Phẫu Thuật Gân Bàn Tay (Tendon Surgery of the Hand)

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Chapter 44:  Molecular Biology of Tendon Healing
binds to the β receptor. Investigations have focused
on the roles of PDGF-BB in tendon healing. Exog­
enous PDGF-BB stimulates collagen, proteogly­
can, and DNA synthesis of the tenocytes.18
Expression of PDGF-BB is increased after tendon
injuries in canine and chicken models.34,37
4. Vascular endothelial growth factor (VEGF).
VEGF has five isoforms (i.e., 121, 145, 165, 189,
and 206) distinguished by their number of amino
acids. Biological effects of these isoforms are
similar. VEGF121 and VEGF165 are the predomi­
nant isoforms secreted by most cells. VEGFs bind
to one of three VEGF receptors (VEGFR 1, 2, and
3) on the cell surface to exert their biologic effects.
The primary role of VEGF is to induce angiogen­
esis, including that in pathological conditions. In
a canine model, VEGF mRNA expression was
increased in healing flexor tendons.17,38,39 VEGF
expression may differ between the cells in endo­
tenon and epitenon at the repair site: 67% of the
cells in the endotenon at the repair site express
VEGF, but 10% of epitenon cells express VEGF.
Direct injection of VEGF increased the healing
strength of Achilles tendon in a rat model.
However, the effectiveness of direct use of VEGF in
synovial tendons has not been tested. We found
that AAV2-VEGF treatment significantly increased
the healing strength of the chicken flexor tendons
at postoperative weeks 3, 4, and 6.
5. Basic fibroblast growth factor (bFGF). bFGF
commonly presents as an 18-kDa, single-chain
polypeptide of 146 amino acids; other forms of
greater molecular weights (22, 22.5, and 24 kDa)
also exist. bFGF has a wide range of biological
effects, including induction of cell proliferation
and migration as well as stimulation of fibroblasts
to produce collagens and collagenase. There have
been several specific investigations of the roles of
bFGF in flexor tendon healing. Duffy and col­
leagues detected presence of bFGF in normal intra­
synovial flexor tendons.16 Chang and colleagues
found that bFGF levels were increased in flexor
tendons and sheath during healing from day 1 to
week 8.12 Tang and colleagues observed that exog­
enous bFGF acts on cultured chicken tenocytes to
accelerate cell proliferation and to promote col­
lagen I gene expression.27,28
Both direct delivery of bFGF and transfer of
bFGF cDNA via appropriate vectors to the healing
tendons have been tested to enhance tendon
healing.31,40-43 Direct delivery of bFGF was achieved
with direct injection of the bFGF,40 use of bFGF-
coated suture,41 or bFGF delivery through con­
trolled release system.42,43 Direct injection of bFGF
did not improve the healing strength of the tendon,
nor did bFGF delivered through controlled release
stage occurs after 10 weeks, and there is an increase in
cross-linking of the collagen fibrils, which makes the
tissue stiffer.
MOLECULAR BIOLOGY OF TENDON HEALING
Roles of Individual Growth Factors
A variety of molecules are involved in tendon healing.36
The roles of six growth factors have been studied associ­
ated with tendon healing in vivo or tenocyte prolifera­
tion in vitro:
1. Transforming growth factor (TGF). This molecule
is secreted by all of cell types participating in the
healing process and plays a role in wound healing
and scar formation. TGF-β has three isoforms: TGF-
β1, TGF-β2, and TGF-β3; they play different roles
in scar formation. While TGF-β1 and -β2 are known
to induce fibrotic changes and scar formation,
TGF-β3 may inhibit scar formation.37 Three iso­
forms are 60% to 80% homologous and are dimers
of 12.5-kDa polypeptides cleaved from larger pre­
cursors after being secreted from the cells into the
ECM. TGF-β is a master mediator in the pathogen­
esis of fibrosis and scar formation. Regarding
specific roles of TGF-β in flexor tendon healing,
Chang and colleagues found increased levels of
TGF-β1 mRNA in the sheath and the tendon itself
after tendon trauma. TGF-β receptors 1, 2, and 3
were upregulated as well. In in vitro studies, TGF-
β1 induced collagen I production by tenocytes.11
Chang and colleagues applied TGF-β1 neutralizing
antibodies to injured digital flexor tendons, and
this therapy increased the range of digital motion
of the toes operated upon in a rabbit model.13
2. Insulin-like growth factor (IGF). It is a single-
chain polypeptide hormone. The primary biologi­
cal action of IGF-1 is mitogenic activity for a broad
range of cells. Extracts from the epitenon and
internal compartment of avian flexor tendons
were found to contain IGF-1; these extracts could
stimulate DNA synthesis by tenocytes.8 In in vitro
culture of tenocytes, IGF-1 was found to increase
cell proliferation as well as stimulate synthesis of
DNA, collagen, and proteoglycan.9 Both IGF-1 and
IGF-2 were shown to promote proliferation of
tenocytes in vitro tenocyte culture.8-10
3. Platelet-derived growth factor (PDGF). PDGF
consists of a group of dimers, each of two chains
(A and B). Various grouping of these chains form
three isoforms (AA, BB, and AB). PDGF acts as a
chemoattractant and mitogen for fibroblasts,
endothelial cells, and smooth muscle cells. The
cell surface contains two kinds of receptors (α and
β) for PDGF binding. In fibroblasts, the β receptor
is predominant. Only the isoform BB of PDGF

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Chapter 44:  Molecular Biology of Tendon Healing
BMP-14 gene therapy increases tendon tensile strength
in a rat model of Achilles tendon injury 2 and 3 weeks
after surgery.
Chhabra and colleagues47 found that GDF-5 defi­
ciency delays Achilles tendon healing in GDF-5 −/−
mice. After injury, these mice took longer to reach peak
cell density and GAG and collagen content in the repair
site compared with normal control littermates. Aspen­
berg and Forslund48 found that implanting GDF-5 and
GDF-6–containing collagen sponge enhanced tendon
healing strength at 2 weeks after surgery in a rat Achilles
tendon model. Other studies also identified that exog­
enous GDFs stimulated healing of the Achilles tendon,
but this response was influenced by loading; without
loading, cartilage and bone formation was initiated.
Roles of Growth Factors and Cytokines
In Vivo
Chen and colleagues investigated the differences in
expression levels of six growth factors in lacerated and
surgically repaired flexor tendon in chicken toes.32 Con­
nective tissue growth factor (CTGF) and TGF-β had high
levels of gene expression in the early healing period
(Figure 44-1). Levels of expression of VEGF and IGF-1
genes were high or moderately high. Expression of the
TGF-β gene was upregulated after injury, whereas the
bFGF gene was downregulated at all time points
observed (Figures 44-1 and 44-2) and expressed at the
lowest levels among six growth factor genes 2 to 3 weeks
after surgery. The PDGF-B gene was minimally expressed
in injured tendon. Findings in immunohistochemical
staining corresponded to TGF-β, bFGF, and IGF-1 gene
expression (see Figure 44-2).
Schulze-Tanzil and colleagues49 reviewed the reports
of cytokines and growth factors on tendon healing and
summarized interrelations known between the interleu­
kin (IL)-1β, transforming growth factor (TNF)-α, IL-6,
and VEGF in tendon to assess their role in tendon
damage and healing. Multiple interrelations between
cytokines and ECM synthesis, catabolic mediators such
as matrix-degrading enzymes, inflammatory and angio­
genic factors (cyclo-oxygenase [COX]-2, prostaglandin
[PG]E2, VEGF, nitric oxide [NO]), and cytoskeleton
assembly are evident. Proinflammatory cytokines affect
ECM homeostasis, accelerate remodeling, amplify bio­
mechanical adaptiveness, and promote tenocyte apop­
tosis. This multifaceted interplay might both contribute
to and interfere with healing, which has relevance for
the development of novel therapeutic strategies.
Extracellular Matrix
Cao and colleagues in our laboratory studied expression
of ECM components from postsurgical day 3 to week
12 in a chicken model. Tendons exhibited drastic upreg­
ulation in the expression of collagens I, III, XII, and XIV
as early as 3 days after injury. After day 3, expression of
system.40,43 After delivery of bFGF to the tendon,
biological reactions and increases in cellular pro­
liferation in the healing tendons were observed,
but mechanically, the healing strength was not
increased.43 Tendon repair with bFGF-coated surgi­
cal suture increased the tendon strength at week 3
after surgery, but not at week 6, in a rabbit model.41
AAV2-bFGF–treated tendons had a significantly
greater breaking strength than the nontreatment
control at weeks 2, 3, and 4 in a chicken model.31
6. Bone morphogenetic proteins (BMPs). BMPs are
a group of growth factors originally discovered by
their ability to induce the formation of bone and
cartilage. BMPs are considered to constitute a
group of pivotal morphogenetic signals, orches­
trating tissue architecture throughout the body.
There are BMPs 1 through 15 in this superfamily.
BMP14 is called growth differentiation factor-5
(GDF-5) as well; this factor was particularly studied
regarding its role in tendon healing and repair.
Hogan and colleagues44 found that growth differ­
entiation factor-5 (GDF-5, or BMP14) regulates
ECM gene expression in murine tendon fibro­
blasts. They isolated mice Achilles tendon fibro­
blasts and treated them with rGDF-5 (0 to 100 ng/
mL) for 0 to 12 days in cell culture. The temporal
effect of rGDF-5 on ECM gene expression was
analyzed for type 1 collagen and aggrecan expres­
sion. They found that expression of extracellular
matrix (ECM) genes procollagen IX, aggrecan,
matrix metalloproteinase 9, and fibromodulin
were upregulated. Proinflammatory reaction genes
were downregulated. rGDF-5 led to an increase
in total DNA, glycosaminoglycan (GAG), and
hydroxyproline (OHP). rGDF-5 treatment showed
improved collagen organization over controls.
No studies have directly investigated expression profile
of BMPs during intrasynovial tendon healing process.
However, studies were performed to determine relation
of BMPs with the healing in rat Achilles tendon. Elias­
son and colleagues45 investigated how mechanical
loading influences the gene expression of the BMP sig­
naling system in intact and healing tendons and how
the BMP signaling system changes during healing. They
studied four BMPs (OP-1/BMP-7, GDF-5/CDMP-1/BMP-
14, GDF-6/CDMP-2/BMP-13, and GDF-7/CDMP-3/
BMP-12), two receptors (BMPR1b and BMPR2), and the
antagonists follistatin and noggin. The Achilles tendon
was transected in rats. Ten tendons were analyzed before
transsection and in the early healing period after surgery.
All genes except noggin were expressed at all time points.
Loading strongly decreased the expression of follistatin.
They concluded that BMPs are involved in tendon
healing, and change after tendon loading. Bolt and col­
leagues46 showed that adenoviral vector–mediated

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Chapter 44:  Molecular Biology of Tendon Healing
during the study period, whereas MMP-3 returned to
normal levels within the first week after injury. TIMP-3
was downregulated in the tendon sheaths. Cathepsin K
was upregulated in tendons and sheaths after injury.
Nerve growth factor (NGF) was present in both tendons
and sheaths, but unaltered. IGF-1 exhibited a late
increase in the tendons, while VEGF was downregulated
at the later time points. They demonstrated the presence
of NGF in flexor tendons and concluded that MMP-13
expression appears to play a more protracted role in
flexor tendon healing than MMP-3. The relatively low
levels of endogenous IGF-1 and VEGF mRNA following
injury support their potential beneficial role as exoge­
nous modulators to optimize tendon healing and
strength without increasing adhesion formation.
Intracellular Signal Pathways
Only the NFκB pathway was investigated in in vitro
tenocytes treated with exogenous bFGF and in in vivo
flexor tendon healing.38,51 Each of the key factors in the
NFκB pathway was found to be activated after exoge­
nous application of bFGF to the tenocytes’ culture
medium. In the healing flexor tendon in a chicken
model, NFκB gene was found to be upregulated.51
TENOCYTE APOPTOSIS DURING
TENDON HEALING
Apoptotic events in the healing digital flexor tendon
have been investigated recently.34,52 Nevertheless, teno­
cyte apoptosis can be an important event in the healing
collagen I declined somewhat but remained at moder­
ately high levels after week 3. The collagen III gene was
upregulated progressively from day 3, with a drastic
increase from week 2 to 5. The fibronectin gene was
upregulated from week 2 to 8. Expression of aggrecan
and fibromodulin genes did not change after tendon
injury.
Matrix metalloproteinases (MMPs) act to modulate
metabolism of tendon healing. They play an important
role in the degradation and remodeling of the ECM.
They break down structural proteins of the ECM. Certain
MMPs, such as MMP-1, -2, -8, -13, and -14, have colla­
genase activity, capable of degrading collagen fibrils. The
activities of the MMPs are inhibited by endogenous
tissue inhibitors of metalloproteinases (TIMPs), a family
of four protease inhibitors (TIMP 1–4). Using the same
chicken model, Cao and colleagues investigated levels of
gene expression of MMPs and TIMPs from the early to
late healing periods in digital flexor tendons. MMP1 of
the tendon was upregulated and remained high in the
first 6 weeks after injury and dropped thereafter. TIMP2
and TIMP3 were downregulated after tendon injury in
the first 6 weeks after injury but were upregulated later.
Berglund and colleagues50 studied molecular events
during flexor tendon healing in a rabbit model of flexor
tendon injury. The mRNA expression for the growth
factors, MMPs, and TIMPs were measured in tendon and
tendon sheath tissue at several time points (3, 6, 21, and
42 days) representing different phases of the healing
process. They found that MMP-13 remained increased
Figure 44-1  Changes in level of expression of six growth factor genes in the early healing period of a chicken FDP tendon
with real-time PCR analysis. Growth factor expression peaked at day 3, and CTGF and TGF-β expressed in the highest level.
(Modified from Chen CH, Cao Y, Wu YF, et al: Tendon healing in vivo: gene expression and production of multiple growth
factors in early tendon healing period, J Hand Surg [Am] 33:1834–1842, 2008.)
0.35
0.3
0.4
0.25
0.2
0.15
0.1
0.05
0
0
3
14
21
9
Levels of gene expression (target/GAPDH)
VEGF
TGF-beta
CTGF
PDGF
bFGF
IGF-1
Time-points of the early healing period (days)
*
*
*
**
**
**
*
*
**

e30
Chapter 44:  Molecular Biology of Tendon Healing
antiapoptotic effects. Apoptosis of tenocytes peaked at
day 3 (see Figure 44-3), which is followed about 10 days
later by the peak proliferation period. At days 14 to 28,
the number of apoptotic cells decreased significantly
compared with days 3 and 7, yet numbers remained
greater than those at day 0. At days 7 to 14, the number
of PCNA-positive cells peaked (see Figure 44-4). At days
7 and 14, the cells positively stained with Bcl-2 peaked.
These findings indicate that tenocyte apoptosis is accel­
erated within several days post-injury, followed by
digital flexor tendon and can affect healing strength.
Investigations of Wu and colleagues have been aimed at
elucidating the relationship between cellular apoptosis
and proliferation in early tendon healing.34 At postop­
erative days 3, 7, 14, 21, and 28, Wu and colleagues
quantitatively analyzed the presence of apoptotic cells
in tendons using an in situ TUNEL assay (Figure 44-3),
and performed immunofluorescence staining with anti­
bodies to proliferating cell nuclear antigen (PCNA) to
assess proliferation (Figure 44-4), and Bcl-2 to assess
Figure 44-2  Immunohistochemical staining of three growth factors in the healing tendons. Great amount of TGF-β is
present in the tendon. Both bFGF and IGF-1 are present in a much lower amount compared with TGF-β. (Modified from
Chen CH, Cao Y, Wu YF, et al: Tendon healing in vivo: gene expression and production of multiple growth factors in early
tendon healing period, J Hand Surg [Am] 33:1834–1842, 2008.)
Day 0
TGF-beta
IGF-1
bFGF
3
5
7
21

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Chapter 44:  Molecular Biology of Tendon Healing
TUNEL assay showed few positive staining cells in the
wound at days 4 and 7. The percentages of TUNEL-
positive fibroblast-like cells showing morphological
characteristics of apoptosis increased sharply and
reached the maximum on day 28 (median, 31.4%). No
fibroblast-like cell was stained at month 6 and the
healed tissue was similar to that in a normal uninjured
tendon. A similar trend was observed with active
caspase-3 immunohistochemistry. They concluded that
an increase in apoptosis at the end of tendon healing
coincided with a decrease in cellularity.
The findings of Skutek and colleagues54 corroborate
that mechanical stretching directly activates intracellular
increases in cellular proliferation and activation of
molecular events to inhibit apoptosis in 2 to 4 weeks.
After 4 weeks, tenocyte proliferation persisted, but at a
rather lower level. Tenocyte apoptosis also declined
drastically (Figures 44-5 and 44-6). In the late healing
period, tenocyte apoptosis persisted, likely in response
to tendon remodeling, while tenocyte proliferation was
minimal or undetectable.52
Lui and colleagues53 found increases in tenocyte
apoptosis at the end of patellar tendon healing. They
investigated the role of apoptosis in cell turnover in a
rat central 1/3 patellar tendon donor site injury model.
The observations were made at days 4, 7, 14, and 28 and
months 2 and 6 after surgery. The total fibroblast-like
cell density in the center of the wound increased from
day 4 and thereafter steadily returned to normal. In situ
Figure 44-3  Tenocyte apoptosis is most obvious at day 3 after tendon laceration. The pictures show the cells with dark
brown nucleus stained with TUNEL are apoptotic cells (A ×200, B ×400). Nearly 50% of the tenocytes in the endotenon are
apoptotic at day 3.
A
B
Figure 44-4  Tenocyte proliferation peak at postsurgical
day 14. The picture shows positive PCNA-stained tenocytes,
which peak in number at day 14 (×200). Positive PCNA
staining indicates proliferation of the cells.
Figure 44-5  Changes of PCNA- and Bcl-2–positively
stained cells (Bcl-2 is an antiapoptotic protein) in the early
tendon healing period in a chicken model. Numbers plotted
in the graph show positively stained cells in the field under
high magnification (×400) over five time-points. (Data from
Wu YF, Chen CH, Cao Y, et al: Molecular events of cellular
apoptosis and proliferation in the early tendon healing
period, J Hand Surg [Am] 35:2–10, 2010.)
40
35
30
25
20
15
10
5
0
0
3
7
14
21
28
Positively-stained cells/field
Days
Bcl 2-positive cells
PCNA-positive cells

e32
Chapter 44:  Molecular Biology of Tendon Healing
of the roles of growth factors and ECM components
during tendon healing process is incomplete. Informa­
tion obtained thus far reflects several instances of genetic
profiling. In the future, effort should be directed to char­
acterizing the molecular events in the in vivo tendon
healing process, under different injury conditions.
Enhancing tendon healing strength and preventing
adhesion formation will continue to be major subjects
of investigation and be at the center of basic science
investigations of tendon repair.
Growth factor–coated suture, controlled-release
system, and gene therapy are appealing approaches to
enhancing flexor tendon healing. Delivery of cells
(including stem cells) and genes critical to the healing
process would ameliorate weakness in healing strength
produced by the paucity of cellular components and
insufficient, or inappropriate, production of growth
factors or ECM. The ideal therapies should not increase
the healing strength at the cost of increasing adhesion
formation. We should be able to control the biological
regulation of tendon healing and avoid any detrimental
effects. A controlled-release system is another way to
provide continuous and controlled supplies of growth
factors, but its effectiveness in improving healing
strength remains to be addressed.
Almost all exogenously applied growth factors are
found to accelerate proliferation of tenocytes to some
extent in vitro. However, our understanding of growth
factor activity in tendon healing is incomplete, and not
all of these growth factors have been characterized as to
their effects on tendon healing in vivo. Further investi­
gations should be able to elucidate the exact roles of
these growth factors in tendon healing.
signaling pathways, which in turn induce apoptosis.
They investigated the response profile of human tendon
fibroblasts in terms of apoptosis in response to cyclic
stretching. They also found that cyclic mechanical
stretching activated stress-activated protein kinase
(SAPK)/Jun N-terminal kinase (JNK).
FUTURE FOR TENDON HEALING BIOLOGY
INVESTIGATION AND APPLICATION
The molecular mechanisms underlying tendon healing
are still poorly understood currently. Our understanding
Figure 44-6  Changes of percentage of PCNA- and
Bcl-2–positively stained cells in the field under high
magnification (×400) in a total population of the cells.
(Data from Wu YF, Chen CH, Cao Y, et al: Molecular events
of cellular apoptosis and proliferation in the early tendon
healing period, J Hand Surg [Am] 35:2–10, 2010.)
50
40
30
20
10
0
0
3
7
14
21
28
Positively-stained cells (%)
Days
Bcl 2-positive cells
PCNA-positive cells
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PDGF-BB for tendon repair: controlled release and biologic
activity by tendon fibroblasts in vitro, Ann Biomed Eng
38:225–234, 2010.
20. Thomopoulos S, Das R, Silva MJ, et al: Enhanced flexor
tendon healing through controlled delivery of PDGF-BB,
J Orthop Res 27:1209–1215, 2009.
21. Khan U, Kakar S, Akali A, et al: Modulation of the formation
of adhesions during the healing of injured tendons, J Bone
Joint Surg (Br) 82:1054–1058, 2000.
22. Akali A, Khan U, Khaw PT, et al: Decrease in adhesion forma­
tion by a single application of 5-fluorouracil after flexor
tendon injury, Plast Reconstr Surg 103:151–158, 1999.
23. Jones ME, Mudera V, Brown RA, et al: The early surface cell
response to flexor tendon injury, J Hand Surg (Am) 28:221–
230, 2003.
24. Wong JK, Cerovac S, Ferguson MW, et al: The cellular effect
of a single interrupted suture on tendon, J Hand Surg (Br)
31:358–367, 2006.
25. Mehta V, Kang Q, Luo J, et al: Characterization of adenovirus-
mediated gene transfer in rabbit flexor tendons, J Hand Surg
(Am) 30:136–141, 2005.
26. Mehta V, Mass D: The use of growth factors on tendon inju­
ries, J Hand Ther 18:87–92, 2005.
27. Tang JB, Xu Y, Ding F, et al: Tendon healing in vitro: promo­
tion of collagen gene expression by bFGF with NF-κB gene
activation, J Hand Surg (Am) 28:215–220, 2003.
28. Tang JB, Xu Y, Wang XT: Tendon healing in vitro: activation of
NIK, IKKα, IKKβ, and NF-κB genes in signal pathway and
proliferation of tenocytes, Plast Reconstr Surg 113:1703–1711,
2004.
29. Wang XT, Liu PY, Tang JB, et al: Tendon healing in vitro:
adeno-associated virus-2 effectively transduces intrasynovial
tenocytes with persistent expression of the transgene, but
other serotypes do not, Plast Reconstr Surg 119:227–234,
2007.
30. Zhu B, Cao Y, Xin KQ, et al: Tissue reactions of adenoviral,
adeno-associated viral, and liposome-plasmid vectors in
tendons and comparison with early-stage healing responses
of injured flexor tendons, J Hand Surg (Am) 31:1652–1660,
2006.
31. Tang JB, Cao Y, Zhu B, et al: Adeno-associated virus-2-medi­
ated bFGF gene transfer to digital flexor tendons significantly
increases healing strength. An in vivo study, J Bone Joint Surg
(Am) 90:1078–1089, 2008.
32. Chen CH, Cao Y, Wu YF, et al: Tendon healing in vivo: gene
expression and production of multiple growth factors in early
tendon healing period, J Hand Surg (Am) 33:1834–1842,
2008.
33. Chen CH, Zhou YL, Wu YF, et al: Effectiveness of microRNA
in down-regulation of TGF-β gene expression in digital flexor
tendons of chickens: in vitro and in vivo study, J Hand Surg
(Am) 34:1777–1784, 2009.

e34
CHAPTER
45 
MOLECULAR METHODS TO
PREVENT ADHESION
FORMATION
Armin Kraus, MD, and James Chang, MD
immediate tendon repair in zone 2 was considered to
be generally possible by a skillful surgeon. Nevertheless,
the results have since remained often less than
satisfactory.
From clinical experience, it can be seen that three
factors (“quality of repair,” “motion” in the sense of
early exercise, and “inflammation”)1 have an impact on
the degree of adhesion formation. While the quality of
a tendon repair is still up to the surgeon, strategies from
the toolbox of molecular medicine are under investiga­
tion to modulate tendon healing on the molecular or
cellular levels, to decrease those inflammatory effects
that are responsible for adhesion formation, and to find
new ways to prevent loss of tendon gliding.
PATHOPHYSIOLOGY
In its healing process, the tendon undergoes three
distinct phases: inflammation, proliferation, and
maturation/remodeling. The inflammatory phase is
characterized by the migration of T-lymphocytes and
phagocytotic cells into synovial sheath and epitenon.
Platelets adherent at the injury site release a variety of
cytokines such as platelet-derived growth factor (PDGF),
transforming growth factor (TGF)-β, or insulin-like
growth factor (IGF) that activate the migrating cells.2
These migrating cells are responsible for phagocytosis
of cell debris and for deposition of a preliminary extra­
cellular matrix.
In the proliferation phase, collagen synthesis and vas­
cularization are enhanced.3 The remodeling phase is
characterized by rearrangement and organization of col­
lagen fibers.4 At this state, adhesions become more
apparent.
In contrast to many other tissues, there are two dif­
ferent mechanisms involved in tendon healing: the
extrinsic and the intrinsic pathway. In extrinsic healing,
extracellular matrix producing cells are invading the lac­
erated tendon from its periphery. This pathway described
by Potenza and colleagues5 was for some time consid­
ered to be the prevailing and maybe only mechanism
of healing in a lacerated tendon.
OUTLINE
Tendon adhesions are a significant problem, especially
after repair in zone 2. Tendon healing undergoes three
different phases—inflammation, proliferation, and
maturation—which can all be altered to reduce adhe­
sions. Intrinsic healing without contact to surrounding
tissue and therefore low adhesive potential can be
distinguished from extrinsic healing, where cell inva­
sion and vascularization take place from the surround­
ing with concomitant adhesions. Motion has shown
to decrease adhesions by mechanical disruption of
adhesions and by molecular alteration of tendon cells.
Artificial tendon grafts can be seeded with cells to form
an epitenon layer that could enhance gliding. Adding
or blocking various cytokines can reduce adhesion for­
mation, but cytokine interaction has shown to be
complex. Gene transfer or RNA interference are further
methods under investigation. Mesenchymal stem cells
have anti-inflammatory effects and may have the
potential to differentiate into a tenocyte-like pheno­
type, so that they could contribute to adhesion free
tendon healing. Despite promising results in the field
of molecular research, many of these insights remain
to be translated into clinical application.
CLINICAL SIGNIFICANCE
In the repair of flexor tendons, hand surgeons attempt
to achieve two main goals: stability of the repair and
gliding of the tendon. The problem of adhesion forma­
tion has been a challenge since the beginning of the
20th century. Initially this lead to the concept of a “no
man’s land” in the area of zone 2, a zone were primary
tendon repair was not indicated. As the tendon is gliding
through a tight fibro-osseus canal in this area, the likeli­
hood of adhesion formation was considered so high
that no direct tendon repair was recommended. As a
secondary procedure, tendon continuity was restored by
grafting. With the advent of more sophisticated suture
materials and surgical techniques and particularly with
more aggressive methods of early mobilization, an
This chapter does not appear in the print edition.

e35
Chapter 45:  Molecular Methods to Prevent Adhesion Formation
showed a reduction of adhesions at the plantar site, but
mild to moderate adhesions both at the ends of the
sheaths and at the plantar contact site to the bone. Ishi­
yama and colleagues reported a phospholipid polymer
hydrogel to effectively prevent adhesion formation in a
rat and in a chicken model.10 They explained this by a
microstructure with a pore size less than 8 to 10 µm that
is capable of preventing extrinsic inflammatory cells
from getting into contact with the tendon surface but
allowing the passage of cytokines and growth factors
required for healing. Tenenhaus and colleagues11
claimed a similar mechanism to be active in adhesion
prevention when they wrapped tendon repair sites with
a collagen-GAG membrane (Integra) in a chicken model.
This material has been used particularly in burn surgery
and is known to possess good biocompatibility.
Motion
From clinical experience, it is known that early active
motion treatment helps to prevent adhesion formation
after tendon repair. Various explanations for this obser­
vation can be conceived. First, it might be due to
mechanical reasons that newly forming adhesions are
interrupted by motion. Recent research, however, has
also shown an effect of motion on a molecular level.
Strain and shear forces can be exerted onto cultured cells
by using a cell bioreactor, which is simulating the condi­
tions of motion.12 By exercising mechanical shear stress
on tenocytes in vitro (Figure 45-1), Fong and colleagues
showed an “antifibrotic” gene expression pattern—that
is, an upregulation of matrix-metalloproteinases and
a downregulation of collagen I and III as well as of
TGF-β.13 Not only cells in culture but also cell-seeded
grafts made from acellularized cadaver tendons can be
treated by mechanical force before implantation. Ange­
lidis and colleagues used a cell bioreactor to exert a
cyclic load of 1.25N on cell-seeded tendon scaffolds
Lundborg and others, however, have shown that
tendon healing is also possible independent from the
adjacent tissue. When a sutured tendon was kept inside
the knee joint space of a rabbit without contact to a
tendon sheath or other connective tissue surfaces, the
tendon healed without forming adhesions. This intrin­
sic healing process allows a restitution of tendon conti­
nuity by cells out of the epitenon and endotenon
without forming adhesions to its surrounding.6
McGrouther and colleagues showed in vitro that the
extrinsic pathway naturally is the more active one and
starts to be active at an earlier time-point.7 This means
that tendon healing naturally tends toward forming
adhesions and that a therapeutic approach should aim
at enhancing the intrinsic pathway and suppressing the
extrinsic.
TREATMENT
Quantification of Tendon Adhesions
Measurement of the degree of adhesion formation is
mainly semiquantitative. In addition to macroscopic
observation, investigators use either biomechanical
testing or image analysis of histologic sections to quan­
tify the degree of adhesions. Biomechanical testing is
also dependent on factors such as joint stiffness. Histol­
ogy is dependent on section location and direction and
cannot quantify the rigidity of adhesions. Therefore, the
ideal measurement for the quantitative analysis of adhe­
sion formation remains elusive.
Conventional Pharmacological Treatment
Before the era of molecular medicine, various pharma­
cological agents have been investigated. Local and sys­
temic steroids, nonsteroidal anti-inflammatory drugs,
hyaluronic acid, 5-fluorouracil, and others have been
used. However, none of these substances have been suit­
able for routine clinical use. Lubricin, a mucinous gly­
coprotein responsible for the boundary lubrication of
articular cartilage, has been used to prevent adhesion
formation in a canine model of tendon repair.8 The
application of this substance led to a decreased adhe­
sion formation, although it is at the expense of repair
strength. Clinical value of this agent therefore is yet to
be elucidated.
Biomaterials to Prevent Adhesion Formation
As described earlier, the majority of adhesion formation
is considered to be caused by extrinsic rather than by
intrinsic healing. Therefore, attempts with blocking
materials and membranes have been made to prevent
adhesion formation caused by the exterior. Before the
area of molecular treatment, attempts have been made
to use materials such as silicone or gelatin sponge. Using
hydroxyapatite or alumina sheaths for covering a tendon
suture site in the chicken model,9 Siddiqi and colleagues
Figure 45-1  Tenocytes may be exposed to shear forces
induced by a cone viscometer to simulate tendon motion in
vitro. An “antifibrotic” gene expression pattern can thereby
be obtained.
Tissue culture plate
Tenocytes
0.5°
Rotating cone

e36
Chapter 45:  Molecular Methods to Prevent Adhesion Formation
susceptible to adhesion formation. Furthermore, the
function of artificial grafting materials has been poor.
On the other hand, the use of allografts or xenografts is
limited due to immunological reasons, as these anti­
genic stimuli generally lead to excessive fibrosis, a fact
that is most detrimental in the gliding region of zone
2.14 Acellularization of cadaver tendons could be a way
to obtain a nonimmunogenic scaffold for tendon repair
with the right mechanical properties. Zhang and col­
leagues acellularized rabbit tendons by treating them
with trypsine/EDTA + Triton-X solution.15 These acel­
lularized scaffolds could be repopulated with epitenon
and endotenon cells. Reseeding the acellularized
tendons with tenocytes has been shown to improve
their biomechanical properties, mainly ultimate tensile
strength and elastic modulus.16 It may be speculated
that the newly formed epitenon layer (Figure 45-2) can
also inhibit adhesion formation, which has to be proved
in further preclinical studies.
for 5 days. Subsequent biomechanical testing showed
higher tensile strength of the bioreactor-treated tendons
compared to untreated controls. Moreover, the seeded
cells (adipoderived stem cells and skin fibroblasts)
showed an orientation parallel to the direction of force
on the scaffold. Further studies will have to show
whether this orientation also helps to prevent adhesion
with the surroundings.
The concept of mimicking the molecular events
induced by motion stress seems appealing, as this could
increase repair strength, decrease the formation of adhe­
sions, and minimize the risk of dehiscence caused by
motion therapy.
Prevention of Adhesions in Tendon Grafting
The formation of adhesions is an even greater problem
in tendon grafting than it is in tendon repair. Com­
monly used grafts such as the palmaris longus tendon
lack an extrasynovial sheath and are therefore highly
Figure 45-2  Acellularized tendon scaffolds seeded with various cell types after 6 weeks in vivo. A, Epitenon tenocytes.
B, Sheath fibroblasts. C, Bone marrow–derived MSCs. D, Adipocyte-derived stem cells. Note preservation of collagen
framework, single epitenon-like layer on surface (individual cells indicated by black arrows), and distribution of endotenon-like
cells in center of grafts (individual cells indicated by white arrows).
A
B
C
D

e37
Chapter 45:  Molecular Methods to Prevent Adhesion Formation
Insulin-Like Growth Factor
IGF is a cytokine also of interest in the process of tendon
healing. It has been shown to posses anti-inflammatory
properties19 and to increase the production of collagen
and proteoglycan as well as DNA synthesis in flexor
tendon specimens in vitro.20 However, the ultimate
proof of whether IGF is effective in preventing intrasy­
novial tendon adhesions is yet to be determined.
Transforming Growth Factor-β
TGF-β is a cytokine that is related to various processes
in wound healing. Because TGF-β was upregulated espe­
cially in the inflammatory cells of the tendon sheath,21
this cytokine has become a target in the effort to prevent
adhesion formation.
By using mannose-6-phosphate as an inhibitor of
TGF-β production in an in vivo model of tendon repair
in rabbits, Bates and colleagues could achieve a signifi­
cantly improved range of motion in the operated digits
(Figure 45-4).22 Similarly, mannose-6-phosphate has
been shown to be effective in blocking TGF-β–induced
production of collagen I in tenocytes in vitro.23 Because
mannose-6-phsophate is nontoxic, nonimmunogenic,
and easy to produce, it will be an interesting agent for
future clinical applications.
In the intracellular pathway triggered by TGF-β, the
Smad proteins play a vital role. Katzel and colleagues
showed decreased scarring after FPL repair in Smad3-
deficient mice.24 By using a blocking agent of the Smad
pathway, likewise, Au and colleagues found diminished
connective tissue deposition and a decreased number of
myofibroblasts in rat skin wound healing.25
Smad 2 and 3 are phosporylated by TGF-β receptors
while Smad 1, 5, and 8 are phosphorylated by bone
Cytokines
As a variety of cytokines are active in the process of
tendon healing (Figure 45-3), blocking the “proadhe­
sion” and substituting the “antiadhesion” ones could be
a powerful strategy in preventing tendon adhesions.
However, there are several obstacles to overcome before
this approach will come to fruition. The number of pos­
sible cytokines involved is large, and there may be
several cytokines that are still unidentified. Second, the
above classification into “proadhesion” and “antiadhe­
sion” is overly simplified. A cytokine may perform con­
tradictory effects depending on the time and location of
its activity. The exact regulation of cytokine secretion
and activation is regulated by various paracrine feed­
back loops that will be very difficult to simulate. Never­
theless, promising results already have been obtained
when certain cytokines were either substituted or
blocked.
Platelet-Derived Growth Factor and
Fibroblast Growth Factor
By exogenous application of the cytokines PDGF-BB
and bFGF, Gelberman and colleagues have shown an
increased expression of lubricin and hyaluronic acid,
which promote gliding.17 By local administration of
PDGF to a tendon repair site in a canine model, the
same group showed an increase in cell proliferation and
matrix maturation without an increase of adhesion
formation.18
Figure 45-3  Although the interaction of cytokines is highly
complex, each cytokine is supposed to make a major
contribution to one or several certain aspects of tendon
healing in the three distinct phases.
INFLAMMATORY
PROLIFERATIVE
FLEXOR TENDON WOUND HEALING CASCADE
REMODELING
Neutrophil and
macrophage
chemotaxis

PDGF
TGF-β
Angiogenesis

VEGF
bFGF
PDGF
Cell proliferation

IGF-1
bFGF
PDGF
Collagen synthesis and
extracellular matrix deposition

TGF-β
bFGF
PDGF
Collagen
reorganization
Figure 45-4  Range of motion of rabbit forepaws treated
with the TGF-β antagonists decorin and mannose-6-
phosphate (M6P). Significant improvement (*) was achieved
by local administration of low-dose M6P (1 mg/100 µL).
RANGE OF MOTION
Control
Low-dose Decorin
High-dose Decorin
Low-dose M6P
High-dose M6P
1
*p <0.05
*
Range of motion (degrees)
40
35
30
25
20
15
10
5
0

e38
Chapter 45:  Molecular Methods to Prevent Adhesion Formation
of medical research where gene silencing offers promise,
such as in HIV therapy, cancer treatment, or the therapy
of neurological disorders, protective treatment against
tendon adhesion by gene silencing may be possible.
Because the site of tendon repair is easy to access, selec­
tive local administration could rule out systemic adverse
events. By coupling silencing RNA with target-selective
carriers such as ligand-coated nanoparticles, an even
more specific way of delivering the agent to its domain
could be provided. Adverse effects of silencing RNAs
such as unspecific downregulation of genes and compe­
tition with endogenous silencing RNAs36 are still to be
overcome. Unlike in chronic diseases that would require
lifelong administration of RNA interference, short-term
treatment during the period of tendon healing should
be more easily tolerated.
Stem Cells
With the knowledge that scarless healing is possible
in the fetal stage,37 one might conceive that stem cell
mechanisms are a key to adhesion free tendon healing.
From embryonic stem cells, pluripotent cells that
can renew indefinitely in vitro can be derived. These
cells are capable of differentiation into tissues of all
three germ lines. The use of donor embryonic stem
cells raises various ethical concerns in humans and
involves the drawback of immune rejection by the
recipient.
Recent research has shown that somatic cells can also
be altered to become pluripotent. These cells are called
“induced pluripotent stem cells” (iPS). Takahashi and
colleagues transfected adult human fibroblasts with the
developmental genes Oct3/4, Sox2, Klf4, and c-Myc and
could thereby successfully transform these cells into a
phenotype that was similar to embryonic stem cells in
morphology, proliferation, surface antigen profile, gene
expression, epigenetic status of pluripotent cell-specific
genes, and telomerase activity.38 Theoretically, this
method could produce a self-renewing cell for every
individual with a capacity to transform into every
favored tissue type without the problem of immune
rejection. Thus, tendon healing free of scars and there­
fore free of adhesions may be conceived in the future as
this technology is further developed.
Despite these groundbreaking achievements, various
obstacles are still to be overcome before clinical use of
this technology is possible. When retroviral transfection
is used, this will yield high efficiency but contains the
risk of tumorigenesis as the viral genome is incorpo­
rated into the genome of the host cell. This problem
could be overcome by modern vectors completely
devoid of prokaryotic elements such as plasmids or
linear dumbbell-shaped expression cassettes, as their
integration rate into the host genome is far below the
spontaneous mutation rate.39 Furthermore, iPS seem to
be highly susceptible for tumor induction themselves.
morphogenetic protein (BMP) receptors and mediate
BMP signals.26 The group of BMPs is characterized by
high complexity of their signaling functions. BMP-12 is
known to play a role in the differentiation of stem cells
into tenogenic cells.27 It further has been shown to
increase proliferation of tenocytes and the production
of procollagen I and III and to decrease the production
of decorin.28 A role in the formation of adhesions there­
fore is likely for BMP-12, but the exact mechanisms are
yet to be elucidated.
Vascular Endothelial Growth Factor
There is evidence from in vivo studies that tendon
healing is possible without vascularization, but just by
mere diffusion.29 If neovascularization should contrib­
ute to adhesion-free tendon healing, it would have to
occur from intratendinous vessels. Gelberman and col­
leagues have shown that this type of neovascularization
takes place in a canine model of tendon repair.30 New
blood vessels were formed in tendon regions during the
healing process that were previously avascular. However,
vascular endothelial growth factor (VEGF), a cytokine
playing a role in angiogenesis, has not been found to
improve tendon vascularity and adhesion prevention
yet. In an in vitro model, VEGF gene transfer led to an
increase in TGF-β production, which was related to
increased adhesion formation.31 The authors concluded
that VEGF was not a critical factor to substitute in order
to promote tendon strength or to decrease adhesion
formation.
Epidermal Growth Factor
Epidermal growth factor (EGF) is another cytokine that
plays a role in tendon healing. It has been shown to be
present not in tenocytes but in migrating inflammatory
cells during the healing process.32 Another study showed
EGF to have a stimulatory effect on tenoblast migration
in culture.33 Further studies must elucidate whether EGF
would increase or decrease adhesion formation in zone
2 tendon repair.
Gene Silencing
In addition to blocking the effect of a cytokine by an
antagonist protein or natural inhibitor, blocking the
gene expression of an adhesion-causing protein such as
TGF-β is another strategy. The use of micro-RNA
(miRNA) or small interfering RNA (siRNA) is a method
to silence gene expression.34 miRNA typically consists of
single-stranded RNA at a length of 19 to 25 nucleotides
that binds to a corresponding sequence of messenger
RNA and inhibits the translation of the respective
protein. siRNA binds to complementary RNA and leads
to degradation of this complex by endonuclease cleav­
age. Chen and colleagues showed an effective decrease
in TGF-β production using miRNA directed against
TGF-β RNA both in vitro and in vivo.35 As in other fields

e39
Chapter 45:  Molecular Methods to Prevent Adhesion Formation
Despite these difficulties, recent studies on nonhu­
man cells give promising evidence that a tenogenic dif­
ferentiation of mesenchymal stem cells toward tenocytes
may be achieved. In vitro studies in animal models have
shown the expression of the tenogenic genes decorin and
tenomodulin, Collagen Ia1, six1, six2, scleraxis, eya1, and
EphA4 after exogenous exposure to BMP-12.47 After
BMP-12 gene transfer, an upregulation of collagen type
I and scleraxis in rhesus monkey MSCs could be shown.27
There is also some evidence that interaction with teno­
cytes could induce mesenchymal stem cells toward a
tenogenic line. Luo and colleagues co-cultured rat bone
marrow MSCs and tenocytes in an indirect co-culture
system that allowed passage of soluble factors.48 They
noted an increased expression of the tendon-related
genes collagen I, collagen III, tenascin C, and scleraxis
compared to the control group. This gives evidence that
no direct cell contact is needed for tenogenic differentia­
tion of MSCs. The soluble factors that play the key role
in this process remain to be identified.
Further evidence is required to prove whether these
differentiated cells will be able to overtake the relevant
functions of tenocytes at a site of tendon repair and
contribute to scarless and adhesion-free healing.
Gene Therapy
Gene therapy is a strategy that may deliver the cytokine
genes to the tendon repair site. For the insertion of genes
into a recipient cell, nonviral and viral vectors are avail­
able. Nonviral gene transfer includes chemical methods
such as lipofection and physical methods such as elec­
troporation, microbubble-enhanced ultrasound, ballis­
tic delivery (“particle gun”), magnetofection, and laser
poration.
Nonviral methods are nonpathogenic but have lower
efficiency than viral methods. Furthermore, chemical
nonviral vectors may be toxic, and physical manipula­
tion may be harmful to the cells. On the other hand,
viral vectors are more efficient but have the potential
risk of immunogenicity and of causing genetic muta­
tions in the host cell. Various attempts of gene transfer
to tendons have been made. Nakamura and colleagues
successfully transferred the PDGF gene into rat tendons
in a liposome-mediated manner.49 Despite a transfec­
tion rate of only 2%, there was enhanced angiogenesis
and collagen I synthesis over a period of 4 weeks. As this
was not a model of intrasynovial tendon repair, further
studies will have to show whether PDGF is a suitable
cytokine to prevent adhesion formation in such a
setting. In another model of extrasynovial tendon
healing (gap formation in the medial collateral liga­
ment of the rabbit, no suture), the same group admin­
istered
antisense-oligonucleotide
against
decorin
mRNA.50 They noted a higher abundance of larger col­
lagen fibrils, higher tensile strength, and better biome­
chanical properties compared to the control group.
In Takahashi and colleagues’ experiments, subcutane­
ous implantation of iPS into mice lead to teratoma
formation in 25% of the cases.
Conversely, multipotent adult stem cells do not raise
the same ethical concerns as do embryonal stem cells,
immunogenic reactions can be avoided by taking the
cells from the recipient individual, and their teratoge­
nous potential seems to be far lower than that of embry­
onal stem cells.40 Mesenchymal stem cells (MSCs) were
initially derived from the bone marrow, but that method
of harvest is a major procedure. Adipocyte-derived stem
cells are an interesting alternative as they are abundant
in adipose tissue and are easier to harvest by
liposuction.
MSCs have been successfully used in various disor­
ders such as myocardial infarction, meniscus repair, or
treatment of spinal cord injury. Concerning their use in
tendon healing, MSCs exert two main functions that can
be important for adhesion free healing.
First, stem cells are known to possess immunosup­
pressive capabilities.41 Their ability of homing at a site
of inflammation by chemotaxis toward inflammatory
cytokines makes them particularly suitable for suppres­
sion of local inflammatory processes. Initially, MSCs
are activated by immune cells that are secreting pro­
inflammatory cytokines such as interferon (IFN)-γ,
tumor necrosis factor (TNF)α, interleukin (IL)-1α, or
IL-1β.42 Subsequently, MSCs produce soluble mediators
such as nitric oxide, prostaglandin E2, indoleamine
2,3-dioxygenase, IL-6, and human leukocyte antigen
(HLA)-G. These mediators have an influence on a variety
of immune cells. Particularly, regulatory T cells are
induced and dendritic cells are directed toward an anti-
inflammatory phenotype.
Second, MSCs are known to be able to differentiate
into various cell lines—bone, cartilage, muscle, bone
marrow stroma cells, adipose tissue, and connective
tissue. A differentiation of MSCs toward mature teno­
cytes could therefore be conceived. Characterization of
the mature tenocyte phenotype is difficult, as a defini­
tive marker is missing. Various markers have been pro­
posed by different groups, such as collagen I, collagen
III, tenascin C, tenomodulin, scleraxis, decorin, aggre­
can, elastin, thrombospondin 4, thrombospondin 5
(also called cartilage oligomeric matrix protein, COMP),
and others.43 Scleraxis, a basic helix-loop-helix tran­
scription factor, is regarded to be highly specific for
tenocytes by some authors44,45 and is thought to regulate
the expression of tenomodulin, a transmembrane gly­
coprotein with an antiangiogenetic C-terminal domain.
However, scleraxis also has been detected in other cell
types such as osteocytes and chondrocytes.43 Tenascin is
an extracellular matrix protein that is highly expessed in
musculoskeletal tissues mainly during regenerative and
healing processes.46 It is upregulated by mechanical
strain but is also not exclusively tendon specific.

e40
Chapter 45:  Molecular Methods to Prevent Adhesion Formation
inflammation and fibrosis. Embryonal stem cells have
the ability to promote scarless wound healing, but their
utilization is limited by ethical concerns, the potential
of tumorigenesis and various technical difficulties. MSCs,
on the other hand, could be harvested from the potential
recipients themselves in large amounts. They could con­
tribute to adhesion-free tendon healing by their capaci­
ties of homing and their potential ability to differentiate
into a tenogenic phenotype. Furthermore, they possess
immunosuppressive and anti-inflammatory properties,
which could be useful in adhesion prevention.
Despite the great potential that these molecular strat­
egies have to offer, they yet have to be tested in routine
clinical use. Research at the interface of surgery and
molecular biology will bring further insights into the
pivotal mechanisms of adhesion formation. Together
with sound surgical technique, surgeons will hopefully
be able to restore full finger motion in the area once
considered to be the “no man’s land.”
CONCLUSIONS
The repair of flexor tendons that is free of adhesions in
zone 2 of the hand is a very complex problem. Various
efforts have been made in the past with pharmacologi­
cal agents, mainly to reduce inflammation, and with
physical barriers to reduce adhesion formation. More
recent attempts have used various cytokines with prom­
ising results. The blockade of TGF-β seems to effectively
reduce adhesion formation in the experimental setting.
For more specific cytokine delivery, genetic modification
strategies at a tendon repair site are possible, but obsta­
cles such as vector toxicity, low transfection efficiency,
unstable transfection, and the possibility of mutagene­
sis remain to be overcome.
To solve the problem of adhesion formation after
tendon grafting, seeding of a graft with recipient cells
could prevent adhesion formation by providing a gliding
layer and by reducing immune response with subsequent
References
1. Potenza AD: Critical evaluation of flexor-tendon healing and
adhesion formation within artificial digital sheaths, J Bone
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2. Gelberman RH, Vandeberg JS, Manske PR, et al: The early
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4. Lane JM, Black J, Bora FW Jr: Gliding function following
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14. Wojciak B, Crossan JF: The accumulation of inflammatory
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108–114, 1993.
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17. Thomopoulos S, Das R, Sakiyama-Elbert S, et al: bFGF and
PDGF-BB for tendon repair: controlled release and biologic
activity by tendon fibroblasts in vitro, Ann Biomed Eng
38:225–234, 2010.
18. Thomopoulos S, Zaegel M, Das R, et al: PDGF-BB released
in tendon repair using a novel delivery system promotes
cell proliferation and collagen remodeling, J Orthop Res 25:
1358–1368, 2007.
19. Kurtz CA, Loebig TG, Anderson DD, et al: Insulin-like
growth factor I accelerates functional recovery from Achilles
tendon injury in a rat model, Am J Sports Med 27:363–369,
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20. Abrahamsson SO, Lohmander S: Differential effects of
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14:370–376, 1996.
21. Chang J, Most D, Stelnicki E, et al: Gene expression of trans­
forming growth factor beta-1 in rabbit zone II flexor tendon
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Reconstr Surg 100:937–944, 1997.
22. Bates SJ, Morrow E, Zhang AY, et al: Mannose-6-phosphate,
an inhibitor of transforming growth factor-beta, improves
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(Am) 88:2465–2472, 2006.
23. Xia CS, Yang XY, Yingzhen W, et al: Inhibition of TGF-beta-
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40. Momin EN, Vela G, Zaidi HA, et al: The oncogenic potential
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tions for future research, Curr Immunol Rev 6:137–148, 2010.
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43. Pauly S, Klatte F, Strobel C, et al: Characterization of tendon
cell cultures of the human rotator cuff, Eur Cell Mater 20:84–
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44. Schweitzer R, Chyung JH, Murtaugh LC, et al: Analysis of the
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and ligaments, Development 128:3855–3866, 2001.
45. Shukunami C, Takimoto A, Oro M, et al: Scleraxis positively
regulates the expression of tenomodulin, a differentiation
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49. Nakamura N, Shino K, Natsuume T, et al: Early biological
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50. Nakamura N, Hart DA, Boorman RS, et al: Decorin antisense
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(BMP) 12 gene transfer, J Biosci Bioeng 100:418–422, 2005.
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1180, 2010.

e42
CHAPTER
46 
TENDON REPAIRS IN
REPLANTATION SURGERY
Ren Guo Xie, MD, Jun Tan, MD, and Jin Bo Tang, MD
46-5). In our unit, we use a cruciate or an U-shaped
four-strand repairs (Figures 46-5 and 46-6). We do not
repair the FDS tendon. The FDS tendons are excised,
because it is not possible to obtain good gliding and
prevent adhesions after injuries to multiple tissues
including bones involved in digital amputation. During
surgery, we attempt to preserve the annular pulleys and
synovial sheath as much as possible. Frequently, we
incise or left open the sheath around the area of digital
amputation. It is not possible to perform complicated
pulley reconstruction during the replantation surgery, as
this is not possible and lengthen the surgery. It is a
practical way to leave completely disrupted annular
pulleys open without surgical repair or reconstruction.
It is not infrequent that we see that the A2 pulley is
almost entirely damaged by the trauma, or is signifi­
cantly shortened during surgery. In the case of thumb
amputation, the FPL tendon must be repaired.
As for extensor tendon repair, shortening of the digits
has great impact on function of extensors. We usually
manage to repair the extensor tendon with running con­
tinuous or locked running stitches or figure-of-eight
suture. When phalanges are shortened, extensor tendons
can be sutured with some overlapping of the cut
portions.
Postoperative Care
To avoid disturbance to vascular circulation and ensure
stable fixation of phalanges, replanted digits do not
undergo early mobilization. For the first 3 or 4 weeks,
the reattached digits are immobilized. After 3 or 4
weeks, the patients can be instructed to perform light
passive motion of the digits. Active motion of the fingers
can be started from 4 or 5 weeks (or even later) after
surgery. Therapies should be given to lessen digital
edema and improve digital circulation when the digit
motion starts.
Outcomes
Recovery of active range of finger motion after digital
replantation is generally poor. Many replanted digits
have only limited active flexion. The specific reports that
discussed digital motion range after digital replantation
Tendon injuries are an integral part of complex tissue
injuries involved in the digital and forearm amputation.
Recovery of active movement of the hand and wrist after
replantation of digits or forearm depends on ample
tendon gliding. Tendon injuries in the amputation can
present as tidy cut or avulsion injuries of the tendons,
caused by knife or machine cuts, or by crush avulsion
injuries, respectively. Loss of a segment of bones or a
part of soft tissues in the trauma area is very common.
After patients are brought into the hospital, the
patients should be thoroughly evaluated regarding the
conditions of entire body and degrees of tissue loss or
contusion locally. The wound should be carefully
assessed about severity of contamination and potential
of infection.
SURGERIES AND TENDON REPAIRS
Digital Replantation
Surgery
Digital amputation after clean-cut injuries does not
have loss of tendon substance (Figure 46-1), but the
level of tendon cut may not be the same as those in the
tendons, particularly the flexor tendon. The proximal
tendon ends retracted to the proximal phalanx or the
palm. During crush and avulsion injuries, both flexor
and extensor tendons can be avulsed from more proxi­
mal parts of the tendon (Figures 46-2 and 46-3). Addi­
tional incisions are needed to find the proximal ends
and do end-to-end repair. In the thumb, both flexor
pollicis longus (FPL) and extensor pollicis longus (EPL)
tendons are usually cut without loss of tendon sub­
stance (Figure 46-4), and tendon avulsion from the
thumb is also sometimes seen. Surgical priority should
be given first to the bony fixation and re-establishment
of vascular circulation. Ideally, tendons are repaired in
all the cases. During replantation surgery, though slightly
shortening of phalanges are necessary, tendons do not
usually require shortening. Trimming the rugged tendon
ends is required, which usually only produces about
0.5 cm shortening of the tendon substance.
Both 2-strand Kessler and cruciate repair methods are
now used popularly for flexor tendon repair (Figure
This chapter does not appear in the print edition.

e43
Chapter 46:  Tendon Repairs in Replantation Surgery
are rare. In our experience, we observed total range of
active motion of the distal and proximal interphalan­
geal (DIP and PIP, respectively) joints of about 60° to
80° degrees of digital flexion. These degrees of motion
in IP joints provide the hand with rather practical func­
tion for making a light grip or picking up. Powerful grip
is usually not possible and making a full fist is rarely
achievable. Joint stiffness occurs to a great percentage of
the replanted digits. In our unit, we note varied degrees
of finger joint stiffness (i.e., limitations in passive digital
motion) in almost all the cases. Limitations of digital
motion and function are actually due largely to the loss
of passive digital motion range, rather than impaired
tendon function.
A few reports indicated effectiveness of tenolysis after
digital replantation. In 1989, Jupiter and colleagues
reported 37 replanted digital units and four thumb
replantations with a flexor tendon tenolysis at an average
of 10 months after replantation.1 The results were
assessed by measuring total active range of motion
(TAM), potential active motion, and by the Strickland
criteria. The TAM increased from a mean pretenolysis of
72° to 130°. The potential active motion increased from
a mean of 43% to 70% after tenolysis. Both of these
improvements were statistically significant. By Strick­
land criteria, 13 digits were rated excellent, 11 good, 6
fair, and 11 poor. The thumbs had two fair results and
two poor results. Poor results were also seen in crush or
avulsion amputations, hands with more than two digits
amputated, and those requiring a PIP joint capsulotomy.
Complications included tendon rupture and infection.
The results support flexor tendon tenolysis after replan­
tation of fingers but not replanted thumbs.
Ross and colleagues (2003) specifically reported
the tendon function after digital replantation.2 They
Figure 46-1  A clean-cut total amputation through the
middle phalanx of the index finger, presenting an ideal
indication for repair of the flexor and extensor tendons. In
this kind of tidy digital amputation, the phalanx was not
shortened, and flexor and extensor tendons were repaired
in the same way as usually do for clean-cuts of flexor or
extensor tendons.
A
B
Figure 46-2  A crush-avulsion amputation of the index
finger.
Figure 46-3  Both the flexor and extensor tendons were
pulled out after disruption at the palm and wrist levels. The
tendons were repaired through additional incision in the
palm and wrist.

e44
Chapter 46:  Tendon Repairs in Replantation Surgery
injury. TAM values were not affected by age, type of
bone fixation, number of arteries repaired, or number
of digits injured. Digits with both the FDP and FDS
tendons repaired had significantly better TAM values
relative to one-tendon fingers. Similarly, fingers treated
with an “early” mobilization regimen also exhibited
better movement.
Secondary Tenolysis
Tenolysis is indicated for the patients who have suffi­
ciently ample passive motion of the digits but whose
degrees of active digital flexion are markedly smaller.
retrospectively reviewed 48 patients (103 digital rays)
who underwent replantation. Average TAM (sum of the
DIP, PIP, and MCP joints) for all digits was 129°. Zone
1 and zone 5 injuries had better TAM than injuries in
zones 2, 3, and 4, which had TAM values not signifi­
cantly different from one another. Avulsion injuries
fared significantly worse than other mechanisms of
Figure 46-4  A, Thumb amputation distal to the IP joint.
B and C, Both FPL and EPL tendons were repaired directly
and the replanted thumb has good cosmetic appearance
and function after surgery.
A
B
C
Figure 46-5  Two methods often used in flexor tendon
repair during replantation surgery. A, Two-strand modified
Kessler repair. B, Four-strand cruciate repair.
A
B
Figure 46-6  A four-stand repair method, i.e., the U-shaped
repair, the senior author developed using a looped suture.
A–C, Method of repair is shown. This is used to repair the
FDP tendon during replantation.
A
B
C

e45
Chapter 46:  Tendon Repairs in Replantation Surgery
lead to amputation through palm. At this level, the
amputation involves multiple flexor and extensor
tendons, and intrinsic muscles. Chances of infection
increase in palm amputation. Thorough irrigation and
débridement are important. Similarly, surgical priority
should be given to stable fixation of the metacarpal
bones and reestablishment of vascular circulation.
Both core and peripheral repairs are used for flexor
tendons, but for extensor tendons, a running or cross-
stitch suture of sufficient suture purchase or a core
suture (mostly two-strand repair) should be used.
Peripheral sutures can be loosely added for flexor
tendons. This is less important in the palm area than in
the digital area, because this area accommodate more
space for the bulky repair site. Strength of the flexor
tendon remains important; we recommend four-strand
repair made with 4-0 or 3-0 sutures rather than two-
strand repair in the flexor tendons of the palm. Using a
looped suture or a system with one needling leading
two suture strands greatly simplify the surgery and
reduce operation time. In our unit, we also use a cruciate
four-strand repair. The FDS tendons are excised and
not repaired; some surgeons attempt to repair one or
two FDS tendons in the palm, which is also a feasible
option. Palm amputation may not involve a FPL tendon
cut. If the FPL tendon is lacerated, the FPL must be
repaired.
Postoperative Care
After surgery, the hand is placed in protective cast with
the wrist in slight extension and the MCP joint slightly
flexed and IP joints extended. Some surgeons place the
wrist in slight flexion. For the first 3 weeks, the hand is
immobilized. Passive digital flexion can be prescribed,
but generally motion range should be limited and
should be initiated after 10 days or 2 weeks when edema
subsides. Light active motion over a very limited range
can be ordered as well, just producing mild finger
motion. Starting passive motion of the digits prevents
digital stiffness. Motion also helps reduce persistent
edema of the hand and digits. After 3 weeks, the patients
can be instructed to perform passive motion of the
digits, together with active motion of the fingers. Hand
edema can be serious in the first days after surgery, and
when persistent, therapies should be given to lessen
digital edema and improve digital circulation when the
digit motion starts.
Outcomes
After palm replantation, the hand can be expected to
recover to rather realistic hand functions. Ample active
digital flexion can expected if no serious adhesions
occur. The overall digital function is better after surgery
of palm than digital replantation. Stiffness in the digital
joints does not usually develop if the passive motion
therapies are properly initiated. Nevertheless, when
Therefore, only a very limited number of patients are
ideally indicative of secondary tenolysis because loss of
passive digital motion is common. Tenolysis is usually
carried out about 6 months or one year after surgery.
Postoperative 3 months are too early for this surgery.
Most patients seen in our department who needs
secondary tenolysis are operated one year after replanta­
tion surgery. When passive motion is restricted, a con­
siderable number of patients may not want to accept a
secondary operation to improve passive joint motion
followed by tenolysis. Under this circumstance, we do
not strongly urge the patients to have the surgery,
because the improvement after tenolysis is not as great
in these patients. Adhesions in extensor tendons are
common, but they are not as problematic as for flexor
tendons. Should these cases undergo the tenolysis,
simple release of the extensor tendon adhesions usually
is required. Care should be given especially to the pres­
ervation of integration of reattached vessels, and the
dissection should not extend too far away. Early passive
and active motion of the digit should be initiated after
tenolysis if the tendons are not found frayed.
Yu and colleagues (2003) reported that 79 digits of
55 patients received 102 secondary procedures follow­
ing replantation.3 They divided the procedures into two
groups, occurring before or after 2 months following
replantation. The procedures in the early group were
mainly for soft tissue coverage (92%), and those in that
late group were mainly for tendon (67%) to improve
function. Factors associated with higher incidence of
early secondary procedures included multiple-finger
injury, avulsion or degloving injury, and level of injury
proximal to zone 3 in finger replantation. However,
younger patients and those with proximal level replan­
tation in fingers had more late secondary procedures.
Flexor tenolysis procedure significantly improved the
digital function after replantation.
Eggli and colleagues (2005) reported 23 patients
with restricted motion after 32 combined digital injuries
or amputations in zone 2 treated with tenolysis.4 With
an average follow-up of 5 years, significant functional
improvement was achieved in 28 of 32 digits (88%).
TAM improved on average 51° after dorsal tenolysis, 55°
after palmar tenolysis, and 63° after combined dorso­
palmar tenolysis. Using Buck-Gramcko’s criteria, 15
digits were rated excellent, 8 good, 4 fair, and 5 poor.
Complications consisted of 16% flexor tendon ruptures
after palmar or combined tenolyses. In contrast, dorsal
tenolysis proved to be a safe procedure. Prerequisites for
success are compliant patients who are willing to
undergo therapy for at least 3 months postoperatively.
Palm Replantation
Surgery
Amputation through palm is rarely caused by clean cuts.
Most often, machine cutting or crush-cutting injuries

e46
Chapter 46:  Tendon Repairs in Replantation Surgery
FPL must be repaired and major wrist flexors (flexor
carpi radialis and ulnaris, FCR and FCU) should be
repaired. Almost all the extensor tendons are worth
repairing, except for the extensor indicis proprius (EIP)
and extensor digiti minimi (EDM). Preferably the EPL
tendon should be repaired with a stronger surgical
method.
Postoperative Care
After surgery, the hand is placed in a well-padded pro­
tective cast with the hand in the functioning position or
neutral position, with the thumb web widely opened.
For the first 3 weeks, the hand is immobilized. After 1
week, after serious hand edema subsides, passive digital
flexion can start, but generally only a mild range of
passive motion should be prescribed. Light active
motion over a very limited range can be ordered as well.
Motion helps reduce persistent edema of the hand.
Early dynamic splinting and digital motion can be initi­
ated in selected patients who can follow the instruction
of the therapist in a setting with well-established reha­
bilitation guideline. After 3 weeks, the cast fixation
should be continued, with the hand in functional posi­
tion. Passive and active finger motion programs can be
upgraded gradually. Similarly, hand edema is serious in
the first week after surgery and, if persistent, therapies
should be given to lessen digital edema and improve
digital circulation when the digit motion starts. After 6
to 8 weeks, when the radiograph confirms that bony
healing is solid, the amplitude of motion and repetition
of the motion can be increased. For the patient with
forearm replantation, much progress can be expected
even months after surgery, and continuation of thera­
pies to 6 months or one year is worthwhile.
Outcomes
Outcomes of the forearm replantation vary greatly,
depending on the degree of injuries, structures repaired,
and, in particular, the recovery of nerve function. Passive
motion of the hand may not be impaired, but hand
function may be greatly reduced due to usually partial
or poor recovery of nerve function. Grip and pinch
strengths reduce substantially.
Scheker and colleagues (1995) reported that the
results of replantation at the wrist and distal forearm are
better than at the metacarpal level.5 Their study evalu­
ated a new postoperative protocol for replantation at
the metacarpal, wrist, and distal forearm levels. Three
days after replantation, the patient was placed in a
dynamic crane outrigger splint with MCP joint control,
compensating for intrinsic muscle function loss. From
4 to 12 weeks, an anticlaw splint alternated with the
outrigger splint. After 12 weeks, a dynamic wrist exten­
sion orthosis was added to the anticlaw splint. Eleven
patients (4 replantations at the transmetacarpal level,
3 at the wrist area, and 4 in the distal forearm) had
postsurgical therapy guidelines are not established or
timely ordered, the hand with successfully replanted
palm may end up with very limited function. Due to the
damage to intrinsic muscles, function of the digital MCP
joint can be affected, and grip and pinch strengths
reduce substantially. Therapies should continue to post­
surgical 6 months or over one year.
Tenolysis
Tenolysis in the palm can be much more safely done
than in the replanted digits. The passive motion of the
digits and wrist are usually ample. Consequently, a
higher percentage of the patients with palm replanta­
tion are indicative of secondary tenolysis. The palm pro­
vides greater space to release the tendon from adhesions
with less danger to damage the reestablished vascular
supplies, although surgeons should still take great care
not to hamper the vessels. Tenolysis is carried out about
6 months after surgery and should be under the condi­
tion that solid union of the metacarpus is achieved.
After tenolysis, the patients are instructed to perform
early active motion to prevent reoccurrence of the adhe­
sion, and the motion therapies should continue for 2
or 3 months.
Foream Replantation
Surgery
Amputation through forearm, especially distal forearm,
is caused by work-related injuries or crushing during
accidents. At this level, the amputation involves multi­
ple flexor and extensor tendons, major arteries, and
nerve trunks. Bony fixation should be accomplished first
during the surgery, followed by vascular anastomosis to
establish circulation. The radius and ulna are usually
shortened for 2 to 3 cm.
There is no need to particularly shorten the tendon,
but the rugged tendon parts are excised to obtain healthy
tendon substance for surgical repair. A core suture
(mostly two-strand repair or a four-strand repair) should
be used for both extensor and flexor tendons. Peripheral
sutures can be loosely added. Whether the repair site is
bulky or not is not a great concern, because this area
accommodates more space for tendon to glide. The
surgeons should pay particular attention not to mis­
match the tendon ends. Strength of the flexor tendon
remains important; we recommend four-strand repair
such as cruciate repair or U-shaped repair (see Figure
46-5 and Figure 46-6), made with 4-0 or 3-0 sutures.
Our colleagues (Zun Shan Ke, MD) used the U-shaped
4-strand repair made with looped nylon suture, supple­
mented with locking running peripheral suture in cases
of forearm replantation, followed by early tendon mobi­
lization. They impressively obtained good function.
Repair of the FDS tendon is not a necessity. To reduce
operation time, the FDS tendon may not be repaired or
may be connected with simpler suture. The lacerated

e47
Chapter 46:  Tendon Repairs in Replantation Surgery
FUNCTIONAL EVALUATION
In the early days of digital replantation, flexor tendons
were not repaired, and secondary tendon reconstructed
was preferred.6,7 The treatment guidelines for the tendon
repairs in replantation have been changed. Currently,
under favorable conditions, repairs of both extensors
and flexor tendons are an integral and important part
of replantation surgery.8,9
Functional evaluations of patients after digital replan­
tation include (1) range of motion, passive and active;
(2) recovery of sensation; (3) muscle power; (4) grip
strength; (5) pain; (6) cold tolerance; (7) ability to
resume previous or new occupation; (8) ability to inte­
grate the replanted parts into daily life and functional
use; (9) patient satisfaction with the replanted part; and
(10) cosmetic appearance.10 While all the above criteria
are important to the normal life, Buncke and colleagues11
stated that among all factors influencing outcomes,
“experience has shown that the two most critical issues
are sensibility and tendon gliding.”
this protocol. For distal forearm replantations, TAM of
fingers averaged 216°, grip strength 42 lb, and pinch
strength 7.2 lb with 75% good or excellent results. For
wrist replantations, TAM of fingers averaged 243°, grip
strength 37 lb, and pinch strength 10.6 lb with 100%
good or excellent results. For transmetacarpal replanta­
tions, TAM of fingers averaged 189°, grip strength 37 lb,
and pinch strength 5.6 lb, with 75% good and excellent
results.
Tenolysis
Tenolysis can improve function of most patients after
replantation in the forearm. Surgery can be performed
from 6 months to several years after surgery. Function
of both extensor and flexor tendons can be improved
after surgical release. Similarly, tenolysis should not be
performed within 6 months after surgery, and before
solid union of the radius and ulna is achieved. After
tenolysis, the patients are instructed to perform early
active motion immediately after surgery, and the motion
therapies should continue for months.
References
1. Jupiter JB, Pess GM, Bour CJ: Results of flexor tendon tenoly­
sis after replantation in the hand, J Hand Surg (Am) 14:35–
44, 1989.
2. Ross DC, Manktelow RT, Wells MT, et al: Tendon function
after replantation: prognostic factors and strategies to enhance
total active motion, Ann Plast Surg 51:141–146, 2003.
3. Yu JC, Shieh SJ, Lee JW, et al: Secondary procedures following
digital replantation and revascularisation, Br J Plast Surg
56:125–128, 2003.
4. Eggli S, Dietsche A, Eggli S, et al: Tenolysis after combined
digital injuries in zone II, Ann Plast Surg 55:266–271,
2005.
5. Scheker LR, Chesher SP, Netscher DT, et al: Functional
results of dynamic splinting after transmetacarpal, wrist, and
distal forearm replantation, J Hand Surg (Br) 20:584–590,
1995.
6. Komatsu S, Tamai S: Successful replantation of a completely
cut-off thumb, Plast Reconstr Surg 42:374–377, 1968.
7. Tamai S: Digit replantation: analysis of 163 replantations in
an 11 year period, Clin Plast Surg 5:195–209, 1978.
8. Meyer VE, Chen ZW, Beasley RW: Basic technical consider­
ations in reattachment surgery, Orthop Clin North Am 12:871–
895, 1981.
9. Morrison WA, O’Brien BM, Macleod AM: Digital replantation
and revascularization: A long term review of one hundred
cases, Hand 10:125–134, 1978.
10. Steichen JB: Management of flexor tendon injury associated
with digital replantation or revascularization. In Hunter JM,
Schneider LH, Mackin EJ, editors: Tendon Surgery in the Hand,
St Louis, 1987, CV Mosby, pp 156–169.
11. Buncke HJ, Alpert BS, Johnson-Giebink R: Digital replanta­
tion, Surg Clin North Am 61:383–394, 1981.

446
Appendix
Peter Amadio:  How about treatment of the partially
lacerated FDP tendon and the FDS tendon? I repair
a partial cut of the FDP when the cut is over 60% to
70% of the cross-section. If the cut is less than 50%
to 60%, trimming the tendon wound is an option.
This reduces the chance of triggering, but does not
reduce the tendon strength. I repair the FDS tendon
if possible, but prefer to remove a slip of the FDS
tendon when the gliding of the FDP appears tight
with the sheath or pulleys.
Michale Riccio:  I agree that we may not need to repair
the FDS tendon in all occasions. In some cases, it is
very difficult to repair this tendon; we have to leave
it unrepaired. Otherwise, the both tendons would be
bulky, but whether not repairing the FDS reduces the
flexion power of the finger is a concern, which
remains uncertain.
Audience:  This is a question for Dr. Tang. First I appreci­
ate the incredibly excellent work done in flexor tendon
from Dr. Tang. One thing I did not understand in the
work you’re doing: how far to place the grasping
suture. To my knowledge, the grasping and locking
suture should be placed 3 or 4 mm away from the cut
edge of the tendon. As to the traditional technique,
too much of the distance will bring about more tissues
within the suture, which will affect tendon gliding.
Jin Bo Tang:  Our original speculation is if a suture is
placed with sufficient grasping or locking area, these
repairs would produce equal strength. However,
during the test, the repair with shorter suture pur­
chase had much lower repair strength. This may
relate to the stiffness of the tendon and grasping
power of the suture. With smaller suture purchase,
the stiffness may be much less and easy to deform
and gap. Also the length of core suture purchase will
affect the share of the loads among the core suture
and peripheral sutures. If the core suture is very short,
the load can be largely loaded into peripheral sutures,
which is disrupted more easily, then the load will be
on the core suture entirely; core suture will be dis­
rupted. This is my explanation. We also found that if
the core suture purchase is beyond 7 mm, such effects
do not exist; almost equal repair strength was found
from 7 mm to 12 mm.
Audience:  We have just heard about venting, removal,
or not repairing a part of important pulleys, such as
the A2. I think this is a dangerous idea. Removal of
the pulley may cause bowstringing and this is oppo­
site to traditional suggestions of not violating these
important structures, such as A2 and A4 pulleys.
SYMPOSIUM DISCUSSION 1
Symposium of Flexor Tendon Injury, The 10th
Congress of International Federation of Societies
for Surgery of the Hand (IFSSH)
March 12, 2007
The Sydney Convention Center, Sydney, Australia
(Figure 1)
The discussion followed the symposium presentations
by panelists.
Panelists: Robert Savage, Jin Bo Tang, Michale Riccio,
and Peter Amadio
Moderators: Peter Amadio and Stephen Coleman
Peter Amadio:  Let’s start the discussion of this session.
It seems all of us are moving towards venting a certain
part of the important pulleys and using strong repairs.
What do you think about importance of individual
annular pulley?
Robert Savage:  If other pulleys are intact, the A2 pulley
may not be as important as thought in terms of
preventing bowstringing and maintaining normal
mechanics of the tendon gliding. I think partial inci­
sion or partial removal of the A2 pulley has no
adverse influence; I leave such partial defects of the
pulley unrepaired. The lack of importance of other
individual pulleys in the presence of a mainly intact
pulley system has been proven biomechanically in
the past more than 10 years.
Peter Amadio:  How about the A4 pulley?
Robert Savage:  It may not be important as well if others
are intact. I would not repair it if it is the only annular
pulley injured.
Peter Amadio:  What method do you use for tendon
repairs?
Jin Bo Tang:  My colleagues and I use the latest modi­
fication of 6-strand repair with looped suture for the
profundus tendon. For FDS tendon, it cannot afford
more than 4-strand core suture, so a four-strand
repair using one group of looped suture is used to
make a U-shaped repair.
Peter Amadio:  What kind of suture material?
Jin Bo Tang:  4-0 nylon.
Peter Amadio:  Dr. Riccio, what sutures are you
using?
Michale Riccio:  Pretty similar, I use 4-0 or 3-0 sutures
to make core stitches, but in children, I use a 5-0
suture instead. It is not necessary to do early motion
of the digit in children.

447
Appendix: Symposium Discussion 2
SYMPOSIUM DISCUSSION 2
Symposium of Flexor Tendon and Carpal
Disorders, The Pre-Congress of The 11th
Congress of International Federation of Societies
for Surgery of the Hand (IFSSH)
October 28, 2010
Affiliated Hospital of Nantong University,
Jiangsu, China (Figure 2)
Panelists: Daniel Mass, Michael Sandow, Robert Savage,
Steve K. Lee, and Jin Bo Tang
Moderator: Jin Bo Tang
Michael Sandow:  Bad repair leads to bad outcomes.
Good repair does not guarantee good outcomes, but
it helps. I used modified Kessler repair (two-strand)
using 4-0 nylon or similar, Kleinert traction, and
flexed wrist splint. We failed to obtain satisfactory
results in some cases. We then changed to a four-
strand single cross grasp repair (“Adelaide repair”)
using 3-0 braided polyester (Ethibond or similar)
with immediate active mobilization, extension block
splint with the wrist extended. I reviewed the results
between 1996 and 2002, 89% follow-up, 71% good
or excellent results, 4.5% rupture rate. Modified
Kessler is a simple repair of poor biomechanics. Its
core suture has inherent grapping potential; its grasps
are easily deformable. The transverse passes in the
tendon may not be a good design.
Michael Sandow:  I have some concern for definitions
of “grasp” and “loop.” I looked up the dictionary:
“Grasp” denotes function, to hold onto something,
but “loop” denotes form, shape. “Locking grasp” and
“looping grasp” appear more appropriate.
Jin Bo Tang:  I probably would not change these terms,
because most hand surgeons are familiar with them,
but we need to give them clearer definitions.
Michael Sandow:  In Green’s textbook about the grasp­
ing, the suture is looped around the tendon sub­
stance, and is pulled to the opposite direction. The
grasping loop slips over the tendon substance in the
illustration. The difference between “grasp” and “lock”
is that if the suture changes its form by tension to the
tendon, it has a poor hold on the tendon and the
strength of repair is decreased. If the suture does not
change its form, it is a lock, and the strength does
not decrease as the hold gets stronger under load.
Jin Bo Tang:  No suture techniques in clinical use actu­
ally have grasping suture pulled at two opposite
directions. The techniques in use have grasp being
pulled in one direction parallel to the longitudinal axis
of the tendon, and in the other side another pull vertical
to the long axis of the tendon. This is the way the grasp­
ing loops act in the Kessler and other grasping repairs.
The drawings in that textbook need to be modified.
Jin Bo Tang:  We perform simple venting of the A2
pulley when other annular pulleys are not injured.
With the other parts of the sheath intact, partial
venting of the A2 pulley is acceptable. Clinically, if
we see a wound limited to the area of the A2 pulley,
or not extending to another annular pulley, we leave
a part of injured A2 pulley unrepaired, or more often,
we incise or remove a part of the A2 pulley to allow
repair or smooth tendon gliding. If the wound is
extensive, with other pulleys, such as A1, PA, injured,
we should take great care to preserve the A2 pulley.
In those cases of tendon injury with A1 and PA lac­
erations, the tendon is usually cut proximal to the
A2. It does not interfere with tendon motion, thus
not needing venting.
Peter Amadio:  What is the length you vent the pulley?
Jin Bo Tang:  I incise the A2 pulley to 2/3 of the length
of this pulley.
Peter Amadio:  How about Dr. Riccio?
Michale Riccio:  About the same.
Jin Bo Tang:  The important message is that we really
need to know the detail of anatomy of the A2 pulley.
In the adult middle finger, this pulley is quite long,
about 2 cm. This pulley even has different density in
its middle, distal, or proximal parts. The diameters of
these parts are also different. I think either distal,
proximal, or their combination with the middle part,
can be incised or excised to free the tendon motion,
without any clinical problems. I have done it over
years, and still continue to do it. I do not suggest the
incision of the entire A2 pulley.
Peter Amadio:  We are at the right time to end this
session now. Great discussion of the panelists and
from the audience! Thank you.
Figure 1  Symposium of flexor tendon injury in The 10th
Congress of the IFSSH, Sydney, March 12, 2007. On the
podium (from left to right): Stephen Coleman, Peter Amadio,
Robert Savage, Jin Bo Tang, and Michale Riccio. (Courtesy of
Bin Wang.)

448
Appendix: Symposium Discussion 2
Figure 2  Panelists touring the Biomechanics Laboratory
of the Hand Surgery Research Center in the Hospital of
Nantong University immediately before the Symposium.
From the left to the right: Robert Savage, Steve K. Lee,
Daniel Mass, Michael Sandow, Ya Fang Wu, and You Lang
Zhou.
splint after surgery. With 3-0 Ethibond suture, we had
no rupture at all in our recent series. I think adding
Silfverskiöld will unnecessarily complicate the repair
of the four-strand core repair. It is much more com­
plicated when we do it.
Jin Bo Tang:  I have never used Silfverskiöld suture, as
we can easily increase the strength of core suture.
Complex peripheral suture brings about a lot of
suture over the tendon surface and this repair is also
difficult to perform. Is that very difficult to perform
such cross-stitch on the dorsal surface of the tendon?
Michael Sandow:  Our discussion here is quite gentle;
actually we had quite hot discussion in Adelaide with
Dr. Silfverskiöld. He works in Adelaide and he pub­
lished the method when he was in Sweden, and then
came back to work in Australia.
Jin Bo Tang:  How about the tension of your core
suture?
Michael Sandow:  The tension is sufficient to maintain
the cooptation of tendon ends. I do not mind having
some gap between the ends, so no bunching or catch­
ing by the sheath.
Jin Bo Tang:  Would other panelists maintain some
tension across the repair site of the tendon, or leave
gaps between the ends?
Michael Sandow:  I mean I will add some tension at the
time of repair when temporary fixation is in place,
but after removal of the fixation, it is best to see that
the tendon is smooth and not bunching, but it is fine
if there are small gaps between the ends. I do not
intentionally leave gaps between the ends when
suturing the tendons.
Steve K. Lee:  I have been using interlocking horizontal
mattress locking sutures. It is similar to Silfverskiöld,
but with interlocks. That is based on the work we
have done in the lab. Michael Hausman called it a
“Chinese finger trap.”
Daniel Mass:  What I usually do is to put epitendinous
stitches to the back of the tendon first. You lock the
stitch each time and make the tendon ends kissing.
Then you put core suture and end with putting the
epitendinous suture in the front of the tendon.
Daniel Mass:  Most people are actually still using the
Kessler. This is what they learned and what they have
used.
Michael Sandow:  I think the Kessler is such a rubbish
method for repairing the tendon; it has very poor
biomechanics, gapping very easily.
Jin Bo Tang:  Many people and papers talk about adding
Pennington locks into the Kessler. Either a grasping
and locking Kessler is not strong. We had a study
several months ago and asked two surgeons to make
two groups of Kessler repairs, with and without
Pennington lock. We couldn’t find any difference in
the strength, except 2 to 3 N differences in the gap
force.
Michael Sandow:  I agree. We put modified Kessler
repair in porcine flexor tendon and observed the
deformation of the tendon after preloading. The
transverse passes of the Kessler repair shortened and
tendon was narrowed remarkably. With two single
cross placed into the tendon, without a transverse
arm across the tendon end, we see little narrowing of
the tendon.
Steve K. Lee:  What do you use for peripheral stitches?
Michael Sandow:  I use a simple peripheral suture. If it
is a big tendon or is not too irregular, I use Silfver­
skiöld method. But, for most tendons, we think
simple epitendinous suture is adequate. Unless you
expect the peripheral stitches to bring about a lot of
strength, simple suture is better.
Daniel Mass:  The complex peripheral stitches may be
caught by pulleys.
Michael Sandow:  Absolutely. In Kessler suture, when
we loaded the tendon, the epitendinous suture failed
first, followed by Kessler suture; when four-strand
single-cross suture is used, the epitendious suture
failed in the same time as the core suture, without
gapping first.
Robert Savage:  Some of the studies showed that Ade­
laide core with Silfverskiöld decrease the rate of
rupture of the repair. Do you feel you will train your
residents to do that repair?
Michael Sandow:  I am very happy you call it “Adelaide”
repair, not the modified …, modified Savage repair.
Robert Savage:  You have done a good job.
Michael Sandow:  We did Adelaide with a simple epi­
tendinous repair and had few ruptures. We had rup­
tures with two repairs of 4-0 nylon that registrars
used to repair these tendons; the hand was out of the

449
Appendix: Symposium Discussion 2
Figure 3  “Work done only a few years, not decades, ahead
of others actually would not make a great difference to the
overall progress in a field.”
—Prof. Seiichi Ishii (back row, second from the left)
commented humbly on May 26, 2010, in Tokyo, when
talking about his early work and contribution on intrinsic
healing capacity of the flexor tendon in early 1970s. The
photograph was taken on that day (second from the right,
back row, Prof. Poong-Teak Kim, and second from the right,
front row, Prof. Masamichi Usui). Prof. Ishii was honored as
“Pioneer of the Hand Surgery” in the Congress of the IFSSH in
October 2010 for his early work on the tendon and other
contributions.
Michael Sandow:  You are right. A study showed what­
ever you put grasping, Pennington locking Kessler or
just a simple loop around the tendon end, the suture
would deform the tendon and form a loop around
the tendon, which actually does not act much
differently.
Jin Bo Tang:  Is the Kleinert method of motion still
common in the United States?
Daniel Mass:  I think it is declining. More therapists use
the Duran method and the place-and-hold exercise.
Jin Bo Tang:  Do you actively move after secondary
tendon graft?
Daniel Mass:  I do active finger motion after tendon
graft, with no-resistance, in a wrist extension splint
or cast putting the wrist in 20° of extension and the
MCP joint in 60° of flexion and the IP straight. For
kids, I put a cast, and in adults, I put a splint. I left
a big hole in the cast, so the finger can move in
kids. In the unreliable patients, you can do the same
thing.
Robert Savage:  Controlled “active” motion began in a
report in 1989 about the Belfast regimen. Variable
results were reported later, including those from
Manchester and Essex, with some ruptures. In a lab
study of pulleys, I noticed, and other noticed too,
that if you do not move the finger through the full
range, you are not putting the maximal load to the
tendon. The other ways of performing active motion
more easily include putting the wrist in extension: to
explain, the wrist flexed position causes the finger
extensors to become tight, and so finger flexion will
become difficult. In wrist extension, the finger exten­
sors are slack and flexion of the fingers requires much
less force. Also if the MCP joints are held in a neutral
or slightly flexed position, you will find it easy to flex
the DIP joint.
Steve K. Lee:  Most people who do primary repair may
still have up to 10% rupture after early active motion;
that’s 1 out of 10. Those results are not that great.
Dr. Richard Gelberman came to speak to the New
York Society for Surgery of the Hand, saying “tenoly­
sis was necessary in 20% of (his) patients. There
is still a lot of research to be done.” We looked at
the strength of different repair and materials. Fiber­
wire has the greatest strength and the least knot
volume (bulk). We recommend 6 knots with Fiber­
wire for repairs. Among epitendinous sutures, the
interlocking horizontal mattress suture provides
good strength. In doing this repair, each bite has to
be slightly away from the cut edge to not converge.
Daniel Mass:  I use running locks in epitendionus
suture, instead of interlocking suture. We tested it,
without a core suture; it is adequately strong. Prob­
ably it is not as strong, but the superficialis is flat, and
people don’t get the rotation right and actually
narrow the Camper’s chiasm. Just doing one slip is
easier and adequate.
Steve K. Lee:  For the superficialis tendon, I would repair
both slips, but quickly reduce it to one slip if there is
any issue with tendon gliding. The Mayo group wrote
about the benefits of repairing just one slip. It seems
many people are moving in that direction.
Jin Bo Tang:  Great talks and discussion. Thank you!

450
A Postscript About Progression of Thought
on Primary Tendon Repair
Jin Bo Tang, MD
I have set out to describe how my thinking pertaining
to flexor tendon surgery has progressed over more than
20 years.
My first work on the tendon started in 1988 with a
study of sheath closure using chicken models. Direct
closure of the sheath was found to be no better than
partial excision, and direct sheath closure at the delayed
primary stage was actually harmful to tendon gliding.
This conclusion differed from a mainstream tenet at that
time that sheath closure was beneficial to preventing
adhesions and maintaining nutrition. My ensuing work
fostered an idea that ample space inside the sheath cavity
(not closure or reconstructive surgery of the sheath per
se) is vitally important to healthy tendon healing and
gliding. A key piece of evidence that led me to this con­
sideration was that, given an equal extent of adhesions,
tendons whose sheaths were enlarged with interposing
grafts exhibited better gliding than those within tightly
closed sheaths. Increasing the volume inside the sheath
is thus considered imperative to both healing and
gliding of the tendon. I should give great credit to Pro­
fessor Seiichi Ishii, who earnestly mentored and sup­
ported my investigations in 1988 and 1989. Particular
credit is due to this great man for creating the adhesion
grading criteria used in the investigation. Prof. Ishii is
an early pioneer in the area of “intrinsic healing” of the
tendon. He initiated in vitro culture work to demon­
strate the capability of tenocytes to proliferate and to
repair wounds as early as 1971, and published 3 years
later. In 2010, when I talked to him about this early
work, he calmly commented that work done only a few
years, not decades, ahead of others actually would not
make a great difference to the overall progress in a field.
He is an exemplary pioneer in science, humble in accept­
ing credit, yet dedicated and nurturing toward young
investigators.
My second work was on subdivision of zone 2 in late
1989. At that time, I began independently treating hand
cases and regularly repaired zone 2 tendon injuries. In
practice, I found that recording the site of injuries and
outcomes of treatment in subdivisions of zone 2
appeared not only necessary, but important in discuss­
ing treatment of these tendons. Literature in the 1970s
and 1980s had been unclear regarding the exact site in
reporting methods and outcomes. I sketched out zoning
methods by observing hand specimens in the Depart­
ment of Anatomy. Later, in the early 1990s, my case
series indicated differences in results of tendon repairs
between zone 2C and other subzones. The repairs in the
area covered by the A2 pulley were found to produce
the worst outcomes.
It was my awareness of worse outcomes in zone 2C
that directed me to conducting studies focusing on the
A2 pulley and its corresponding tendon segment in
1993–94. Clinically I compared the outcomes of repair
to non-repair of the superficialis tendon in this particu­
lar area, and found worse outcomes when the superfi­
cialis was repaired. These clinical results prompted me
to return to the anatomic laboratory to specifically study
the morphology and mechanics of tendons and pulleys.
There, I began to realize that purposeful incision of a
part of the A2 pulley can be a feasible clinical option to
improve treatment results.
This idea of active release of the A2 pulley encoun­
tered great opposition when presented to a symposium
later. Though this study was published in The Journal of
Hand Surgery (British) in 1995, even with clinical data
the idea of purposeful pulley-venting was printed only
as an abstract in Chinese. There was considerable resis­
tance to this “dangerous” initiative against deeply rooted
traditional recommendations.
In late 1998, I read a report by Dr. David Elliot and
his colleagues of reporting results of tendon repairs in
subzones of zone 2 and venting of the A2 and A4
pulleys, which inspired me to send a letter to start com­
munication with Dr. Elliot and to plan a 5-day visit to
him in June of 1999. In Dr. Elliot’s house in the middle
of a wheat field by Chelmsford, Dr. Elliot and I spent
no less than 3 entire days “randomly” discussing any
topics we could think of relating to tendon repair, taking
notes on ideas that came up during conversations. Dr.
Elliot showed me a manuscript in which he proposed
to subdivide zone 1. We agreed that a precise and clear
determination of the site of tendon laceration is funda­
mental to any discussion of treatment. Dr. Elliot’s take
was as follows: most people who do not feel a need
to subdivide the zones probably have not had enough
cases to allow for observing differences in treatment

451
A Postscript About Progression of Thought on Primary Tendon Repair
who lack background knowledge about the project but
have strong technical skills, so they do not know what
we are trying to prove. We intend not only to publish
our findings, but also to publish with greater confidence,
with results that withstand the test of time.
Our hand surgery service for disorders of hand and
upper extremity became a department in 2002, and has
continuously expanded to its current size of 12 staff
surgeons and 110 hospital beds. Over the past 10 years,
my colleagues and I have steadily modified our surgical
techniques and rehabilitation protocols. Most of the
novel methods or technical modifications that my col­
leagues and I have applied to the clinic were derived
directly from our laboratory results. We also adopted a
few clinical treatment rules directly from laboratory
studies, e.g., optimal core suture purchase and ideal
grasping/locking sizes in a surgical repair, etc. Motion
protocols have been amended with new components,
such as passive motion prior to active motion in each
exercise session and initiation of finger motion 3 to 5
days after surgery. These modifications stemmed from
studies of factors affecting strength of tendon repair,
postoperative edema, resistance to tendon movement,
etc. We have been able to prove the safety of judicious
surgical venting of the pulleys through clinical follow-up
and established simplified multistrand repairs as the
standard method for zone 2 tendon repairs. Though we
still face challenges of composite tissue loss/damage
with tendon injuries—including tendon injuries involv­
ing bones or after multiple reconstructions—It is the my
opinion and that of my colleagues that it is possible to
achieve close-to-normal recovery of function in clean-
cut tendon injuries in the finger. The outcomes of repairs
of tendon injuries in the fingers are no longer unpredict­
able, which is a major advance.
My colleagues and I share the belief that attention to
the intricate details of surgical repair is vital to the
success of any given method. Equally important is the
clear and precise mastery of the surgical anatomy of the
tendon and its pulleys. Junior surgeons may frequently
not attend to details of surgical repair techniques such
as ensuring sufficiently large tendon substance within a
suture’s grasps or locks and adding some tension across
the repair, and may possess no clear mental picture of
anatomy during surgery. Without attention to such
details, the repair may be disrupted or gap easily, and
the sheath or pulleys could be treated erroneously. Sur­
geons who adopt an established method may report the
end-results that vary enormously depending on the sur­
gical details. Thus attention to surgical details should be
adequately emphasized. Technical details and mastery
of anatomy need to be passed from experienced sur­
geons to junior staff members in classrooms and at the
operation table.
results. We discussed the methods of repairs and the
need of stronger surgical repair; in the later years, I
learned that Dr. Elliot and his colleagues started routine
use of the six-strand core repair using the looped suture
that I have favored. We agreed that a part of the pulleys
can be incised and that sheath closure is not important—
still at that time I did not recognize the importance of
pulley-venting to the extent that I would later—the
venting may be vital to achieve predictable treatment
outcomes. We were surprised by our similar approaches
in A2 pulley treatment without prior awareness of one
another. Dr. Elliot actually started to perform pulley-
venting in early 1995.
I established a research center for the hand in 1995
and had a group of investigators working on tendon
projects since then. Before that, I was mostly alone on
my journey. Drs. Ren Guo Xie, Bin Wang, and Yu-tong
Gu were the earliest to join in mechanical testing of
tendon repair strength and in vivo studies, followed by
Drs. Zhi Ming Cui, Jun Tan, Yan Xu, and Zun Shan Ke.
Over the past years, Drs. Yi Cao, Bei Zhu, Chuan Hao
Chen, and Ya Fang Wu performed a series of excellent
mechanical and molecular studies. On the clinical side,
Drs. Ren Guo Xie, Bin Wang, and Jun Tan have been
active in applying novel surgical and rehabilitation
methods for years. All have been extremely dedicated;
to them I should give great credit. The research center
has entered into full function since 1997. Over the past
15 years, we have investigated individual factors that
may affect tendon repair strength with in vitro mechani­
cal testing; modified test models under curvilinear
loading conditions; tested novel surgical repair methods;
examined the effects of pulley integrity or venting on
tendon gliding and adhesions with in vivo models; and
explored molecular methods which may be used in
enhancing tendon healing or limiting adhesions. In
these investigations, the study had been set up with
detailed discussion within the group. In order to allow
myself to remain involved in some vital steps and
monitor or participate the project directly, I rather strictly
limit the number of people participating in investigation
at the same time. In investigations that have led to major
conclusions, I repeated and verified key experimental
steps together with colleagues. Often independent inves­
tigators have worked on projects at different times, with
a portion of study contents overlapping, to verify each
other’s conclusions in a blinded way. To avoid bias, I do
not usually explain expected results to fellow investiga­
tors. I consider our conclusions reliable only when they
are obtained without a clear purpose of proving a pre­
conceived conclusion and are repeatedly proven by dif­
ferent investigators among us. Not infrequently, a study
is published years later, after it has undergone blinded
self-verification, sometimes carried out by researchers

452
INDEX
A
AAV. See Adeno-associated virus (AAV) vector for
gene therapy delivery
AAV2. See Adeno-associated virus serotype 2
(AAV2) vector for gene therapy delivery
Abductor pollicis brevis (APB) tendon, 13
Abductor pollicis longus (APL) tendon, 10–11, 10f,
364
Abrasion of sheath, due to high-friction repair,
17–18
Acellularized scaffold, 75, 76f
Active extension
for boutonnière deformity, 431, 432f
in six-strand Lim/Tsai repair rehabilitation,
119–121, 120f
in tendon transfer for extensor tendon
reconstruction rehabilitation, 370
in vascular tendon transfer rehabilitation, 341,
341f
Active extension-passive flexion. See Kleinert
rehabilitation technique
Active flexion
for boutonnière deformity, 431, 432f
in flexor tendon rehabilitation, 407
in Mantero technique, 205, 205f
in Nantong repair rehabilitation, 147–148, 147f
rupture of repair due to unprotected, 253
in six-strand Lim/Tsai repair rehabilitation, 121
Standford experience and methods, 159
Active mobilization
for flexor tendon rehabilitation, 18, 407–409,
408f
Chelmsford experience, 126
controlling flexion force in, 409–410,
409f–410f
of flexor pollicis longus tendon, 187, 188f,
190t
in flexor tendon grafting, 281
following tenolysis, 263–264
history of, 125
initiating of, 410
in Mantero technique, 205
Standford experience and methods, 159
tendon excursion and, 31
in vascular tendon transfer rehabilitation,
341
for mallet finger, 430, 430f
symposium discussion on, 449
for tendon transfer for extensor tendon
reconstruction, 370
Adductor pollicis tendon
anatomy of, 13, 13f
rehabilitation for, 434–436
Adelaide repair, 40f, 122, 164, 164f, 166, 169
symposium discussion on, 447–448
Adeno-associated virus (AAV) vector for gene
therapy delivery, 62, 64f
Adeno-associated virus serotype 2 (AAV2) vector
for gene therapy delivery, 62, 63f
with basic fibroblast factor, 62–66, 64f–66f
future perspectives, 68
with luciferase, 64, 65f
with vascular endothelial growth factor, 65–66,
66f
Adenoviral vector for gene therapy delivery, 62
Adhesions, 125–126
Australian experience and methods, 163–164
classification of, 411t
loss of motion in formation of, 17
outcomes and, 252–253
partial tendon laceration and, 174–175
pharmacological management of, 19
rehabilitation protocols and, 411, 411t
staged tendon grafting and, 298–299
suppression of formation of
future of, 444
gene therapy associated with micro-RNA
regulation for, 66–67
tendon healing and, 72–73, 323
tenolysis for, 261–265
zone 5 repair and, 198
Adipofascial flap, turnover, 373
Adipose-derived mesenchymal stem cells, 73–74
Age
outcomes and, 182–183
in zone 5 flexor tendon repair, 200
in rehabilitation regimen customization,
418–419, 418f–419f
Aiche’s technique for extensor reconstruction, 389
“Allen test”, 394–395
Allogenous cell seeding of scaffold, 74
Allograft, vascularized tendon, 337–338, 338f
Allograft-matched intrasynovial flexor tendon,
282–283
ALT flap. See Anterolateral thigh (ALT) flap
Amadio-Mayo Group on biomechanics of tendon
repair, 36b
American Society for Surgery of the Hand (ASSH)
method of evaluation, 250–251, 251t
Anatomy of tendon system, 3–15
chiasma tendinum of Camper in, 10
extensor retinaculum in, 4
extensor tendons in
of fingers, 12–13, 12f–13f
rehabilitation and, 427–437, 428f
sagittal band injuries and, 355–357, 356f
variations to the fingers, 11–12
at wrist, 10–11, 10f
flexor retinaculum in, 3
flexor tendon sheaths in, 5–6, 5f–7f
flexor tendons in, 4–5
lumbrical and interosseous muscles in, 9–10
mastery of, 145–146
Nantong experience and, 145–146
pulley system in, 8–9
in thumb, 13–14, 13f
vascularized tendon transfer and, 324–327,
325f–326f, 328f–329f
vincula tendinea in, 6–8, 7f
Anchor(s)
in single-stage free tendon grafting, 267–269,
270f, 275–276, 276f
for traumatic avulsion of flexor tendon repair,
222f–223f, 224t
Anchor point, 242–243, 242f–243f
Annular ligament
anterior, 3
dorsal, 4
posterior, 4
Annular pulleys. See also specific pulleys
anatomy of, 7f, 8–9, 88, 89f, 104–105
function of, 89
incisions in Nantong experience, 138–140
preservation of in secondary tendon surgery,
95–96
in thumb, 13, 13f
venting of, 94–96, 94f
Antebrachial fascia, 3–4
Anterior annular ligament, 3
Anterolateral thigh (ALT) flap, 379–380, 381f
APB. See Abductor pollicis brevis (APB) tendon
APL. See Abductor pollicis longus (APL) tendon
Aponeurosis, pulley system and, 9
A1 pulley
anatomy of, 7f, 8, 88–89
in thumb, 89
function of, 89
reconstruction of in staged tendon grafting, 304
modified Paneva-Holevich technique, 308,
308f–309f
A2 pulley
absence of, 9
anatomy of, 7f, 8, 88–89
investigation of, 92–93, 92f
in thumb, 89
enlargement of, 111–115
function of, 89
length of, 88–89
Mantero technique and, 204f, 205
Omega plasty for treatment of, 107–109
reconstruction of in staged tendon grafting, 304
modified Paneva-Holevich technique, 308,
308f–309f
rupture of, 233–238, 234f–235f
symposium discussion on, 441, 443
venting of, 94–96, 95f, 99–101
investigation of, 92–93, 92f
rehabilitation program and, 418
A3 pulley
absence of, 9
anatomy of, 7f, 8
bowstringing due to excision of, 101–102, 101f
rupture of, 233–234, 234f–235f
venting of, 99
A4 pulley
anatomy of, 7f, 8, 88–89
Australian experience and methods, 166
bowstringing due to snapping or venting of,
101–102, 101f
enlargement of, 111–115
flexor tendon injury under or distal to,
rehabilitation and, 419–420
function of, 89
length of, 88–89
Omega plasty for treatment of, 105, 105f–106f,
107–109, 108f
reconstruction of with modified Paneva-
Holevich technique, 308, 308f–309f
rupture of, 234f
symposium discussion on, 441
venting of, 94–96, 95f, 99–101
investigation of, 93
A5 pulley, 7f, 8
Arthritis
boutonnière deformity due to, 384–385
sagittal band injuries due to, 355, 357, 357f
tendon rupture due to, 228–232, 229f, 230t,
231f
tendon transfer for extensor tendon
reconstruction due to, 366–367
thumb deformity due to, 385, 386f
b indicates boxes, f indicates illustrations, and
t indicates tables.
Annular pulleys (Continued)

453
Index
Arthrodesis
for boutonnière deformity, 387, 387f
for rheumatoid deformity of thumb, 388–389
for swan-neck deformity, 387–388
ASSH. See American Society for Surgery of the
Hand (ASSH) method of evaluation
Assisted active mobilization, 408
Attachment
in single-stage tendon grafting
distal, 267–269, 268f, 270f, 281
of flexor pollicis longus tendon, 291, 291f
proximal, 269, 280–281, 280f
strength of, 37–38, 37f
in two-stage tendon grafting, proximal, 282
Australian experience, 161–167
author’s preferred approach, 166–167
current practice, 165–166
outline, 161–167, 162f
recent advances 2000-2010, 163–165,
163f–164f
Autogenous cell seeding of scaffold, 74
Avulsion of flexor tendons, 219–227
authors’ personal experience, 225–226, 225f,
226t
classification of, 220–221, 220f
diagnosis of, 221–224, 221f–224f, 224t
of FDP tendon, rehabilitation for, 420
mechanism of injury, 219–220, 220f
outcomes, 224–225
postoperative care, 224, 224f
traumatic avulsion as, 219
B
Barb-wire suture, 225
Basic fibroblast factor (bFGF)
gene therapy with, 61–66, 64f–66f
future perspectives, 68
sutures for delivery of, 77
in tissue engineering, 76
Becker flap, 378
Becker repair
augmented, for partial tendon laceration,
175f
strength of, 39
Belfast regimen, 126, 409
modified
Billericay/Chelmsford, 126–128, 127f–128f
Wellington, New Zealand experience and
methods, 168
Bern experience, 116–124
complications, 122, 122t
discussion, 122–123
methods and outcomes, 116–119, 117t, 118f,
121–122, 121t–122t
operative technique, 119, 119f
postoperative care, 119–121, 120f
bFGF. See Basic fibroblast factor (bFGF)
Billericay/Chelmsford variation of Belfast regimen/
splint, 126–128, 127f–128f
Bioactive suture, 71–77, 77f
Biological factors in tendon-bone development,
51–52
Biologically-based treatments, 59, 61
future of, 444
gene therapy as, 59–70
Singapore experience and methods, 154
for tendon-bone repair, 55–56, 56f
Biologic scaffold, 74–75
Biomechanics
of partial tendon laceration, 172–174
of sagittal band, 355–357
of surgical repair
considerations in design and use of repair
methods and, 46–47
core sutures, 38–40, 39t, 40f–41f
current techniques and, 36–37
factors affecting, 41–44, 42f
historical reviews of, 36, 36b
increasing of strength and, 44–45, 45f, 45t
outline of, 35–47
peripheral sutures, 40–41, 41f
test setup and measurement of, 45–46, 46f
types of tendon-suture junctions and, 37–38,
37f
of tendon-bone insertion, 50
of tendon motion, 29–32, 29f–32f
of Teno Fix Tendon Repair System, 208, 209f
Bipedicle flap reconstruction for skin deficiencies,
303, 303f
Bite, metacarpophalangeal joint injury due to, 351,
351f
Black box, zone 2 as, 129–130
Blood supply. See also Vascular system
to flexor tendons, 7f, 17f, 72
BMD. See Bone mineral density (BMD)
BMP-2. See Bone morphogenetic protein 2
(BMP-2)
BMSCs. See Bone marrow-derived stem cells
(BMSCs)
Bone
loss of following tendon or ligament injury, 54,
54f
rehabilitation regimen based on injury to,
416–417
Bone marrow-derived stem cells (BMSCs)
for augmentation of tendon healing, 19, 61
Singapore experience and methods, 154
for tissue engineering, 73–74
in zone 2 tendon healing, 17
Bone mineral density (BMD), decrease following
tendon or ligament repair, 54, 54f
Bone morphogenetic protein 2 (BMP-2), 55
Bony pulleys, 8
Botulinum toxin A
as adjunct to surgery in children, 182
tendon-bone insertion site development and,
52–53, 52f
tendon-bone insertion site healing and, 55
Boutonnière deformity, 350
outline, 383–392
post-traumatic, 383–384, 384f
nonoperative treatment of, 385–386
operative treatment of, 386
reconstruction for, 389–390, 390f
rehabilitation for, 430–432, 431f–432f
rheumatoid, 384–385, 386f
general management of, 387
nonoperative management of, 387
operative management of, 387, 387f
of thumb, 385, 388–389
Bowstringing, 8–9
active force and, 31, 32f
distal, 101–102, 101f–102f
due to absence of pulleys, 89
due to rupture of pulleys, 233–234, 234f–236f
following enlargement of sheath and pulleys,
112–113
Nantong experience and methods, 149, 150f
venting of pulleys and, 94, 94f
“Boxer’s knuckle”, 357, 360
Boxing glove-type dressing, 418–419, 419f
Boyes-Lister method for evaluation, 251–252,
252t
Boyes’ preoperative classification, 266, 267t
modified by Merle and Dautel, 266, 267t
Boyes test, 383–384
Boyes transfer for digital extension restoration,
369
Braided polyester suture, 164–166
Brand tendon transfer, 368–369, 368f
Brewerton view, 357–358, 358f
Bridge grafts in flexor pollicis longus tendon
repair, 290
Bridge splint, sagittal band, 359, 360f
Bruner incision
for flexor tendon reconstruction
in modified Paneva-Holevich technique, 308,
308f
single-stage, 280
two-stage, 277, 277f
Nantong experience and methods, 138, 140f
in pediatric repair, 184, 184f
Standford experience and methods, 158
Buck-Gramcko criteria, 122t, 251–252, 252t
Buddy splint for sagittal band injury, 359, 360f
Bulk after tendon repair, minimizing of, 25
Bundle, collagen, 29
Bunnell, S, 239–240
Bunnell’s intrinsic tightness test, 384
“Buttonhole” deformity, 383
C
Cage activity for tendon-bone healing, 54–55
Calcification in tendon-bone insertion, 50
Caliber of sutures, 243–244
Australian experience and methods, 165–166
in flexor pollicis longus tendon repair, 190
for increased strength of surgical repair, 44–45,
45f, 45t
for pediatric repair, 184
rehabilitation program and, 418
Stanford experience, 157
symposium discussion on, 442
of zone 5 flexor tendon repair, 201
CAM. See Controlled active mobilization (CAM)
Capener splint, 431, 431f
Capillary refill in pediatric diagnosis, 181
Carbodiimide-derivatized hyaluronic acid mixture,
282–283, 283f
Carpal disorders
symposium of, 447–449
tendon rupture after, 228–232, 229f, 230t,
231f
Carpal ligament
dorsal, 4
transverse, 3
pulley system and, 9
Carpal tunnel
anatomy of, 3
as flexor tendon zone 5, 6f
release of, 3
sliding unit in, 6f
Carpometacarpal (CMC) joint, rheumatoid
deformity of, 385, 388–389
Cartilage, lubrication mechanism of, 27–28
Cascade, flexor tendon grafting and, 281, 281f,
283f
Cast immobilization
in children, 182, 184
for tendon-bone insertion site healing, 55
for zone 5 flexor tendon repair, 199–200,
199f
Catheter technique for tendon retrieval, 161–162,
162f
Cells
in tendons, 72
for tendon tissue engineering, 73–74
future of, 441–442
Central slip
anatomy of, 12, 12f
injury to, 350, 383–384
(See also Boutonnière deformity)
primary repair of, 389
reconstruction using local tissue for, 389,
390f
reconstruction using tendon graft for,
389–390
rehabilitation for, 430–432, 431f–432f
Chelmsford experience, 125–132
complex suturing, 130–131
early active mobilization, 126
early results, 126–127
economic factors, 131
etiology of ruptures, 127–128
5% rupture rate, 127
flexor pollicis longus repair, 130
passive mobilization, 126
rupture re-repair, 128–129
splinted wrist position, 128
stronger repairs, 129
venting of pulleys, 129
zone 2 as a black box, 129–130
Chiasma tendinum of Camper, 10
Children, flexor tendon injury in, 179–185
adjuncts to surgery, 182
complications, 183
current treatment recommendations, 184–185,
184f
diagnosis of, 179–181, 180f–181f
flexor tendon grafting for, 183–184
incidence of, 179
Biomechanics (Continued)

454
Index
major reports and important information on,
250
Nantong experience and methods, 146–147
outcomes, 182
rehabilitation, 182, 418–419, 418f–419f
treatment of, 182
Chondrocytes in tendon-bone insertion site
development, 51–52
Circle-lock tendon-suture junction, 37, 37f
strength of, 38
“Clean-cut” wound repair, 84, 85f
“Climber’s finger”, 234f
Clinical reports, 247t, 248–250
Closed rupture of tendon, 83
CMC. See Carpometacarpal (CMC) joint
Cobra splint and rubber band rehabilitation, 119,
120f
Collagen, 29, 72
for augmentation of tendon healing, 19–20,
19f
gene therapy and, 62–63, 66–67, 68f
for scaffold in tissue engineering, 74–75
in tendon-bone insertion, 49–50
development of, 51
stress and strain concentration and, 50–51
in tendon healing, 72
in tendon lubrication
extrasynovial, 28–29, 29f
intrasynovial, 27–28, 28f
Complete closure. See Direct closure
Complete injury, rehabilitation regimen for, 417
Complete laceration, 85
Compliance, rehabilitation regimen and, 418
Complications
in children, 183
of modified Paneva-Holevich technique,
310–312
of partial tendon laceration, 175–176, 176f
of single-stage free tendon grafting, 272
of six-strand Lim/Tsai repair, 122, 122t
Computed tomography (CT) of fracture or carpal
disorder-associated rupture, 231, 231f
“Concertina effect”, 89
Connective tissue, subsynovial, 5, 6f–7f
Contamination of wound, 83
Contracture, flexion, of interphalangeal joint,
421–422
Controlled active mobilization (CAM), 244
symposium discussion on, 449
Controlled-release delivery system for
administration of growth factors, 61
Core suture lock, importance of length of, 42,
42f
Core suture purchase
grasping and locking junctions and, 37
importance of length of, 42
Stanford experience and, 157
Core suture repair, 35–37
biomechanics of, 36–37
set up and measurement of, 45–46, 46f
in children, 184
grasping and locking junctions in, 37–38
history of developments in, 241–244
of partial tendon laceration, 174–175, 175f
strength of, 38–40, 39t, 40f–41f
Australian experience and methods and,
163–164
in early healing, 42–43
during early tendon healing, 42–43
factors affecting, 41, 42f
finger flexion and, 43, 44f
in flexor pollicis longus tendon repair, 187
future of, 443
increasing of, 44–45, 45f, 45t
Stanford experience and, 157
suture purchase and lock (grasp) size in, 42
tension of suture repair in gap formation and,
41–42
traumatized tissue softening and, 43–44
C1 pulley
anatomy of, 7f, 8
bowstringing due to excision of, 101–102, 101f
rupture of, 233–234, 234f–235f
C2 pulley
anatomy of, 7f, 8
bowstringing due to excision of, 101–102, 101f
C3 pulley, 7f, 8
Creep, 29–30, 30f
“Crimp grip”, 233, 234f
Criteria, development of, 254–255, 256f, 257t
Cross finger flap, 301–302, 302f
reverse, 373, 374f
Cross-lock tendon-suture junction, 37, 37f
strength of, 38, 39t
Cross-stitch suture, 41f, 248–249. See also
Silfverskiöld (cross-stitch) suture
strength of, 40–41
Cruciate pulleys. See also Specific pulleys
anatomy of, 7f, 8–9, 88, 89f
bowstringing due to excision of, 101–102,
101f
function of, 89
preservation of in loss of annular pulleys,
95–96
Cruciate repair
Australian experience and methods, 164
Nantong experience and methods, 141f
strength of, 38, 39t
Crush injury repair, 84, 85f
CTGF gene, gene therapy for suppression of,
66–67, 68f
Current status of tendon repair, 441–443
Customization of flexor tendon rehabilitation,
415–426
age in, 418–419, 418f–419f
extent of injury in, 415–417, 416f
length of time from injury to repair in,
417–418
patient characteristics and compliance in, 418
type and quality of repair in, 418
type of injury in, 417
zone if injury in, 419–424
zone 1, 419–421, 420f–421f
zone 2, 421–422, 423f
zone 3, 422–423
zone 4, 422–423
zone 5, 424
Cutaneotendinous free flap, dorsalis pedis, 394,
397–398, 397f–399f
Cyclic loading measurement, 46
Cytokines
for augmentation of tendon healing, 19f
future of, 441–442
in tendon healing, 17
D
DBS. See Dorsal blocking splint (DBS)
Débridement, wound, in soft tissue coverage for
extensor tendon reconstruction, 371–372,
372f
Decision-making process
in primary flexor tendon repair, 84f
in six-strand Lim/Tsai repair, 84f
Delayed flexor tendon repair, 86
absolute contraindications to, 87
annular pulley preservation in, 95–96
in children, 183
flow-chart of decision-making process in, 84f
indications for, 84–85
borderline, 85–87
Omega pulley plasty in, 107, 109f
timing of, 83–84, 84f
Delivery
of drugs using sutures, 77
of gene therapy, 61–62, 64f
in tissue engineering, 76
Dermal fibroblasts for tissue engineering, 73
Digital flexor tendon sheath. See also Flexor
tendon sheath
anatomy and structure of, 5–6, 88–89
vencula in, 6
in zone 2, 6f
“Digital sheath syndrome”, 91
DIP. See Distal interphalangeal (DIP) joint
Direct closure of flexor tendon sheath, 91f,
93–94
problems with, 98
Dislocation as sagittal band injury, 357, 357f
in thumb, 361
Distal bowstringing, 101–102, 101f–102f
Distal interphalangeal (DIP) joint
arthrodesis of for swan-neck deformity, 387–388
assessment of, 82, 83f
early passive mobilization and, 406, 407f
flexion of in swan-neck deformity, 384–385
(See also Swan-neck deformity)
general management of injuries of, 347–349,
348f
hyperextension of in boutonnière deformity, 383
immobilization of, 429, 429f
manipulation of for Omega plasty of A4 pulley,
105, 105f–106f
motion of following enlargement of sheath and
pulley, 112, 113t
pulley venting in zone 2 and, 99–100
stiffness of, 253–254
traumatic tendon avulsion and, 220–221, 221f,
223, 224t, 225
Distal junction suture
in single-stage tendon grafting, 267–269, 268f,
281
of flexor pollicis longus tendon, 291, 291f
in vascular tendon transfer, 327–329
Distal phalanx, pulley system in, 8
Documentation of rehabilitation for extensor
tendon repair, 429
Dorsal annular ligament, 4
Dorsal blocking splint (DBS), 157, 159–160
Dorsal carpal ligament, 4
Dorsal hood, 12
Dorsal interosseous muscles, 9–10
Dorsalis pedis cutaneotendinous free flap, 394,
397–398, 397f–399f
Dorsal metacarpal artery (DMA) flap
first, 373–375, 375f
perforator-based, 376–377, 376f
second, 375–376
Dorsal radial artery thumb flap, 377, 377f
Dorsum of hand, injuries over, 352
Dressings, rehabilitation and, 416, 416f
in children, 418–419, 419f
Drugs
sutures for delivery of, 77
for tendon healing manipulation, 19
Duran Houser technique, 126
Duran postoperative protocol
modified, 406–407
Mayo Clinic experience, 136
symposium discussion on, 449
E
Early mobilization, 18–19
in children, 182
in partial tendon laceration, 173
rupture and, 172–173
in Standford experience and methods, 159
for tendon-bone healing, 54
in zone 5 repair of FDS tendon, 196
Early mobilization, active
for flexor tendon repair rehabilitation, 407–409,
408f
Chelmsford experience, 126
controlling flexion force in, 409–410,
409f–410f
of flexor pollicis longus tendon, 187, 188f,
190t
following tenolysis, 263–264
in Mantero technique, 205
in St. Andrews regimen, 128
Standford experience and methods, 159
strength of sutures and, 129
in tendon transfer for extensor tendon
reconstruction rehabilitation, 370
Early mobilization, passive
for flexor tendon rehabilitation, 406–407,
406f–407f
Standford experience and methods, 159
in tendon transfer for extensor tendon
rehabilitation, 369–370
Early tendon healing, strength during, 42–43
Ecchymosis in traumatic tendon avulsion, 221, 221f
Children, flexor tendon injury in (Continued)

455
Index
ECM. See Extracellular matrix (ECM)
Economic factors
Chelmsford experience regarding, 131
in staged tendon grafting, 299
ECRB. See Extensor carpi radialis brevis (ECRB)
tendon
ECRL. See Extensor carpi radialis longus (ECRL)
tendon
ECU. See Extensor carpi ulnaris (ECU) tendon
EDC. See Extensor digitorum communis (EDC)
tendon
Edema
prevention of in vascular tendon transfer
rehabilitation, 341
rehabilitation and, 410–411
rupture of repair due to, 253
EDL. See Extensor digitorum longus (EDL) tendon,
harvesting and grafting of
EDM. See Extensor digiti minimi (EDM) tendon
Eight-strand core suture repair, 36–37
EIP. See Extensor indicis proprius (EIP) tendon
Elasticity, Young’s modulus of, 29–30
Elastin in tendon, 29
Elongation of tendon, 29–30, 30f
Elson test, 349–350, 383–384
End-to-end repair, 35
biomechanics of
essential mechanical requirements in, 35–36
historical reviews of, 36, 36b
outline of, 35–47
evolution of, 239–245, 241f–243f
Energy to failure, measurement of, 45–46
Enlargement
of pulley, 111–115
of tendon sheath, 111–115, 113t, 114f
investigation of, 89–92, 92b
Enthesis. See Tendon-bone insertion
Entrapment, partial tendon laceration and,
175–176, 176f
EPB. See Extensor pollicis brevis (EPB) tendon
Epitendinous sutures, 35. See also Peripheral suture
repair
Epitenon
anatomy of, 6, 6f
cells of
tendon friction and, 26, 26f
in tendon healing, 16–17, 17f
tendon lubrication and, 27–28, 28f
EPL. See Extensor pollicis longus (EPL) tendon
Ethilon material, Australian experience and
methods, 164
Evaluation, 81–83, 83f
development of comprehensive universally
acceptable criteria for, 254–255, 256f,
257t
methods of, 250–252, 251t–252t
Excision, flexor tendon sheath, 94
investigations regarding, 89–92
Excursion, flexor tendon, 30
force and, 31
joint moment arm and, 30–31, 31f
joint motion and, 30
Exercise. See Rehabilitation
Expertise level of surgeon
development of comprehensive universally
acceptable criteria for, 255–256, 257t
effects on outcomes, 254
future of, 445
zone 5 flexor tendon repair outcomes and,
200–201, 200f
Extension
active
for boutonnière deformity, 431, 432f
in six-strand Lim/Tsai repair rehabilitation,
119–121, 120f
in tendon transfer for extensor tendon
reconstruction rehabilitation, 370
in vascular tendon transfer rehabilitation, 341,
341f
digit, tendon transfer for restoration of,
368–369, 368f
thumb, tendon transfer for restoration of,
367–368
wrist, tendon transfer for restoration of, 367
Extension deficit
as evaluation criteria, 252t
following vascular tendon transfer, 342–343
in Lim/Tsai method versus modified Kessler
method, 121, 121t
Extensor carpi radialis brevis (ECRB) tendon
anatomy of, 10f, 11, 364
tendon transfer for reconstruction of, 367,
367t
Extensor carpi radialis longus (ECRL) tendon,
10f, 11, 364
Extensor carpi ulnaris (ECU) tendon, 364
Extensor digiti minimi (EDM) tendon, 10f, 11
Extensor digitorum communis (EDC) tendon
anatomy of, 10f, 11, 364
for digital extension restoration, 361
rehabilitation for, 433
ulnar slip of for sagittal band reconstruction,
361
Extensor digitorum longus (EDL) tendon,
harvesting and grafting of, 269f
Extensor expansion, 12
Extensor hood reconstruction, 362f
Extensor indicis proprius (EIP) tendon
anatomy of, 10f, 11, 364
for tendon transfer for EPL rupture, 366,
366f–367f
Extensor pollicis brevis (EPB) tendon
anatomy of, 10–11, 10f, 364
rehabilitation for, 434–436
in thumb, 14
Extensor pollicis longus (EPL) tendon
anatomy of, 10f, 11, 364
rehabilitation for, 434–436
rerouting of for rheumatoid deformity of
thumb, 388
rupture of, 352
tendon transfer for traumatic injury to,
366–368, 366f–367f, 367t
in thumb, 14
Extensor retinaculum
anatomy of, 4
grafting of for rupture of pulley, 233–238, 235t,
236f–237f
rehabilitation for, 434
Extensor tendon anatomy, 364
of fingers, 12–13, 12f–13f
rehabilitation and, 427–437, 428f
variations to the fingers, 11–12
at wrist, 10–11, 10f
Extensor tendon repair and reconstruction
of boutonnière deformity
outline, 383–392
post-traumatic, 383–386, 384f
reconstruction for, 389–390, 390f
rheumatoid, 384–385, 387–389, 387f
of distal interphalangeal joint, 347–349, 348f
of metacarpophalangeal joint, 351–352
of middle finger, 349, 350f
outline, 347–353
over dorsum of hand, 352
of proximal interphalangeal joint, 349–350
of proximal phalanx, 351
rehabilitation for, 427–438
of sagittal band injuries, 355–363
anatomy and biomechanics, 355–357, 356f
causes, 357, 357f
classification, 357, 357f
diagnosis, 357, 358b
differential diagnosis, 357–358, 358f
immobilization for, 359, 359f–360f
surgery for, 359–361, 361f–362f
to thumb, 361
treatment methods, 358–361, 358b
soft tissue coverage for, 371–382
anterolateral thigh flap, 379–380, 381f
discussion, 380–382
evaluation and treatment, 371
free flaps, 378–379
intrinsic flaps, 372–373
lateral arm flap, 379, 379f–380f
local flaps, 377–378
metacarpal artery island flaps, 373–377,
375f–376f
outline, 371–382
reverse cross-finger flap, 373, 374f
scapula/parascapular flap, 379
secondary procedures, 380
thumb dorsal radial artery flap, 377, 377f
timing of, 372
turnover and distally based adipofascial flap,
373
wound débridement, 371–372, 372f
of swan-neck deformity
post-traumatic, 384, 386–387, 386f
reconstruction for, 390–391, 391f
rheumatoid, 385, 386f, 387–389
tendon transfer for, 364–370
methods of treatment, 366–369, 366f–368f,
367t
outline, 364–370
principles of, 365t
rehabilitation following, 369–370
treatment alternatives for, 369, 369f
vascularized tendon graft for, 394–402
discussion, 397–400, 397f–401f
operative techniques, 394–395, 395f
outcomes, 396, 396f
outline, 394–401
postoperative care, 395–396
of wrist and distal and proximal forearm,
352–353
in zone 1, 347–349
in zone 2, 349
in zone 3, 349–350
in zone 4, 351
in zone 5, 351–352, 351f
in zone 6, 352
in zone 7,8, and 9, 352–353, 352f–353f
Extent of flexor tendon injury, rehabilitation
regimen based on, 415–417, 416f
Extracellular matrix (ECM), 29
in tendon healing, 16–17
Extrasynovial tendons
flexor tendons as, 5f
friction of, 26–27, 26f–27f
gliding mechanism of, 28–29, 29f
lubrication of, 28–29, 29f
nutrition for, 16
Extrinsic tendon healing, 72–73
F
Failure load, measurement of, 45–46
Failure region of stress-strain curve, 29–30, 29f
Fascicles, collagen, 29
Fasciocutaneous flap, 379
FCR. See Flexor carpi radialis (FCR) tendon
FCU. See Flexor carpi ulnaris (FCU) tendon
FDMA. See First dorsal metacarpal artery (FDMA)
flap
FDP. See Flexor digitorum profundus (FDP)
FDS. See Flexor digitorum superficialis (FDS)
FiberWire, 169
Fibrils, collagen, 29
Fibroblasts
5-fluorouracil for suppression of, 19
in tendon-bone insertion, 49–50
for tissue engineering, 73
future of, 441–442
Fibrocartilage in tendon-bone insertion, 49–50,
50f
Fibrochondrocytes in tendon-bone insertion,
49–50
Fibrous sheath, Omega pulley plasty and,
104–105, 107
Fibrous transition at tendon-bone insertion site,
49–50
Fibrovascular scar in tendon-bone healing, 53,
53f
“Fight bite” injury, 351, 351f, 357
Figure-of-eight ring splinting for swan-neck
deformity, 386, 386f
Finger(s)
cascade of, flexor tendon grafting and, 281, 281f,
283f
“climber’s”, 234f
Extensor tendon repair and reconstruction
(Continued)

456
Index
extensor tendons of, 11–12, 12f–13f
“jersey”, 83, 219
mallet, 347–349, 348f
rehabilitation for, 429–430, 429f–430f
pulley system in, 8
“rugby”, 219
strength of suture repair during flexion of, 43,
44f
supple, as criteria for tenolysis, 261
tendon transfer for restoration of extension of,
368–369, 368f
Finger-to-palm distance method for evaluation,
251–252, 252t
First dorsal metacarpal artery (FDMA) flap,
373–375, 375f
5% rupture rate, 127
Flap coverage/reconstruction
for extensor tendon injuries, 371–382
anterolateral thigh flap, 379–380, 381f
discussion, 380–382
dorsalis pedis cutaneotendinous free flap,
394, 397–398, 397f–399f
evaluation and treatment, 371
free flaps, 378–379
intrinsic flaps, 372–373
lateral arm flap, 379, 379f–380f
local flaps, 377–378
metacarpal artery island flaps, 373–377,
375f–376f
outline, 371–382
radial artery forearm island flap with
vascularized tendons, 394–395, 398–399,
400f
reverse cross-finger flap, 373, 374f
scapula/parascapular flap, 379
secondary procedures, 380
thumb dorsal radial artery flap, 377, 377f
timing of, 372
turnover and distally based adipofascial flap,
373
wound débridement, 371–372, 372f
for flexor tendon injuries, 301–303, 302f–304f
rehabilitation and, 416
for open mallet injury, 349, 349f
ulnar artery-based
(See also Vascularized tendon transfer/graft)
for extensor tendon injuries, 395–396,
395f–396f
for flexor tendon injuries, 327–332,
330f–332f
Flexion
active
for boutonnière deformity, 431, 432f
in flexor tendon rehabilitation, 407
distal interphalangeal joint
for early passive immobilization, 406, 407f
for mallet finger, 430, 430f
in swan-neck deformity, 384
metacarpophalangeal joint
lumbrical muscles and, 9
in swan-neck deformity, 385
(See also Swan-neck deformity)
proximal interphalangeal joint
in boutonnière deformity, 383
(See also Boutonnière deformity)
following repair of ruptured pulley, 235
strength of suture repair during, 43, 44f
tendon excursion and, 31, 32f
work of, 407
Flexion-block splint for sagittal band injury, 359f
Flexion contractures of interphalangeal joint,
421–422
Flexion deformity of distal interphalangeal joint,
347–348, 348f
Flexion mobilization
active
in Mantero technique, 205, 205f
in Nantong repair rehabilitation, 147–148,
147f
rupture of repair due to unprotected, 253
in six-strand Lim/Tsai repair rehabilitation,
121
in Standford experience and methods, 159
controlling force during, 409–410, 409f–410f
passive
in Nantong repair rehabilitation, 147–148,
147f
in Singapore repair rehabilitation, 154
in six-strand Lim/Tsai repair rehabilitation,
119–121, 120f
in Standford experience and methods, 159
in vascular tendon transfer rehabilitation, 341,
341f–342f
Flexor carpi radialis (FCR) tendon
anatomy of, 4–5
for tendon transfer, 368–369, 368f
Flexor carpi ulnaris (FCU) tendon
anatomy of, 5
tendon transfer
for digital extension restoration, 369
for extensor tendon reconstruction, 395, 395f,
398–399
Flexor digitorum profundus (FDP) tendon
accessory slips for, 4
Australian experience and methods, 161,
164–165
early passive mobilization and, 406, 407f
enlargement of sheath and pulley in repair of,
112–113, 113t, 114f
examination of, 82, 83f
fracture or carpal disorders-associated rupture
of, 228–232, 230t, 231f
Mantero technique in repair of, 203–207
Mayo Clinic experience and methods, 133–136,
134f–135f
Nantong experience and methods, 140–141,
143–144
Omega pulley plasty in repair of, 105,
105f–106f, 107, 108f
pediatric repair of, 146–147, 184
pulley venting in repair of, 99–101, 100f
rehabilitation for, 419–421
severity of injury to, 85
sheaths of, 5–6
Standford experience and methods, 158
tendon excursion of, 30, 31f
tendon grafting for repair of
historical perspective, 275–276
modified Paneva-Holevich technique,
307–313
single-stage, 266–273, 279–281
two-stage, 281–282, 297–306
traumatic avulsion of, 219–227
in zone 1, 6f
in zone 2, 6f
Flexor digitorum superficialis (FDS) tendon
accessory slips for, 4
Australian experience and methods, 161
enlargement of sheath and pulley in repair of,
113t
examination of, 82, 83f
fracture or carpal disorder-associated rupture of,
228–232, 230t
modified Paneva-Holevich technique for repair
of, 307–313
Nantong repair of, 140–141
in zone 2, 142–143, 144f–146f
in zone 3, 143
pediatric repair of, 184
severity of injury to, 85
sheaths of, 5–6
Singapore experience and methods, 154
single-stage free tendon grafting for repair of,
266–273
Standford experience and methods, 158
for tendon transfer
in flexor pollicis longus tendon
reconstruction, 292, 292f
in restoration of thumb extension, 368
traumatic avulsion of, 219–227
for vascularized tendon grafting, 327–329,
328f–330f
(See also Vascularized tendon transfer/graft)
in zone 2, 6f
zone 5 repair of, 195–196
Flexor pollicis brevis (FPB) tendon, 13, 13f
Flexor pollicis longus (FPL) tendon
anatomy of, 4–5, 13
no repair of, 289, 289f
repair of, 186–193
before 1989, 186–187
from 1989-1999, 186–187
from 1999-2004, 187, 188f
from 2004-2009, 187, 190f, 190t
Chelmsford experience and methods, 130
interphalangeal joint motion and, 289–290
lengthening of tendon in, 286, 288f
major reports and important information on,
250
management of, 190–191, 191f
Mantero technique for, 203–207
Nantong experience and methods, 144–146
preference for, 285
primary grafting in zone 3 and 4, 285–286
problems of, 186
rehabilitation for, 406, 407f, 417, 417f
re-repair of, 191
rupture of, 187
summary of major studies of, 189t
techniques to extend, 286–289, 287f–288f
in zone 2, 186
in zone 3, 285–286
in zone 4, 285–286
secondary reconstruction of, 285–296
bridge grafts, 290
distal and proximal attachment, 291, 291f
FPL muscle and, 290
outcomes and prognosis, 295
rehabilitation, 295
setting of tension in, 291–292
tendon transfer and, 289f, 292–293
thenar tunnel and, 291
two-stage, 293–295, 293f–294f
wrist-to-distal phalanx graft, 291
Flexor retinaculum
anatomy of, 3
release of for carpal tunnel disease, 3
Flexor retinaculum carpi, 3
Flexor superficialis indicis tendon, 4
Flexor tendons
anatomical divisions of, 81, 82f
anatomy of, 4–5
biomechanics of, 30–32
bowstringing of, pulley system and, 8–9
grafting of in children, 183–184
healing of in zone 2, 17
zones of, 6f, 81, 82f
Flexor tendon injury
etiologies and evaluation of, 81–83, 83f
symposium of, 446–449
Flexor tendon repair. See also Primary flexor
tendon repair; Secondary flexor tendon repair
absolute contraindications to, 87
Bern experience, 116–124
Chelmsford experience, 125–132
in children, 179–185
current status of, 441
early mobilization following, 18–19
early strategies in, 239–240
evolution of, 239–245, 241f–243f
of flexor pollicis longus tendon, 186–193
flexor sheath and pulley treatment in, 88–97
anatomy and, 88–89, 89f
considerations in, 96–97
enlargement of sheath and pulley in, 111–115
function and, 89
guidelines for, 93
historical review of, 89, 90b–91b
indications and operative methods for,
93–96
investigations associated with, 89–93,
91f–92f, 92b
Omega pulley plasty in, 104–110
venting of pulleys in, 94–96, 94f–95f,
98–103
flow-chart of decision-making process in, 84f
future of, 441–445
indications for, 84–85, 85f
borderline, 85–87
Mayo Clinic experience regarding, 133
Finger(s) (Continued)
Flexion mobilization (Continued)

457
Index
Mantero technique for, 203–207
outcomes (See Outcomes)
of partial tendon laceration, 171–178
reconstruction (See Reconstruction)
rehabilitation after, 405–426
(See also Rehabilitation)
relation of postsurgical mobilization methods to
surgical technique in, 244
rupture of (See Rupture)
splint-free, 153
strength of (See Strength)
Teno Fix Tendon Repair System for, 208–213
tenolysis, 261–265
timing of, 83–84, 84f
of traumatic avulsion, 219–227
authors’ personal experience, 225–226, 225f,
226t
background, 219
classification of, 220–221, 220f
diagnosis of, 221–222, 221f
mechanism of injury, 219–220, 220f
outcomes, 224–225
postoperative care, 224, 224f
treatment of, 222–224, 222f–224f, 224t
in zone 5, 194–202
Flexor tendon sheath
anatomy of, 5–6, 5f–6f, 72, 88–89, 89f
Omega pulley plasty and, 104–105
function of, 89
healing of, history of views on, 240–241
rupture of primary flexor tendon repair and,
214–215
treatment of (See Flexor tendon sheath
treatment)
Flexor tendon sheath treatment
considerations in, 96–97
direct closure in, 93–94
enlargement in, 111–115, 113t, 114f
investigation of, 89–92
excision in, 94
guidelines for, 93
historical review of, 89, 90b–91b
indications and operative methods for, 93–96
investigations of, 89–93, 91f, 92b
reconstruction by grafts, 94
venting of pulleys in, 94–96, 94f–95f
Flow-chart of decision-making process
in primary flexor tendon repair, 84f
in six-strand Lim/Tsai repair, 84f
5-Fluorouracil (5-FU) for tendon healing, 19
Force
controlling flexion, 409–410, 409f–410f
for tendon-bone healing, 54
tendon excursion and, 31
Forearm flap, radial, 378
with vascularized tendons, 394–395, 398–399,
400f
Forearm injury, 352–353, 353f
rehabilitation for, 434
Four-strand cruciate repair, 40f
strength of, 39t
Four-strand Kessler repair
of flexor pollicis longus tendon, 190t
strength of, 38
Four-strand MGH repair, 39t
Four-strand repair, 36–37
Adelaide repair as, 164, 164f, 166
symposium discussion on, 444–445
in children, 182
of flexor pollicis longus tendon, 187–189,
190t
major reports and important information on,
249
Nantong experience and methods, 141f
rehabilitation program and, 418
Standford experience and methods, 158
strength of, 38, 39t
suture caliber and, 44–45, 45f
strength-versus-force graph for, 163f
Wellington, New Zealand experience, 169
of zone 5 flexor tendon injuries, 201
Four-strand Strickland repair, 40f
strength of, 38, 39t
Four-strand Tsuge-type repair, 188–189
4-0 sutures
Australian experience and methods, 165–166
strength of repair with, 44, 45f, 45t
FPB. See Flexor pollicis brevis (FPB) tendon
FPL. See Flexor pollicis longus (FPL) tendon
Fracture, 86
mallet, 347–348, 348f
tendon rupture after, 228–232, 229f, 230t,
231f
Free flap reconstruction for extensor tendon
injuries, 378–379, 394
Free tendon grafting
single-stage, 266–273
vascularized, 336–338, 337f
Friction, tendon
in different tendon surroundings, 26–27,
26f–28f
effects on tendon healing, 17–18, 18f
in pathological conditions, 25–26
in physiological conditions, 24–25, 25f–26f
pulley system and, 9
reduction of after repair, 25
sliding system and, 324
Frictional coefficient, 24
Frictional force, 24–25, 26f
of repaired tendon, 25–26
with gap formation, 25–26
5-FU. See 5-Fluorouracil (5-FU)
Function grade in evaluation, 251t
Future
of flexor tendon surgery, 441–442
secondary, 282–283, 283f
of gene therapy, 68
of tendon surgery, 442–445
of vascularized tendon transfer for extensor
reconstruction, 336–338, 337f–338f
G
Galen, 274
Gap formation/gapping
FPL tendon, lengthening for, 286
frictional force and, 25–26
measurement of, 46
partial tendon laceration and, 172–173
tension of suture repair and, 41–42
Gapping force(es)
measurement of, 45–46
in “safe zone”, 18, 19f
Gap resistance
measurement of, 46
tension of repair and, 42
GDF-5. See Growth differentiation factor-5
(GDF-5)
Gelberman-St. Louis Group on biomechanics of
tendon repair, 36b
Gene expression in tendon-bone insertion, 50
Gene therapy, 59–70
associated with micro-RNA regulation, 66–67,
67f–68f
choosing of genes and delivery methods for,
61–62, 61f, 63f–64f
future perspectives, 68
growth factors for
in vitro testing of, 62–63, 64f
in vivo testing of, 64–66, 65f–66f
“no-gain” period in strength and, 60, 60f
outline, 59–68
overall concepts and methods of, 60
Gliding/gliding system
anatomy of, 324–327, 325f–326f
enlargement of sheath and pulley and, 91,
111–115
of extrasynovial autografts, improving of, 282
of extrasynovial tendon, 28–29, 29f
mechanical resistance to, 32
partial tendon laceration and, 173–174
pulley system in, 89
rehabilitation protocol and, 410
staged tendon grafting and, 297–298
vascular tendon transfer and, 323–327,
325f–326f, 330f
(See also Vascularized tendon transfer/graft)
venting of pulleys and, 92f, 93–96
Gliding resistance
in choosing rehabilitation protocol, 410
following enlargement of tendon sheath and
pulleys, 113, 114f
partial tendon laceration and, 174–175
pulley system and, 9
Gliding velocity, tendon friction and, 24–25, 26f
Graft(s)/grafting
allograft-matched tendon, 282–283
for arthritis or carpal disorder-associated rupture
repair, 228–232, 230t
in children, 183–184
enlargement plasty of tendon sheath by, 89–92,
92b
flexor pollicis longus tendon
bridge grafts, 290
distal and proximal attachment, 291
FPL muscle and, 290
outcomes and prognosis, 295
rehabilitation, 295
setting of tension in, 291–292
tendon transfer and, 292–293, 292f
thenar tunnel and, 291
two-stage, 293–295, 293f–294f
wrist-to-distal phalanx graft, 291
rehabilitation and, 416
for rupture of pulley, 233–238, 236f
sheath reconstruction by, 94
single-stage tendon, 266–273, 275–276
complications, 272
indications, 266–267, 267t, 279–280, 280f
methods, 280–281, 280f–281f
operative methods, 267–271, 268f–270f
outcomes, 271–272, 272t, 281
postoperative care, 270–271
prognosis factors, 272
for tendon sheath and pulley enlargement, 112
two-stage tendon, 274, 276–278, 276f–277f,
297–306
clinical principles of, 300–305
correction of skin deficiencies at first stage of,
301–303, 301f–303f
first stage of, 300–301, 300f–301f
indications, 281–282
joint deficiency correction at first stage of,
304–305
method, 282, 282f
with modified Paneva-Holevich technique,
307–313
outcomes and prognosis, 282, 305–306
outline, 297–306
pseudo-sheath and, 298
pulley deficiency correction at first stage of,
304, 305f
second stage of, 305
single-stage versus, 298–300
skin deficiency correction at first stage of,
304f
vascularized
for extensor tendon reconstruction, 394–402
for flexor tendon reconstruction, 323–343
“Grasping jersey” mechanism, 219
Grasping tendon-suture junction, 36–38, 37f, 40f,
242, 242f
symposium discussion on, 442–445
Grip strength
in evaluation criteria, 251t, 252, 254
following rupture of pulleys repair, 235
in Lim/Tsai method versus modified Kessler
method, 121, 121t
Groin flap, 397
Growth differentiation factor-5 (GDF-5), 20, 77
Growth disturbances, pediatric, 183
Growth factors, 19–20, 19f, 62–66
controlled-release delivery system for
administration of, 61
for enhancement of tendon healing, 61
sutures for delivery of, 77
for tendon-bone healing, 55
in tissue engineering, 76
in vitro testing of, 62–63, 64f
in vivo testing of, 64–66, 65f–66f
Guard, splint, 418–419, 418f
Guyon’s canal, 5
Flexor tendon repair (Continued)

458
Index
H
HA. See Hyaluronic acid (HA)
Halsted peripheral suture, 241
major reports and important information on,
249
Hamate hook fracture, tendon rupture due to,
228–232, 230t
Hand, injuries over dorsum of, 352
Hand Clinics, 246
Healing
in children, 182
tendon, 16–17, 72
biological methods for enhancement of, 61
biology of, 16–17, 17f
cytokines for augmentation of, 19–20
effects of physical factors on, 17–19, 18f
extrinsic versus intrinsic, 72–73
future of, 441–442
gene therapy for, 59–70
history of views on, 240–241
“no-gain” period in strength and, 60f
partial tendon laceration and, 172
pharmacological manipulation of, 19
“safe zone” and, 18–19, 19f
stem cells for augmentation of, 19, 19f
strength during early, 42–43
tendon-bone, 53–56
biologically-based treatments for, 55–56, 56f
bone loss and, 54, 54f
rehabilitation-based treatments for, 54f
science of healing in, 53–54, 53f
Hemitrapeziectomy, carpometacarpal joint,
388–389
Herpes simplex virus vectors for gene therapy
delivery, 62
Historical reviews
of biomechanics of surgical repair, 36, 36b
of flexor sheath and pulley treatment, 89,
90b–91b
History
of flexor tendon reconstruction, 274–278
of primary flexor tendon repair, 125, 239–240
of venting of pulleys, 98–99
Homograft, vascularized tendon, 337–338, 338f
Hook of hamate fracture, tendon rupture due to,
228–232, 230t
Human dermal fibroblasts for tissue engineering,
73
Hunter rod, 277, 277f, 297–298
Hunter technique, Paneva-Holevich technique
modifications of, 307
Hyaluronic acid (HA)
carbodiimide-derivatized, 282–283, 283f
in tendon lubrication, 27–28, 28f
Hyperextension
of distal interphalangeal joint in boutonnière
deformity, 383
of metacarpophalangeal joint in boutonnière
deformity, 383
of proximal interphalangeal joint in swan-neck
deformity, 384
Hypertrophic zone in tendon-bone insertion site
development, 51
I
ICAM. See Immediate active controlled motion
(ICAM) technique
IGF-1. See Insulin-like growth factor-1 (IGF-1)
IHH. See Indian Hedgehog (IHH) in tendon-bone
insertion site development
Immediate active controlled motion (ICAM)
technique, 433
Immobilization
in extensor tendon repair rehabilitation
for boutonnière deformity, 431
for mallet injury, 348, 429–430, 429f
for proximal interphalangeal joint, 350
for sagittal band injuries, 359, 359f–362f
in flexor tendon repair rehabilitation, 405–406
in children, 182, 184, 418–419, 419f
early, 405–406
early passive, 406–407, 406f–407f
in rupture of pulleys repair and rehabilitation,
235
in single-stage free tendon grafting
rehabilitation, 270
tendon-bone healing and, 54–55
tendon healing and, 72
in thumb, 434–436, 435f–436f
in traumatic avulsion of flexor tendon repair
rehabilitation, 224, 224f
for zone 5 flexor tendon repair, 199–200,
199f
Implant, silicone
in modified Paneva-Holevich technique,
307–308, 308f
in two-stage tendon grafting, 282, 282f,
297–298, 300–301, 301f
Incision(s)
in A2 and A4 pulleys, 95–96
for correction of skin deficiencies, 301–302,
301f–302f
for flexor tendon reconstruction
in modified Paneva-Holevich technique,
308–310, 308f–309f
single-stage, 267, 268f, 280
two-stage, 277, 277f
Nantong experience and methods
sheath and pulleys incisions, 138–140
skin incisions, 138, 140f
in pediatric repair, 184, 184f
for release of pulleys, 95f
Standford experience and methods, 158
for tenolysis, 262, 262f
for two-stage flexor tendon reconstruction, 277,
277f
for ulnar artery harvesting with vascularized
tendons, 395, 395f
in vascular tendon transfer, 327, 332f
Index finger, extensor tendons in, 11
Indianapolis program, 408, 408f
Indian Hedgehog (IHH) in tendon-bone insertion
site development, 51
Indications for flexor tendon repair, 84–85
borderline, 85–87
Mayo Clinic experience regarding, 133
single-stage tendon grafting, 266–267, 267t,
279–280, 280f
two-stage tendon grafting, 281–282
using Mantero technique, 203
using modified Paneva-Holevich technique,
307–308
Infection
following modified Paneva-Holevich technique,
311–312
rehabilitation and, 416
sagittal band injury due to, 357
Inflammatory stage of tendon healing, 72
Infratendinous layer of extensor retinaculum, 4
Insulin-like growth factor-1 (IGF-1), 61
in tissue engineering, 76
Interosseous artery flap, posterior, 378
Interosseous muscles
anatomy of, 9–10
extensor mechanism of fingers and, 12
Interphalangeal (IP) joint. See also Distal
interphalangeal (DIP) joint; Proximal
interphalangeal (PIP) joint
flexion contractures of, 421–422
flexor pollicis longus tendon repair and,
289–290
secondary reconstruction of, 289–290
tendon lengthening and, 286–289
tension setting and, 291–292
rheumatoid deformity of in thumb, 385,
388–389
splinting position of
in Mayo Clinic experience and methods, 136
in vascular tendon transfer, 340–341
Interrupted peripheral suture repair, strength of,
40–41
“Intersection syndrome”, 11
Intertendinous lamina, 12
Intrasynovial tendons, 5f, 72
friction of, 26–27, 26f–27f
lubrication of, 27–28, 28f
nutrition for, 16
Intrinsic tendon healing, 72–73
In vitro testing of growth factors for gene therapy,
62–63, 64f
In vivo testing of growth factors for gene therapy,
64–66, 65f–66f
IP joint. See Interphalangeal (IP) joint
Island flap
metacarpal artery, 373
first dorsal, 373–375, 375f
perforator-based dorsal, 376–377, 376f
second dorsal, 375–376
radial artery forearm, 394–395, 399–400,
400f–401f
ulnar artery-based, 395, 395f
Island tendon transfer for extensor reconstruction,
323–343
anatomical studies and surgical basis, 324–327,
325f–326f, 328f–329f
future challenges, 336–338, 337f–338f
operative procedures, 327–332, 330f–334f
outline, 323–338
physiotherapy after, 340–343, 341f–343f
results and outcomes, 332–336, 335f
J
“Jersey” finger, 83, 219
Joint
deficiency of, correction of in staged tendon
grafting, 304–305
motion of
pulley system and, 9
tendon excursion and, 30
positioning of after vascularized tendon transfer,
340–341
rehabilitation regimen based on injury to,
416–417
stiffness of, effects on outcomes, 253–254
tendon rupture due to disorders of, 228–232,
229f, 230t, 231f
Joint moment arm, 30–31, 31f
Jones transfer for digital extension restoration,
368–369
Journal of Hand Surgery (British Volume), 248
Journal of Hand Surgery (European Volume),
249–250
JT. See Junctura tendinae (JT)
Junction
in single-stage tendon grafting
distal, 267–269, 268f, 270f, 281
of flexor pollicis longus tendon, 291, 291f
proximal, 269, 280–281, 280f
strength of, 37–38, 37f
in two-stage tendon grafting
in modified Paneva-Holevich technique,
308–309, 308f, 310f
proximal, 282
in vascular tendon transfer, 327–329, 328f,
331f
Junctura tendinae (JT)
anatomy of, 10f, 12
for radial sagittal band reconstruction, 360–361,
362f
K
Kapandji’s method, 188f
Kessler-type repair, 40f
Australian experience and methods, 161, 164f
in enlargement of tendon sheath and pulleys,
112
of flexor pollicis longus tendon, 187–188, 188f,
190t
history of modifications to, 241–244
Nantong experience and methods, 141f
of partial tendon laceration, 174, 175f
six-strand Lim/Tsai repair versus, 117, 117t,
121–122, 121t
Standford experience and methods, 158,
158f
strength of, 38, 39t
symposium discussion on, 444–445
Kienböck’s disease, tendon rupture due to,
228–232
Kinetic frictional force, 24
Kite flap, 373–375, 375f
Immobilization (Continued)

459
Index
Kleinert rehabilitation technique, 406
Chelmsford experience and, 126
in FDS zone 5 repair, 195–196
following enlargement of tendon sheath and
pulleys, 112
future of, 444
modifications of, 406–407
in Omega plasty of A4 pulley, 105
symposium discussion on, 449
Kleinert repair technique, 240–241
Knives, tenolysis, 262–263, 262f
Knot(s)
Mayo Clinic experience, 133–136
reduction of friction and, 25
in tendon retrieval, 161–162, 162f
K-wire for repair of mallet injury, 348–349,
349f
L
Laceration, partial. See Partial tendon laceration
lacZ gene, 62–63
Lahey technique, 239–240
Lateral arm flap, 379, 379f–380f
Lateral bands
anatomy of, 12, 12f–13f
tenodesis of, 390–391, 391f
Lateral incision for release of pulleys, 95f
Leddy and Packer’s classification of traumatic
tendon avulsion, 220, 220f
Lee repair, modified, for partial tendon laceration,
175f
Length
of A2 and A4 pulleys, 88–89
of suture purchase and lock (grasp), 42, 42f
Nantong experience and methods, 142
Standford experience and, 157
Lengthening in flexor pollicis longus tendon
repair, 286, 288f
Lentiviral vectors for gene therapy delivery, 62
Le Viet technique, 286, 288f
Lim/Tsai repair with place-and-hold exercises,
116–124
complications, 122, 122t
discussion, 122–123
methods and outcomes, 116–119, 117t, 118f,
121–122, 121t–122t
operative technique, 119, 119f
postoperative care, 119–121, 120f
two-strand modified Kessler method versus, 117,
117t, 121, 121t
Linea jugata, 4
Linear region of stress-strain curve, 29–30, 29f
Liposome-mediated gene transfer, 62
Literature review, 247t, 248–250
Little finger
development of comprehensive universally
acceptable criteria for repair in, 255,
256f
extensor tendons in, 11
rupture repair in, 217–218
Littler and Eaton’s technique for extensor
reconstruction, 389
Load/loading
effects on tendon healing, 17–18
in mallet finger rehabilitation, 430
tendon-bone insertion site development and,
52–53
tendon-bone insertion site healing and, 55
tendon friction and, 24–25, 26f–27f, 27
Teno Fix Tendon Repair System and, 208,
209f
Load-to-failure test/curve, 45–46, 46f
Local flap for extensor tendon reconstruction,
377–378
Localized soft tissue injury, 85–86
Locking core suture
importance of length of, 42, 42f
Stanford experience and, 157–158, 158f
symposium discussion on, 442–443
Locking cross-stitch suture, 41f
strength of, 40–41
Locking loops of Pennington repair, 37, 37f
Mayo Clinic experience, 133, 134f–135f
strength of, 38
Locking running peripheral suture repair, 41f
strength of, 40–41
Locking tendon-suture junction, 36–38, 37f
Looped suture repair and modifications
history of, 242
in modified Paneva-Holevich technique,
308–310, 308f
Nantong experience and methods, 140–141
Singapore experience and methods, 153–154,
155f
strength of, 39
symposium discussion on, 444–445
Loop junction in modified Paneva-Holevich
technique, 308, 308f
Loop-lock tendon-suture junction, 37, 37f
Loop release knot in tendon retrieval, 161–162,
162f
Loosely supervised rehabilitation, 444
Lubrication
cartilage, 27–28
tendon, 27–29, 28f–29f
Lubricin, 27–28
Luciferase, 64, 65f
Lumbrical muscles
anatomy of, 9–10
in zone 3, 6f
M
Mallet finger, 347–349, 348f
rehabilitation for, 429–430, 429f–430f
Mansat and Bonnevialle classification of traumatic
tendon avulsion, 220–221
Manske-St. Louis Group, on biomechanics of
tendon repair, 36b
Mantero technique, 203–207
discussion, 206–207
in flexor pollicis longus tendon repair, 190
indications, 203
Nantong experience, 143–144, 144f
outcomes, 206, 206f
postoperative care, 205–206
in single-stage free tendon grafting, 267–269
surgical technique, 203–205, 204f–205f
for traumatic avulsion of flexor tendon, 222,
222f
Mason and Allen technique, 240
Mass-Chicago Group, on biomechanics of tendon
repair, 36b
Material testing machine, 45–46
Matev’s technique for extensor reconstruction,
389, 390f
Maximal strength, measurement of, 45–46
Mayo Clinic experience, 133–137
indications, 133
operative techniques, 133–136, 135f
with pediatric patients, 182–183
postoperative care, 136
MCP. See Metacarpophalangeal (MCP) joint
Mechanical factors
in tendon-bone development, 52–53, 52f
in tendon-bone healing, 53–54
Mechanical manipulation in tissue engineering,
76, 76f
Mechanical properties of tendon, 29–30,
29f–30f
Mechanical requirements of surgical repair,
35–36
Mechanism of injury
rehabilitation regimen based on, 415–417
in traumatic avulsion of flexor tendons,
219–220, 220f
Median nerve
anatomy of, 4
transfer to radial nerve, 369, 369f
zone 5 injury of, 198
Merle and Dautel modification of Boyes’
preoperative classification, 266, 267t
Mesenchymal stem cells (MSCs). See also Stem
cells
for tendon-bone healing, 55–56
for tissue engineering, 73–74
Mesotendon
anatomy of, 6
in vascular tendon transfer, 327, 329f–330f
Metacarpal artery island flap, 373
first dorsal, 373–375, 375f
perforator-based dorsal, 376–377, 376f
second dorsal, 375–376
Metacarpophalangeal (MCP) joint
evaluation criteria and, 250–251
extensor mechanism and, 12–13
flexion of
lumbrical muscles and, 9
in swan-neck deformity, 385
(See also Swan-neck deformity)
hyperextension of in boutonnière deformity,
383
(See also Boutonnière deformity)
injuries to
general management of, 351–352, 351f
sagittal band, 355–363
tendon transfer for, 367t
moment arm of, 30–31
no repair of FPL tendon and, 289
pulley system and, 8–9
rehabilitation for, 432–434, 433f
rheumatoid deformity of in thumb, 385,
388–389
sagittal band anatomy and, 355–357, 356f
splinting position of
in flexor tendon injury rehabilitation, 406
in Mayo Clinic experience and methods,
136
in single-stage free tendon grafting
rehabilitation, 270
in Standford experience and methods, 159
in vascular tendon transfer, 340–341
in zone 5 repair, 195
Metallic sutures in single-stage free tendon
grafting, 267–269
MGH repair, strength of, 39, 39t
Micro-anchor sutures. See Mini-anchor sutures
Microfibril, collagen, 29
Micro-RNA (miRNA) for tendon healing, 61f,
66–67, 67f–68f
Microvacuoles in sliding system, 324–325, 325f
Microvideo observations of tendon structure in
zones 3,4,5, 324–326, 325f
Middle finger
extensor tendons in, 11
injuries to, 349, 350f
pulley system in, 8
Midline incision for release of pulleys, 95f
Mineral content in tendon-bone insertion, 50
stress and strain concentration and, 50–51
Mini-anchor sutures
in single-stage free tendon grafting, 267–269,
270f
for traumatic avulsion of flexor tendon repair,
222, 222f–223f, 224t
miRNA. See Micro-RNA (miRNA)
Mixed grasping-locking repair, 36–37
Mobilization. See Active mobilization; Early
mobilization; Flexion mobilization; Passive
mobilization
Modified Duran postoperative protocol, 406–407
Mayo Clinic experience, 136
Modified Kessler repair
Australian experience and methods, 161, 164f
as low friction repair, 25
Nantong experience and methods, 141f
of partial tendon laceration, 174, 175f
Standford experience and methods, 158, 158f
symposium discussion on, 444–445
two-strand
in enlargement of tendon sheath and pulleys,
112
six-strand Lim/Tsai repair versus, 117, 117t,
121–122, 121t
Modified Kleinert splint in vascular tendon
transfer rehabilitation, 340–341, 341f
Modified Paneva-Holevich technique, 307–313
complications, 310–312
discussion, 312
indications, 307–308
operative technique, 308–310, 308f–309f
outcomes, 310, 311f, 311t
postoperative care, 310

460
Index
Modified Pennington repair, Mayo Clinic
experience with, 133
Modified six-strand Tang repair, 40f
Moiemen-Elliot criteria, 251t, 254
Molecular therapy, 444
Moment arm, 30–31, 31f
Monofilament nylon suture, 164
Morrison, W, 162–163
Motion
biomechanics of, 29–32, 29f–32f
effects on tendon healing, 17–18
following enlargement of sheath and pulley,
112, 113t
joint
pulley system and, 9
tendon excursion and, 30–31
for tendon-bone healing, 54–55
tendon friction and, 27, 27f–28f
MSCs. See Mesenchymal stem cells (MSCs)
M-Tang repair, 40f
history of, 242–243
Nantong experience and methods, 141, 141f,
146f, 149
strength of, 39t
Multimicro-Vacuolar Collagenous Dynamic
Absorbing System (MVCAS), 324, 326f
Multiple looped sutures and modifications, 40f
strength of, 39
Multi-strand core suture repair, 36–37
in children, 182
history of, 242
major reports and important information on,
249–250
MVCAS. See Multimicro-Vacuolar Collagenous
Dynamic Absorbing System (MVCAS)
N
Nalebuff classification of swan-neck deformity,
385
Nantong experience, 138–152
anesthesia and skin incisions, 138, 140f
clinical methods, 138–147, 139t
discussion, 149–151
FPL tendon treatment, 144–146
outcomes, 150f, 153–156
pediatric repair, 146–147
postoperative rehabilitation, 147–149,
147f–148f
zone 2 repair, 138–143
FDS tendon repair, 142–143, 144f–146f
incisions in sheath and pulleys, 138–140
tendon repair techniques, 140–142,
141f–142f, 142b
zone 1 repair of FDP, 143–144
zone 3 repair of FDP and FDS tendons, 143
Native tendon in tissue engineering, 75, 76f
Nerve(s), rehabilitation regimen based on injury
to, 417
Neuropeptides for augmentation of tendon
healing, 20
Neurovascular assessment, pediatric, 181
“No-gain” period in strength, 60, 60f
“No man’s land”, 104. See also Zone 2
history of term, 239–240
vincular anatomy and, 8
Noncompliance, rupture due to, 127–128, 214
Norwich exercise regimen, 433, 433f
Nutrition, tendon, 16, 17f, 72
partial tendon laceration and, 174
synovial sheath in, 89
Nylon materials, Australian experience and
methods, 164
O
Oblique retinacular ligament (ORL)
anatomy of, 12, 12f
reconstruction of, 391
Omega (“Ω”) pulley plasty, 104–110
anatomy and, 104–105
of A2 pulley, 107
of A4 pulley, 105, 105f–106f
discussion, 107–109, 108f–109f
outcomes, 107
outline, 104–109
postoperative care, 107
Ω-shaped loop in Mantero technique, 203–205,
204f
Open circle grasping junction, 37
Open loop grasping junction, 37
Open tendon injury, 81–82
Osteoblasts in tendon-bone insertion, 49–50
Osteoclasts in tendon-bone insertion, 49–50
Osteosynthesis in traumatic avulsion of flexor
tendon repair, 223f, 224t
Outcomes, 246–256
age and, 182–183
Bern experience, 116–119, 121–122, 121t–122t
in children, 182–183
development of comprehensive universally
acceptable criteria and, 254–255, 256f,
257t
factors affecting, 158t, 247t
adhesion formation, 252–253
extent of injury, 254
joint stiffness, 253–254
rupture of repair, 253
surgical skill, 254
flexor pollicis longus tendon grafting, 295
major reports and important information
regarding, 248–250
Mantero technique, 206, 206f
modified Paneva-Holevich technique, 310, 311f,
311t
Nantong experience, 150f, 153–156
Omega pulley plasty, 107
over past 20 years, 246–248, 247t
rehabilitation for extensor injury, 436–437,
436t
rerepair of ruptures, 215–217, 216t
rupture of pulleys, 235–236
Singapore experience, 155
single-stage tendon grafting, 271–272, 272t,
281
Standford experience, 158t
tendon rupture after fractures and carpal
disorders, 228–229, 231f
Teno Fix Tendon Repair System, 211
tenolysis, 264
traumatic avulsion of flexor tendons, 224–225
two-stage tendon grafting, 282, 305–306
vascularized tendon transfers
extensor, 396, 396f
flexor, 332–336, 335f
zone 5 repair, 200, 200f, 201t
P
PA. See Palmar aponeurosis (PA)
Palm
FDP and FDS tendon repair in, 143
skin deficiencies of, correction of, 301–303,
301f–304f
structure of sheath at, 5
Palmar aponeurosis (PA), pulley system and, 9
Palmar extension splinting, 421–422, 423f
Palmar interosseous muscles, 9–10
Palmaris longus tendon
anatomy of, 4
grafting of
for flexor pollicis longus repair, 291
for rupture of pulleys, 233–238, 235t
for staged tendon grafting, 300–301
in vascular tendon transfer, 329
harvesting and grafting of, 267, 269f
Palmar pulley in early passive immobilization,
406, 407f
Paneva-Holevich technique, modified, 307–313
complications, 310–312
discussion, 312
indications, 307–308
operative technique, 308–310, 308f–309f
outcomes, 310, 311f, 311t
postoperative care, 310
Parascapula flap, 379
Paratenon
anatomy of, 5, 72, 324, 325f
in extrasynovial tendon lubrication, 28–29, 29f
tendon friction and, 26–27, 26f
Parathyroid hormone-related protein (PTHrP) in
tendon-bone insertion site development,
51–52
Parietal synovium anatomy, 5
Partial injury, rehabilitation regimen for, 417
Partial release of pulleys. See Venting of pulleys
Partial tendon laceration, 85, 171–178
adhesion formation and, 174
biomechanical properties of, 172–174
complications of, 175–176, 176f
diagnosis and physical examination of,
171–172
early mobilization and remodeling in, 173
nonrepair of, 174
rupture and, 172–173
outline, 171–176
physiology of tendon healing and, 172
postoperative rehabilitation in, 175
surgical repair of, 171, 174–175, 175f
symposium discussion on, 442
tendon gliding and resistance and, 173–174
tendon nutrition and, 174
tensile strength and
cross-sectional are and, 172–173
repair and, 173
trimming of, 175, 175f
Passive flexion
in Nantong experience and methods, 147–148,
147f
in Singapore experience and methods, 154
in six-strand Lim/Tsai repair rehabilitation,
119–121, 120f
in Standford experience and methods, 159
in vascular tendon transfer rehabilitation, 341,
341f–342f
Passive mobilization
early, 18
for extensor tendon rehabilitation after tendon
transfer, 369–370
for flexor tendon rehabilitation, 406–407,
406f–407f
Chelmsford experience and methods, 126
Standford experience and methods, 159
after vascular tendon transfer, 341
for tendon-bone healing, 54–55
tendon excursion and, 31
Pathological conditions, tendon friction in,
25–26
Patients
flexor tendon rehabilitation and, 409, 418
involvement of in tenolysis, 262
referral for rehabilitation for extensor tendon
repair, 428
rupture due to noncompliance of, 127–128,
214
rupture of primary flexor tendon repair and,
214
rupture of pulley repair and, 233–234,
234f–236f
six-strand Lim/Tsai repair with place-and-hold
exercises and, 116–119
staged tendon grafting and, 298–299
tendon rupture after fractures and carpal
disorder repair and, 228–229
Teno Fix Tendon Repair System and, 209
zone 5 tendon repair and, 199, 199f
PDGF-B. See Platelet-derived growth factor-B
(PDGF-B)
Pediatric patient. See Children
Pedis cutaneotendinous free flap, dorsalis, 394,
397f–399f, 398
Pennington repair
Australian experience and methods, 161–162
history of modifications to, 241–244
locking loops of, 37, 37f
strength of, 38
Mayo Clinic experience and methods, 133
symposium discussion on, 448–449
Percent return of motion in evaluation criteria,
251t
Omega (“Ω”) pulley plasty (Continued)
Paratenon (Continued)

461
Index
Perforator-based dorsal metacarpal artery flap,
373–375, 376f
Peripheral suture repair, 35–37
Australian experience and methods, 166
biomechanics of, 35, 37
in children, 184
history of, 241–242, 241f
of partial tendon laceration, 174–175
Standford experience and methods, 157–158,
158f
strength of, 39t, 40–41, 41f
symposium discussion on, 448
PET. See Positron emission tomography (PET)
PGA. See Polyglycolic acid (PGA) scaffolds in
tissue engineering
Phospholipids in tendon lubrication, 27–28,
28f
Physical examination
of partial tendon laceration, 171–172
of tendon injury, 81–83, 83f
Physical factors in tendon healing, 17–19
Physiological conditions, tendon friction in,
24–25, 25f–26f
Physiotherapy after vascularized tendon transfer,
340–343, 341f–343f
Pig flexor tendon, 442
Pinch grip, following rupture of pulleys repair,
235
PIP. See Proximal interphalangeal (PIP) joint
Pisohamate ligament, 5
Pisotriquetral disorders, tendon rupture due to,
228–232, 229f, 230t, 231f
PLA. See Polylactic acid (PLA) scaffolds in tissue
engineering
Place-and-hold exercises, 408–410
for boutonnière deformity, 431
in six-strand Lim/Tsai repair rehabilitation, 116,
120f, 121
in Standford experience and methods, 159
in vascular tendon transfer rehabilitation, 341,
342f
Plantaris tendon, harvesting and grafting of, 267,
269f
for flexor pollicis longus repair, 291
Plaster of Paris cast, 421f
Plasty
enlargement sheath, 89–92, 92b
Omega pulley, 104–110
anatomy and, 104–105
of A2 pulley, 107
of A4 pulley, 105, 105f–106f
discussion, 107–109, 108f–109f
outcomes, 107
outline, 104–109
postoperative care in, 107
Platelet-derived growth factor-B (PDGF-B)
gene therapy with, 61
in tissue engineering, 76
PLGA. See Polylactic-co-glycolic acid (PLGA)
scaffolds in tissue engineering
Plowing friction, gap formation and, 25–26
Pluripotential cell on sutures, 77, 77f
Polyester scaffolds in tissue engineering, 75
Polyglycolic acid (PGA) scaffolds in tissue
engineering, 75
Polylactic acid (PLA) scaffolds in tissue
engineering, 75
Polylactic-co-glycolic acid (PLGA) scaffolds in
tissue engineering, 75
Polypropylene material, 164
Positron emission tomography (PET), 411
Posterior annular ligament, 4
Posterior interosseous artery flap, 378
Postoperative care. See Rehabilitation
Post-traumatic deformity
boutonnière deformity, 383–384, 384f
nonoperative treatment of, 385–386
operative treatment of, 386
swan-neck deformity, 384
nonoperative treatment of, 386, 386f
operative treatment of, 387
Preoperative physiotherapy in vascularized tendon
transfer, 340
Primary flexor tendon repair
absolute contraindications to, 87
Australian experience, 161–167
author’s preferred approach, 166–167
current practice, 165–166
outline, 161–167, 162f
recent advances 2000-2010, 163–165,
163f–164f
Bern experience, 116–124
complications, 122, 122t
discussion, 122–123
methods and outcomes, 116–119, 117t, 118f,
121–122, 121t–122t
operative technique, 119, 119f
postoperative care, 119–121, 120f
Chelmsford experience, 125–132
complex suturing, 130–131
early active mobilization, 126
early results, 126–127
economic factors, 131
etiology of ruptures, 127–128
5% rupture rate, 127
flexor pollicis longus repair, 130
passive mobilization, 126
rupture re-repair, 128–129
splinted wrist position, 128
stronger repairs, 129
venting of pulleys, 129
zone 2 as a black box, 129–130
in children, 179–185
early strategies in, 239–240
evolution of, 239–245, 241f–243f
of flexor pollicis longus tendon, 186–193
flexor sheath and pulley treatment in, 88–97
anatomy and, 88–89, 89f
considerations in, 96–97
enlargement of sheath and pulley in,
111–115
function and, 89
guidelines for, 93
historical review of, 89, 90b–91b
investigations of, 89–93, 91f–92f, 92b
Omega pulley plasty in, 104–110
venting of pulleys in, 94–96, 94f–95f,
98–103
flow-chart of decision-making process in, 84f
history of, 125
indications for, 84–85, 85f
borderline, 85–87
Mayo Clinic experience regarding, 133
Mantero technique for, 203–207
Mayo Clinic experience, 133–137
indications, 133
operative techniques, 133–136, 135f
postoperative care, 136
Nantong experience, 138–152
(See also Nantong experience)
anesthesia and skin incisions, 138, 140f
clinical methods, 138–147, 139t
discussion, 149–151
FPL tendon treatment, 144–146
outcomes, 150f, 153–156
pediatric repair, 146–147
postoperative rehabilitation, 147–149,
147f–148f
zone 1 repair of FDP, 143–144
zone 3 repair of FDP and FDS tendons, 143
zone 2 repairs, 138–143
outcomes (See Outcomes)
of partial tendon laceration, 171–178
problems of, 125
relation of postsurgical mobilization methods to
surgical technique in, 244
rupture of (See Rupture)
Singapore experience, 153–156
operative technique, 154, 155f
outcomes, 155
outline, 153–156
postoperative care, 154–155, 155f
Stanford experience, 157–160
operative technique, 158, 158f
outline, 157–160, 158t
postoperative rehabilitation, 159–160
strength of (See Strength)
Teno Fix Tendon Repair System for, 208–213
timing of, 83–84, 84f
Wellington, New Zealand experience, 168–170,
169f, 169t
in zone 5, 194–202
Prolene material, 164
Proliferative stage of tendon healing, 72
Pronator teres (PT), for tendon transfer, 367–368,
367t
Proteoglycan
in tendon, 29, 72
in tendon lubrication, 27–28, 28f
Proximal interphalangeal (PIP) joint
active extension of for boutonnière deformity,
431
arthrodesis of for boutonnière deformity, 387,
387f
assessment of, 82, 83f
early passive mobilization and, 406, 406f
enlargement of sheath and pulley and motion
of, 112, 113t
flexion of in boutonnière deformity, 383
(See also Boutonnière deformity)
flexor tenodesis of, 390, 391f
general management of injuries of, 349–350
hyperextension of in swan-neck deformity,
384–385
(See also Swan-neck deformity)
immobilization of, 431
moment arm of, 30–31
joint flexion and, 32f
passive flexion of following vascular tendon
transfer, 341, 342f
pulley system and, 8
pulley venting in zone 2 and, 99–100
repair of ruptured pulley and motion of, 235
splinting of
for boutonnière deformity, 386, 430–431, 431f
for swan-neck deformity, 386, 386f
stiffness of, 253–254
traumatic avulsion of flexor tendon and, 220,
223, 225
Proximal junction
in single-stage tendon grafting, 269, 280–281,
280f
of flexor pollicis longus tendon, 291, 291f
in two-stage tendon grafting, 282
in vascular tendon transfer, 327–329
Proximal lengthening in flexor pollicis longus
tendon repair, 286
Proximal phalanx
injuries to, 351
rehabilitation for, 432
pulley system in, 8
Pseudo-sheath, staged tendon grafting and,
297–298
PT. See Pronator teres (PT), for tendon transfer
PTHrP. See Parathyroid hormone-related protein
(PTHrP)
Pulleys. See also Specific pulleys
anatomy of, 5–6, 7f, 8–9, 88–89, 89f
function of, 89
Mantero technique and, 204f, 205
rupture of, 233–238
discussion, 236–238
evaluations, 235
operative techniques, 234–235, 235t,
236f–237f
outline, 233–238, 234f
patients, 233–234, 234f–236f
postoperative care, 235
results, 235–236
symposium discussion on, 441, 443
tenolysis and, 262–263, 263f
of thumb, 13, 13f, 89
traumatic avulsion of flexor tendon repair and,
222–223
treatment of (See Pulley repair)
triggering of
following enlargement of tendon sheath and
pulleys, 113
Primary flexor tendon repair (Continued)

462
Index
partial tendon laceration and, 173–176, 176f
rupture of repair due to, 253
venting of, 94–96, 94f–95f, 98–103
author’s clinical research, 99–101, 100f
Chelmsford experience regarding, 128–129
considerations in, 96–97
distal bowstringing due to, 101–102,
101f–102f
history of, 98–99
rehabilitation program and, 418
significance of, 102
Pulley repair
considerations in, 96–97
enlargement in, 111–115
in flexor pollicis longus tendon two-stage
grafting, 293–294, 293f–294f
historical review of, 89, 90b–91b
indications and operative methods for, 93–96
investigations associated with, 89–93, 91f–92f,
92b
Omega pulley plasty in, 104–110
anatomy and, 104–105
of A2 pulley, 107
of A4 pulley, 105, 105f–106f
discussion, 107–109, 108f–109f
outcomes, 107
outline, 104–109
postoperative care in, 107
reconstruction
combined island FDS tendon and palmaris
longus tendon transfer for, 329
in modified Paneva-Holevich technique, 308,
309f
in staged tendon grafting, 304, 305f
two-stage flexor tendon, 276–277, 277f
Pull-out technique. See Mantero technique
Pulvertaft weave, 268f, 280–281, 280f, 291, 291f
Purchase, core suture
grasping and locking junctions and, 37
importance of length of, 42, 43f
Stanford experience and, 157
Q
“Quaba flap”, 376–377, 376f
Quality of motion in evaluation criteria, 251t
R
Radial artery, zone 5 injury of, 194, 198
Radial artery thumb flap, 377, 377f
Radial bursa, 5
Radial forearm flap, 378
with vascularized tendons, 394–395, 398–399,
400f
Radial nerve dysfunction
nerve transfer for, 369, 369f
tendon transfer for, 365, 367, 367t
Radiography, 83
of fracture or carpal disorder-associated rupture,
229f, 231, 231f
of mallet finger injury, 348f
pediatric, 181
in tenolysis, 262–263, 263f
Reconstruction. See also Graft(s)/grafting
extensor tendon
for boutonnière deformity, 389–390, 390f
soft tissue coverage for, 371–382
for swan-neck deformity, 390–391, 391f
tendon transfer for, 364–370
flexor pollicis longus tendon, 285–296
bridge grafts, 290
distal and proximal attachment, 291, 291f
FPL muscle, 290
interphalangeal joint motion and, 289–290
no FPL repair, 289, 289f
outcomes and prognosis, 295
rehabilitation, 295
techniques to extend, 286–289, 287f–288f
tension setting, 291–292
tension transfer, 292–293, 292f
thenar tunnel, 291
two-stage grafting, 293–295, 293f–294f
wrist-to-distal phalanx grafts, 291
for zone 3 and 4 injuries, 285–286
flexor tendon, 274–278
flexor pollicis longus tendon, 285–296
history of, 274–278
outline, 274–278
single-stage, 275–276, 276f
surgical procedure, 275–278
two-stage, 276–278, 276f–277f
vascularized tendon transfer, 323–343
flexor tendon sheath
by grafts, 94, 112
investigations regarding, 89–92
of oblique retinacular ligament, 391
of pulleys
combined island FDS tendon and palmaris
longus tendon transfer for, 329
in modified Paneva-Holevich technique, 308,
309f
in staged tendon grafting, 304, 305f
of radial sagittal band, 360–361, 362f
Record keeping in rehabilitation for extensor
tendon repair, 429
Referral for rehabilitation, 428
Rehabilitation
extensor tendon, 427–438
clinical evidence and outcomes, 436–437,
436t
considerations, 437
general guidelines, 428–429
for mallet injury, 349
for metacarpophalangeal joint injury, 351
outline, 427–437, 428f
patient referral, 428–429
for proximal interphalangeal joint, 350
record keeping, 429
for tendon transfer for extensor tendon
reconstruction, 369–370
of thumb, 434–436, 435f–436f
timing of, 428
after vascularized tendon grafting, 395–396
in zone 3, 430–432, 431f–432f
in zone 4, 432
in zone 7, 434
in zone 8, 434
in zone 1 and 2, 429–430, 429f–430f
in zone 5 and 6, 432–434, 433f
flexor tendon, 405–414
age and, 418–419, 418f–419f
Australian experience and methods,
165–166
Bern experience and methods, 116–119,
118f
in children, 418–419, 418f–419f
controlling flexion force during, 409–410,
409f–410f
customization of, 415–426
early active mobilization in, 407–409,
408f
early passive mobilization in, 406–407,
406f–407f
extent of injury and, 415–417, 416f
for flexor pollicis longus tendon repair,
187–188, 188f, 189t
following re-repair, 424–425
fundamental concepts and techniques of
evaluation and treatment in, 410–412,
411f–412f, 411t
immobilization in, 405–406
(See also Immobilization)
initiation of active mobilization in, 410
length of time from injury to repair and,
417–418
loosely supervised, 444
in Mantero technique, 205–206, 205f
Mayo Clinic experience and methods, 136
after modified Paneva-Holevich technique,
310
Nantong experience and methods, 147–149,
147f–148f
after Omega pulley plasty, 107
outline, 405–413
for partial tendon laceration, 175
passive flexion, active extension in, 119–121,
120f
patient characteristics and compliance and,
418
patient selection, 409
pediatric, 182, 184–185
place-and-hold exercises in, 120f, 121
questions and issues, 412–413
relation to surgical technique, 244
for rupture of pulleys, 235
Singapore experience and methods, 154–155,
155f
after single-stage tendon grafting, 270, 281
after six-strand Lim/Tsai repair, 119–121, 120f,
122t
Stanford experience and methods, 159–160
“stop and go” program in, 116–121, 120f
for tendon-bone repair, 54–55
after tendon grafting of flexor pollicis longus
tendon, 295
for tendon rupture after fractures and carpal
disorders, 229
in Teno Fix Tendon Repair System, 210–211
tenolysis, 263–264
traumatic avulsion of flexor tendons, 224
type and quality of repair and, 418
type of injury and, 417
in vascularized tendon grafting, 340–343,
341f–343f
zone if injury and, 419–424, 420f–421f,
423f
after zone 5 tendon repair, 195, 199–200,
199f
of FDS tendon, 195–196
future of, 442–444
Release
of lateral pulley attachment in Omega pulley
plasty, 104, 109
of A4 pulley, 105, 106f
of pulleys (See Venting of pulleys)
Remodeling stage of tendon healing, 72
early mobilization in partial tendon laceration
and, 173
Repair. See Healing
surgical (See Surgical repair)
Reports, clinical, 247t, 248–250
Rerepair, 86, 214–218
Chelmsford experience, 128–129
of flexor pollicis longus tendon repair, 191
immediate, 215
in little finger, 217–218
patient and, 214
in pediatric child, 183
possible modifications of, 217
rehabilitation for, 424–425
results, 215–217, 216t
rupture of, 217
staged tendon grafting and, 299
suture for, 214
timing of, 84
Reserve zone in tendon-bone insertion site
development, 51
Resistance, gliding, 32
in choosing rehabilitation protocol, 410
following enlargement of tendon sheath and
pulleys, 113, 114f
partial tendon laceration and, 174–175
pulley system and, 9
Resting position of hand in pediatric diagnosis,
181
Results. See Outcomes
Retinacular ligament
oblique, 12, 12f
transverse, 12, 12f
Retinaculum
extensor
anatomy of, 4
grafting of, for rupture of pulleys, 233–238,
235t, 236f–237f
rehabilitation for, 434
flexor, anatomy of, 3
Retrieval of tendon, suction catheter technique for,
161–162, 162f
Retroviral vectors for gene therapy delivery, 62
Reverse cross-finger flap, 373, 374f
Pulleys (Continued)
Reconstruction (Continued)
Rehabilitation (Continued)

463
Index
Reverse flow dorsal metacarpal flap, 376–377,
376f
Rheumatoid arthritis
boutonnière deformity due to, 384–385
general management of, 387
nonoperative management of, 387
operative management of, 387, 387f
sagittal band injuries due to, 355, 357, 357f
swan-neck deformity due to, 384–385
general management of, 387
nonoperative management of, 387
operative management of, 387–388
tendon transfer for extensor tendon
reconstruction and, 366–367
thumb deformity due to, 385, 386f
nonoperative management of, 388–389
operative management of, 388
Ring finger
extensor tendons in, 11
FDS tendon of for tendon transfer
in flexor pollicis longus tendon
reconstruction, 292–293
vascularized, 327–329, 328f–330f
(See also Vascularized tendon
transfer/graft)
traumatic avulsion of flexor tendons in, 220
Rod implant in two-stage tendon grafting, 282,
282f, 297–298, 300–301, 301f
in modified Paneva-Holevich technique,
307–308, 308f
Rotator cuff repair, tendon-bone insertion site
healing following, 54–55
Rubber bands
in early passive mobilization, 406, 406f
flexion contractures of IP joint due to,
421–422
problems with, 126
rupture and, 128
in six-strand Lim/Tsai repair and rehabilitation,
119, 120f
in thumb extensor rehabilitation, 435, 435f
in vascular tendon transfer rehabilitation,
340–341, 341f
“Rugby finger”, 219
Running locking peripheral suture repair, 41f
Running peripheral suture repair, 41f
Mayo Clinic experience, 133
of partial tendon laceration, 174
in six-strand Lim/Tsai repair, 119, 119f
Standford experience, 158, 158f
strength of, 40–41
Rupture
of extensor pollicis longus tendon
general management of, 352
tendon transfer for, 366, 366f–367f
of flexor tendon repair, 125–126
causes of, 253
Chelmsford experience, 126–128
in children, 183
etiology of, 127–128
5% rate of, 127
of flexor pollicis longus tendon, 187–188,
189t–190t
in zone 2, 186
rehabilitation for, 424–425
repair of, 214–218
(See also Rerepair)
immediate, 215
in little finger, 217–218
patients and, 214
possible modifications of, 217
results, 215–217, 216t
suture for, 214
in six-strand Lim/Tsai repair and
rehabilitation, 122, 122t
staged tendon grafting and, 299
strength of suturing and, 129–130
timing of, 215, 215t
after fractures or carpal disorders, 228–232,
229f, 230t, 231f
of partial laceration, 172–173, 175–176, 176f
of pulleys, 233–238
discussion, 236–238
evaluations, 235
operative techniques, 234–235, 235t,
236f–237f
outline, 233–238, 234f
patients and, 233–234, 234f–236f
postoperative care, 235
results, 235–236
of rerepair, 217
S
Safe zone in postoperative management, 18–19,
19f, 410, 411f
Sagittal bands, 12f
anatomy and biomechanics of, 12, 356f
injuries to, 351–352, 355–363
anatomy and biomechanics of, 355–357
causes of, 357, 357f
classification of, 357, 357f
diagnosis of, 357, 358b
differential diagnosis of, 357–358, 358f
immobilization for, 359, 359f–360f
surgery for, 359–361, 361f–362f
to thumb, 361
treatment methods for, 358–361, 358b
Sagittal band bridge splint, 359, 360f
Saline injection
tendon-bone insertion site development and,
52–53, 52f
tendon-bone insertion site healing and, 55
Sandow repair, 161–162, 164, 164f, 242, 242f
Sarcomere length, tendon transfer and,
364–365
Savage repair and modifications, 40f
Australian experience and methods, 166
history of, 242, 242f
for partial tendon laceration, 175f
strength of, 38, 39t
Scaffolds, 74–75
acellularized, 75, 76f
biologic, 74–75
seeding of cells for
autogenous versus allogenic, 74
cell types and sources for, 73–74
in vivo versus in vitro, 74
synthetic, 75
for tendon-bone healing, 56, 56f
Scaphoid nonunion, tendon rupture due to,
228–232, 230t
Scaphotrapeziotrapezoid joint (STT), 4
Scapula flap, 379
Scar/scarring. See also Adhesions
skin deficiencies due to, 301–303, 301f
in tendon-bone healing, 53, 53f
Scleraxis in tendon-bone insertion site
development, 51–52
SDMA. See Second dorsal metacarpal artery
(SDMA) flap
Secondary flexor tendon repair, 279–283
in future, 282–283, 283f
grafting/reconstruction, 274–278
of flexor pollicis longus tendon, 285–296
modified Paneva-Holevich technique,
307–313
single-stage, 266–273, 275–276, 279–280
symposium discussion on, 449
two-stage, 276–278, 281–282, 297–306
vascularized tendon transfer for, 323–343
tenolysis, 261–265
in zone 5, 198–199
Second dorsal metacarpal artery (SDMA) flap,
375–376
Seeding of cells for scaffold in tissue engineering
autogenous versus allogenic, 74
cell types and sources in, 73–74
future of, 441–442
in vivo versus in vitro, 74
Sex determining region Y in tendon-bone
insertion site development, 51
Sheaths. See Synovial sheaths
Sheep flexor tendon, 442
Shortening
of pulley, 95f
of skin, repair of in staged tendon grafting,
301–302, 301f
Silfverskiöld (cross-stitch) suture, 41f
in flexor pollicis longus tendon repair, 187–188,
188f, 190t
history of, 241–242, 241f
major reports and important information on,
248–249
strength of, 40–41
symposium discussion on, 448
Silicone implant
in modified Paneva-Holevich technique,
307–308, 308f
in two-stage tendon grafting, 282, 282f,
297–298, 300–301, 301f
Singapore experience, 153–156
operative technique, 154, 155f
outcomes, 155
outline, 153–156
postoperative care, 154–155, 155f
Single-cross repair, strength of, 39t
Single-stage flexor tendon reconstruction,
266–273, 275–276, 276f
complications, 272
of flexor pollicis longus tendon
bridge grafts, 290
distal and proximal attachment, 291
FPL muscle and, 290
setting of tension in, 291–292
tendon transfer and, 292–293, 292f
thenar tunnel and, 291
two-stage, 293–295
wrist-to-distal phalanx graft, 291
indications, 266–267, 267t, 279–280, 280f
methods, 280–281, 280f–281f
operative methods
for FDP tendon disruption with FDS tendon
intact, 270–271
for injuries to FDP and FDS, 267–271,
268f–270f
outcomes, 271–272, 272t, 281
postoperative care, 270
prognosis factors, 272
two-stage versus, 298–300
Six-strand repair, 36–37
history of, 242, 242f
Lim/Tsai, 116–124
complications, 122, 122t
discussion, 122–123
methods and outcomes, 116–119, 117t, 118f,
121–122, 121t–122t
operative technique, 119, 119f
postoperative care, 119–121, 120f
two-strand modified Kessler method versus,
117, 117t, 121, 121t
major reports and important information on,
249
Nantong experience and methods, 140–141,
141f, 143, 144f–146f, 149
rehabilitation program and, 418
Savage, 40f
history of, 242, 242f
strength of, 39t
Singapore experience and methods, 153–156
strength of, 39t
strength-versus-force graph for, 163f
Tang, 40f
strength of, 39t
of zone 5 flexor tendon injuries, 201
Skill, surgical
development of comprehensive universally
acceptable criteria for, 255–256, 257t
effects on outcomes, 254
future of, 445
Skin
deficiency of, correction of in staged tendon
grafting, 299–303, 301f–304f
pliable, in two-stage reconstruction, 276,
277f
rehabilitation regimen based on injury to,
416, 416f
Skin flap reconstruction
for extensor tendon reconstruction, 371–382
anterolateral thigh flap, 379–380, 381f
discussion, 380–382
evaluation and treatment, 371
Rupture (Continued)

464
Index
free flaps, 378–379
intrinsic flaps, 372–373
lateral arm flap, 379, 379f–380f
local flaps, 377–378
metacarpal artery island flaps, 373–377,
375f–376f
outline, 371–382
rehabilitation and, 416
reverse cross-finger flap, 373, 374f
scapula/parascapular flap, 379
secondary procedures, 380
thumb dorsal radial artery flap, 377, 377f
timing of, 372
turnover and distally based adipofascial flap,
373
wound débridement, 371–372, 372f
for skin deficiencies, 301–303, 302f–304f
ulnar artery-based, 330–332
(See also Vascularized tendon transfer/graft)
anatomical features, 327, 330f
operative procedures, 327–332, 331f–334f
results and discussion, 332–336
Skin incision, 138. See also Incision(s)
Sliding unit in carpal tunnel region, 6f. See also
Gliding/gliding system
Slip. See also Central slip
FDS and FDP, 4
for sagittal band reconstruction, 361
Snow’s technique for extensor reconstruction,
389
Softening, tissue, strength of suture repair and,
43–44
Soft tissue coverage
for extensor tendon reconstruction, 371–382
anterolateral thigh flap, 379–380, 381f
discussion, 380–382
evaluation and treatment, 371
free flaps, 378–379
intrinsic flaps, 372–373
lateral arm flap, 379, 379f–380f
local flaps, 377–378
metacarpal artery island flaps, 373–377,
375f–376f
outline, 371–382
reverse cross-finger flap, 373, 374f
scapula/parascapular flap, 379
secondary procedures, 380
thumb dorsal radial artery flap, 377, 377f
timing of, 372
turnover and distally based adipofascial flap,
373
wound débridement, 371–372, 372f
for flexor tendon reconstruction, 297–306,
301f–304f
SOX-9 in tendon-bone insertion site development,
51–52
SP. See Substance P (SP)
“Spaghetti” wrist, 194–195, 198, 199f, 201t, 202f
Splinted wrist position
Chelmsford experience and methods, 128
in flexor tendon injury rehabilitation, 406
Mayo Clinic experience and methods, 136
in metacarpophalangeal joint injury
rehabilitation, 351
Nantong experience and methods, 147–148,
147f–148f
Singapore experience and methods, 154
in zone 5 flexor tendon repair and
rehabilitation, 199–200, 199f, 424
Splint-free flexor tendon repair and rehabilitation,
153
Splinting
Australian experience and methods, 166–167
for boutonnière deformity, 386–387, 430–431,
431f
in children, 418–419, 418f
for flexor pollicis longus tendon rehabilitation,
187, 188f, 190t
for flexor tendon injury rehabilitation, 405–406
following tendon transfer for extensor tendon
reconstruction
vascularized, 369–370, 395–396
of mallet finger, 429–430, 429f
Mayo Clinic experience and methods, 136
Nantong experience and methods, 147–148,
147f–148f
in Norwich regimen, 433, 433f
in physiotherapy after vascularized tendon
transfer, 340–341
pulley rupture rehabilitation, 235
rupture and, 128
for sagittal band injury, 359, 359f–360f
Singapore experience and methods, 154, 155f
in single-stage free tendon grafting
rehabilitation, 270
six-strand Lim/Tsai repair and rehabilitation,
119, 120f
Standford experience and methods, 157,
159–160
for swan-neck deformity, 386–387, 386f
for thumb extensor injury, 434–436, 435f–436f
in traumatic avulsion of flexor tendon repair,
224, 224f
for zone 5 and 6 flexor tendon repair and
rehabilitation, 199–200, 199f, 424,
432–434
for zone 1 injury, 421, 421f
“Spot-welding”, 125–126
SRY gene in tendon-bone insertion site
development, 51
SSCT. See Subsynovial connective tissue (SSCT)
St. Andrew’s Unit
flexor pollicis longus tendon repair in
1994-1999, 187, 188f
1999-2004, 187, 188f
primary flexor tendon repair in, 125
Staged tendon grafting. See Two-stage flexor
tendon reconstruction
Stanford experience, 157–160
operative technique, 158, 158f
outline, 157–160, 158t
postoperative rehabilitation, 159–160
Stem cells
for augmentation of tendon healing, 19, 19f, 61
future of, 441–442
Singapore experience and methods, 154
for tendon-bone healing, 55–56
for tissue engineering, 73–74
in zone 2 tendon healing, 17
Stiffness
effects on outcomes, 253–254
measurement of, 45–46
“Stop and go” rehabilitation program, 116–121,
120f, 123
Strain, mechanical, in tissue engineering, 76, 76f
Strands, strength associated with number of,
38–40, 39t
Stanford experience and methods and, 157
Strength, 35–47
balanced with friction, 25
of core suture repair, 38–40, 39t, 40f–41f
Australian experience and methods and,
163–164
during early tendon healing, 42–43
factors affecting, 41, 42f
finger flexion and, 43, 44f
in flexor pollicis longus tendon repair, 187
future of, 443
increasing of, 44–45, 45f, 45t
Stanford experience and methods and, 157
suture purchase and lock (grasp) size in, 42
tension of suture repair in gap formation and,
41–42
traumatized tissue softening and, 43–44
factors affecting, 41, 42f
in early tendon healing, 42–43
finger flexion, 43, 44f
suture purchase and lock (grasp) size, 42
tension of suture repair in gap formation,
41–42
traumatized tissue softening, 43–44
following rupture of pulleys repair, 235
increasing of, 44–45, 45f, 45t
“no-gain” period in, 60, 60f
partial tendon laceration and, 172–173
of peripheral sutures, 40–41, 41f
types of tendon-suture junction and, 37–38,
37f
Strength-versus-force graph, 163f
Stress at tendon-bone insertion, 50–51
Stress relaxation, 29–30, 30f
Stress-strain curve, 29–30, 29f
Strickland repair, strength of, 38, 39t, 40f
Strickland scoring system, 250–251, 251t, 254
in enlargement of tendon sheath and pulleys,
112, 113t
in six-strand Lim/Tsai repair and rehabilitation,
121, 122t, 123
in zone 5 flexor tendon repair, 200
Strickland’s graph, 163–164, 163f
STT. See Scaphotrapeziotrapezoid joint (STT)
Subfibril, collagen, 29
Subluxation as sagittal band injury, 357, 357f
in thumb, 361
Substance P (SP), 20
Subsynovial connective tissue (SSCT)
anatomy of, 5, 6f–7f
tendon friction and, 26, 26f
Suction catheter technique for tendon retrieval,
161–162, 162f
Suppleness
as criteria for single-stage grafting, 280, 280f
as criteria for tenolysis, 261
Supraspinatus tendon-bone insertion, 50f
Supratendinous layer of extensor retinaculum, 4
Surface-modified allograft, 282f, 283
Surface morphology, tendon friction and, 27, 28f
Surgeon, expertise level of
development of comprehensive universally
acceptable criteria for, 255–256, 257t
effects on outcomes, 254
future of, 445
zone 5 flexor tendon repair outcomes and,
200–201, 200f
Surgical repair
biomechanics of
considerations in design and use of repair
methods and, 46–47
of core sutures, 39t, 40f–41f, 42
current techniques and, 36–37
factors affecting, 41–44, 42f
historical reviews of, 36, 36b
outline of, 35–47
of peripheral sutures, 40–41, 41f
test setup and measurement of, 45–46, 46f
types of tendon-suture junctions and, 37–38,
37f
essential mechanical requirements of, 35–36
relation of postsurgical mobilization methods to
technique of, 244
strength of, 35–47
of core sutures, 38–40, 39t, 40f–41f
factors affecting, 41–44, 42f
increasing of, 44–45, 45f, 45t
of peripheral sutures, 40–41, 41f
types of tendon-suture junction and, 37–38,
37f
Suture(s)
bioactive, 71–77, 77f
Chelmsford experience, 129–130
for delivery of drugs, 77
increasing of for increased strength of surgical
repair, 44–45, 45f
in single-stage free tendon grafting, 267–269,
268f, 270f
in tendon retrieval, 161–162, 162f
Suture anchor
in single-stage free tendon grafting, 267–269,
270f, 275–276, 276f
for traumatic avulsion of flexor tendon repair,
222f–223f, 224t
Suture caliber, 243–244
Australian experience and methods, 165–166
in flexor pollicis longus tendon repair, 190
for increased strength of surgical repair, 44–45,
45f, 45t
Splinting (Continued)
Skin flap reconstruction (Continued)
Strength (Continued)

465
Index
for pediatric repair, 184
rehabilitation program and, 418
Stanford experience and methods, 157
symposium discussion on, 442
of zone 5 flexor tendon repair, 201
Suture materials
Australian experience and methods, 164–166
strength of, 39t
symposium discussion on, 442
Suture purchase
grasping and locking junctions and, 37
importance of length of, 42
Suture repair, 36–37. See also Core suture repair;
Peripheral suture repair
bioactive, 71–77, 77f
complex, Chelmsford experience regarding,
130–131
in enlargement of tendon sheath and pulleys,
112
grasping and locking junctions in, 37–38, 37f
history of, 239–240
of rupture of primary flexor tendon repair, 214
for sagittal band injury, 359–360, 361f
strength of, 38–40, 39t, 40f–41f
future of, 443
symposium discussion on, 446
tension of
in flexor pollicis longus tendon repair,
291–292
gap formation and, 41–42
Nantong experience and methods, 142,
142b
in single-stage tendon grafting, 270, 276,
276f, 281, 281f
symposium discussion on, 448
in traumatic tendon avulsion, 222, 225
Suture strands, strength associated with number
of, 38–40, 39t
Stanford experience and, 157
Swan-neck deformity
post-traumatic, 384
nonoperative treatment of, 386, 386f
reconstruction for, 390–391, 391f
rheumatoid, 385, 386f
general management of, 387
nonoperative management of, 387
operative management of, 387–388
of thumb, 385, 386f, 388–389
SWM. See Synergistic wrist motion (SWM)
Symposiums, 446–449, 447f–449f
Synergistic wrist motion (SWM), 407
Synovial fluid, 72
in tendon lubrication, 27–28
in tendon nutrition, 16
Synovial sheaths, 72
abrasion of, due to high-friction repair, 17–18
extensor, anatomy of, 10f
flexor (See also Flexor tendon sheath)
anatomy of, 5–6, 5f–6f, 88–89, 89f
function of, 89
treatment of (See Flexor tendon sheath
treatment)
vencula in, 6
healing of, history of views on, 240–241
rupture of primary flexor tendon repair and,
214–215
Synthetic scaffold, 75
T
TAM. See Total active motion (TAM)
Tang criteria for evaluation, 251t, 252
Tang-Nantong group, on biomechanics of tendon
repair, 36b
Tang repair
of flexor pollicis longus tendon, 188–189, 190t
history of, 242–243
six-strand, 40f
modified, 40f
strength of, 39t
Teeth, metacarpophalangeal joint injury due to,
351, 351f
Temperate, tendon friction and, 24–25
Tendons
anatomy of, 3–15, 72
chiasma tendinum of Camper in, 10
extensor retinaculum in, 4
extensor tendons in, 10–13, 10f, 12f–13f
flexor retinaculum in, 3
flexor tendon sheaths in, 5–6, 5f–7f
flexor tendons in, 4–5, 10f
lumbrical and interosseous muscles in, 9–10
pulley system in, 8–9
in thumb, 13–14, 13f
vincula tendinea in, 6–8, 7f
biology of, 71–73
biomechanics of motion of, 29–32, 31f–32f
cells in, 72
edema of
prevention of in vascular tendon transfer
rehabilitation, 341
rehabilitation and, 410–411
rupture of repair due to, 253
lubrication of, 27–29, 28f–29f
mechanical properties of, 29–30, 29f–30f
nutrition for, 16, 17f
partial tendon laceration and, 174
synovial sheath in, 89
Tendon-bone insertion, 49–58
development of, 51–53, 52f
gradations in biomechanical, compositional,
and structural properties along, 50
morphology of, 49–51, 50f
structure and function of, 49
Tendon-bone repair, 53–56
biologically-based treatments for, 55–56, 56f
bone loss and, 54, 54f
rehabilitation-based treatments for, 54–55
science of healing in, 53–54, 53f
Tendon enthesis. See Tendon-bone insertion
Tendon friction
in different tendon surroundings, 26–27,
26f–28f
effects on tendon healing, 17–18, 18f
in pathological conditions, 25–26
in physiological conditions, 24–25, 25f–26f
reduction of after repair, 25
sliding system and, 324
Tendon healing, 16–17, 72
biological methods for enhancement of, 61
biology of, 16–17, 17f
in children, 182
cytokines for augmentation of, 19–20
effects of physical factors on, 17–19, 18f
extrinsic versus intrinsic, 72–73
future of, 441–442
gene therapy for, 59–70
associated with micro-RNA regulation, 66–67,
67f–68f
choosing of genes and delivery methods for,
61–62, 61f, 63f–64f
future perspectives, 68
growth factors in, 62–66, 64f–66f
“no-gain” period in strength and, 60, 60f
outline, 59–68
overall concepts and methods of, 60
history of views on, 240–241
“no-gain” period in strength and, 60f
partial tendon laceration and, 172
pharmacological manipulation of, 19
“safe zone” and, 18–19, 19f
stem cells for augmentation of, 19, 19f
Tendon junction
in single-stage tendon grafting
distal, 267–269, 268f, 270f, 281
of flexor pollicis longus tendon, 291, 291f
proximal, 269, 280–281, 280f
strength of, 37–38, 37f
in two-stage tendon grafting
modified Paneva-Holevich technique,
308–309, 308f, 310f
proximal, 282
in vascular tendon transfer, 327–329, 328f, 331f
Tendon-pulley frictional measurement system, 24,
25f
Tendon sheaths. See Synovial sheaths
Tendon splint, strength of, 39t
Tendon tissue engineering, 71, 73f
cells for, 73–74
growth factors in, 76
mechanical manipulation in, 76, 76f
outline, 71–77, 72f
scaffolds in, 74–75, 76f
tendon biology and, 71–73
Tendon transfer for extensor tendon
reconstruction, 364–370
methods of treatment, 366–369
radial nerve dysfunction, 367, 367t
restoration of digit extension, 368–369, 368f
restoration of thumb extension, 367–368
restoration of wrist extension, 367
systemic disease, 366–367
traumatic injury of EPL, 366, 366f–367f
outline, 364–370
principles of, 365t
rehabilitation following, 369–370
treatment alternatives, 369, 369f
vascularized, 394–402
discussion, 397–400, 397f–401f
operative techniques, 394–395, 395f
outcomes, 396, 396f
outline, 394–401
postoperative care, 395–396
Tendon transfer for flexor tendon reconstruction
basic principles for, 326–327, 326f, 328f
for secondary reconstruction of flexor pollicis
longus tendon, 289f, 292–293
vascularized, 323–343, 330f
anatomical studies and surgical basis,
324–327, 325f–326f, 328f–329f
future challenges, 336–338, 337f–338f
operative procedures, 327–332, 330f–333f
outline, 323–338
physiotherapy after, 340–343, 341f–343f
results and discussion, 332–336, 335f
Tenocytes
anatomy and function of, 72
gene transfer in, 62–63
in tissue engineering, 73
future of, 441–442
Tenodesis
lateral band, 390–391, 391f
loss of in pediatric injury, 181, 181f
PIP joint flexor, 390, 391f
tendon transfer for extensor tendon
reconstruction and, 365t
in traumatic avulsion of flexor tendon repair,
223, 224f
Teno Fix Tendon Repair System, 208–213, 212f
advantages of, 211–212
biomechanical study of, 208, 209f
disadvantages of, 211–212
exclusion criteria, 209–210
inclusion criteria, 209
operative techniques, 210, 210f
outcomes, 211
patients, 209
postoperative care, 210–211
strength of, 37, 39t
Tenolysis, 261–265
following Omega pulley plasty, 107, 109
indications for, 261
in pediatric patients, 183
rehabilitation after, 263–264
results, 264
surgical technique, 262–263, 262f–263f
timing of, 261–262
Tenotomes, 262–263, 262f
Tenotomy, for boutonnière deformity, 390, 390f
Tensile strength
balanced with friction, 25
partial tendon laceration and, 172–173
Tension of suture repair
gap formation and, 41–42
Nantong experience and methods, 142, 142b
in single-stage tendon grafting, 270, 276, 276f,
281, 281f
of flexor pollicis longus tendon, 291–292
symposium discussion on, 448
Suture caliber (Continued)

466
Index
TGF-β. See Transforming growth factor β (TGF-β)
TGF-β1. See Transforming growth factor β1
(TGF-β1)
The Journal of Hand Surgery (British Volume), 248
The Journal of Hand Surgery (European Volume),
249–250
Thenar tunnel, flexor pollicis longus tendon
grafting and, 291
Thigh flap, anterolateral, 379–380, 381f
3-0 sutures
Australian experience and methods, 165–166
in flexor pollicis longus tendon repair, 190
strength of repair with, 44, 45f
Three Tsuge suture technique, 188–189, 190f,
190t
Thumb
anatomy of tendons in, 13–14, 13f
dorsal radial artery flap for injuries of, 377,
377f
FPL tendon repair in, 144–146, 145f
pulley system in, 89, 89f
pulley venting and preservation in, 95–96
rehabilitation for extensors in, 434–436,
435f–436f
rheumatoid deformity of, 385, 386f
nonoperative management of, 388–389
operative management of, 388–389
sagittal band injuries to, 361
tendon transfer for restoration of extension of,
367–368, 367t
vincular system in, 8
Ticron suture, 164–166
Tight closure of sheath, 91, 91f
Timing
of rehabilitation
for extensor tendon repair, 428
for flexor tendon repair, 410
for vascularized flexor tendon transfer, 340
of repair of flexor tendon rupture, 215, 215t
of soft tissue coverage for extensor tendon
reconstruction, 83–84
of tendon repair, 83–84, 84f
of tenolysis, 261–262
of two-stage tendon grafting, 281–282
Tissue engineering, 73f
bioactive suture in, 76–77
cells for, 73–74
future of, 442, 444–445
growth factors in, 76
mechanical manipulation in, 76, 76f
outline, 71–77, 72f
scaffolds in, 74–75, 76f
tendon biology and, 71–73
Tissue softening, strength of suture repair and,
43–44
Toe, vascularized tendon transfer from, 336–338,
337f
Toe region of stress-strain curve, 29–30, 29f
Total active motion (TAM)
early mobilization in children and, 182
as evaluation criteria, 251t–252t, 254
following arthritis or carpal disorder-associated
tendon rupture repair, 229, 230t
following digitorum superficialis tendon zone 5
repair, 195–196
in Lim/Tsai method versus modified Kessler
method, 117, 121, 121t
Tourniquet control during wound débridement,
371–372, 372f
Traction test in tenolysis, 262, 262f
Transfer, tendon. See Tendon transfer
Transforming growth factor β (TGF-β)
in tendon healing, 17, 19–20
in tissue engineering, 76
Transforming growth factor β1 (TGF-β1), 66,
67f–68f
Transverse carpal ligament, 3
pulley system and, 9
Transverse retinacular ligament, 12, 12f
Trapeziectomy, carpometacarpal joint, 388–389
Trauma
avulsion of flexor tendons due to, 219–227
authors’ personal experience, 225–226, 225f,
226t
classification of, 220–221, 220f
diagnosis of, 221–222, 221f
mechanism of injury, 219–220, 220f
outcomes, 224–225
postoperative care, 224, 224f
traumatic avulsion as, 219
treatment of, 222–224, 222f–224f, 224t
boutonnière deformity following, 383–384,
384f
swan-neck deformity following, 384
Triangle flap reconstruction for skin deficiencies,
303, 304f
Triangular ligament (lamina), 12–13
Triggering
following enlargement of tendon sheath and
pulleys, 113
partial tendon laceration and, 173–176, 176f
rehabilitation regimen and, 417
rupture of repair due to, 253
Trimming of partial tendon laceration, 175,
175f
Triple Tsuge suture technique, 188–189, 190f,
190t
Trumble-Seattle group, 36b
Tsuge repair
of flexor pollicis longus tendon, 188–189, 190f,
190t
Mayo Clinic experience with, 133
for partial tendon laceration, 175f
Turnover adipofascial flap, 373
Two-stage flexor tendon reconstruction, 274,
276–278, 276f–277f, 297–306
in children, 183–184
clinical principles of, 300–305
first stage of, 300–301, 300f–301f
joint deficiency correction at, 304–305
pulley deficiency correction at, 304, 305f
skin deficiency correction at, 301–303,
301f–304f
of flexor pollicis longus tendon, 293–295,
293f–294f
indications, 281–282
method, 282, 282f
with modified Paneva-Holevich technique,
307–313
complications, 310–312
discussion, 312
indications for, 307–308
operative technique, 308–310, 308f–309f
outcomes, 310, 311f, 311t
postoperative care, 310
outcomes and prognosis, 282, 305–306
outline, 297–306
second stage of, 305
single-stage versus, 298–300
Two-strand core suture repair, 36–37
in children, 184
history of, 241–244
strength of, 38, 39t
suture caliber and, 44–45, 45f
strength-versus-force graph for, 163f
Two-strand Kessler repair and modifications, 40f
in enlargement of tendon sheath and pulleys,
112
of flexor pollicis longus tendon, 187–188, 188f,
190t
history of, 241–244
major reports and important information on,
249
Mayo Clinic experience with, 133
Nantong experience and methods, 141
six-strand Lim/Tsai repair versus, 117, 117t,
121–122, 121t
strength of, 38, 39t
Two-strand Tsuge repair, Mayo Clinic experience
with, 133
Type I collagen
gene therapy and, 62–63
in tendon, 29
in tendon-bone insertion, 49–50
in tendon-bone insertion site development, 51
in tendon healing, 72
in tendon lubrication, 27–28
Type II collagen
in tendon-bone insertion, 49–50
in tendon-bone insertion site development, 51
Type III collagen
gene therapy and, 62–63
gene therapy for suppression of, 66–67, 68f
in tendon-bone insertion, 49–50
Type X collagen
in tendon-bone healing, 53
in tendon-bone insertion site development, 51
U
Ulnar artery, zone 5 injury of, 194, 198
Ulnar artery-based tendon transfer. See also
Vascularized tendon transfer/graft
for extensor tendon reconstruction, 395–396,
395f
for flexor tendon reconstruction, 330–332
anatomical features of, 327, 328f–329f
operative procedures, 327–332, 331f–332f
Ulnar bursa, 5
Ulnar deviation, due to rheumatoid arthritis, 357,
357f
Ulnar nerve, zone 5 injury of, 198, 201, 202f
“Ulnar trail”, 334f
Ultimate strength, measurement of, 45–46
Undifferentiated cells in tendon healing in zone 2,
17
Universal Tendon Spacer, 300–301, 301f
Unloaded “work of flexion”, 18
in “safe zone”, 18
Unmineralized tissue in tendon-bone insertion,
50
U-shaped repair, 40f
Nantong experience and methods, 140–141,
141f
strength of, 39t
V
Vacuoles in sliding system, 324–325, 325f
Vascular endothelial growth factor (VEGF)
gene therapy with, 65–66, 66f
future perspectives, 68
in tissue engineering, 76
Vascularized soft tissue coverage
interosseous artery flap, posterior, 378
metacarpal artery, 373
first dorsal, 373–375, 375f
perforator-based dorsal, 376–377, 376f
second dorsal, 375–376
radial artery
forearm, 378
for thumb injuries, 377, 377f
ulnar artery dorsal perforator flap, 378
Vascularized tendon transfer/graft
for extensor reconstruction, 394–402
discussion, 397–400, 397f–401f
operative techniques, 394–395, 395f
outcomes, 396, 396f
outline, 394–401
postoperative care, 395–396
for flexor reconstruction, 323–343
anatomical studies and surgical basis,
324–327, 325f–326f, 328f–329f
basic principles, 326–327, 326f, 328f
future challenges, 336–338, 337f–338f
operative procedures, 327–329, 330f–334f
outline, 323–338
physiotherapy after, 340–343, 341f–343f
results and discussion, 332–336, 335f
Vascular system
assessment in pediatric diagnosis, 181
of flexor tendon, 5, 7f, 72
rehabilitation regimen based on injury to, 417
for tendon nutrition, 16, 17f
VBP. See Vinculum brevis profundus (VBP)
VBS. See Vinculum brevis superficialis (VBS)
Vectors for gene therapy delivery, 62, 63f–64f
VEGF. See Vascular endothelial growth factor
(VEGF)
Venting of pulleys, 94–96, 94f–95f, 98–103
Australian experience and methods, 166
author’s clinical research, 99–101, 100f
Chelmsford experience and methods, 128–129
Trauma (Continued)

467
Index
in children, 184
considerations in, 96–97
distal bowstringing due to, 101–102, 101f–102f
history of, 98–99
investigation of, 92–93, 92f
Nantong experience and methods, 149, 150f
Omega pulley plasty versus, 107
rehabilitation program and, 418
significance of, 102
symposium discussion on, 441, 443
Wellington, New Zealand experience and
methods, 168
Verdan technique, 240
Vertical fibers in subsynovial connective tissue,
7f
V incision for correction of skin deficiencies,
301–302, 301f
Vincular system
anatomy of, 6–8, 7f
“no man’s land” and, 8
in tendon nutrition, 16
Vincula brevia, 6, 7f
Vincula longa, 6–7, 7f
Vinculum brevis profundus (VBP), 6, 7f
Vinculum brevis superficialis (VBS), 6, 7f
Vinculum longum profundus (VLP), 7–8, 7f
Vinculum longum superficialis (VLS), 6–8, 7f
Visceral synovium, 5–6
VLP. See Vinculum longum profundus (VLP)
VLS. See Vinculum longum superficialis (VLS)
Volar annular ligament, 3
Volar Bruner incision for flexor tendon
reconstruction
single-stage, 280
two-stage, 277, 277f
Volar plate
incompetence of in swan-neck deformity,
384–385
pulleys of, 8–9
W
Wellington, New Zealand experience, 168–170,
169f, 169t
White method for evaluation, 251–252, 252t
WOF. See Work of flexion (WOF)
Wolfe-Yale-New York Group, 36b
Work of flexion (WOF), 18, 407
measurement of, 46
in “safe zone”, 18
Wound contamination, 83
Wound débridement in soft tissue coverage for
extensor tendon reconstruction, 371–372,
372f
Wound dressings, rehabilitation and, 416, 416f
in children, 418–419, 419f
Wrist
early active mobilization and, 407
extensor tendons at
anatomy of, 10–11, 10f
injuries to, 352–353
tendon transfer for restoration of, 367
flexor tendon injuries at or proximal to,
194–202
flexor tendon sheath at, 5
kinematics of, tendon transfer and, 365
“spaghetti”, 194–195, 198, 199f, 201t, 202f
splinted position of
Chelmsford experience and methods, 128
in flexor tendon injury rehabilitation, 406
Mayo Clinic experience and methods, 136
in metacarpophalangeal joint injury
rehabilitation, 351
Nantong experience and methods, 147–148,
147f–148f
Singapore experience and methods, 154
in vascular tendon transfer, 340–341
in zone 5 flexor tendon repair and
rehabilitation, 199–200, 199f, 424
synergistic motion exercise of, 407
work of flexion and, 407
Y
Young’s modulus of elasticity, 29–30
Z
Zigzag incision, Bruner’s, 138, 140f
Z lengthening in flexor pollicis longus tendon
repair, 286
Zone 1, 6f
extensor tendon injuries in, 347–349
FDP repair in
in children, 184
Nantong experience and methods, 138,
143–144
rehabilitation regimen for injury in
extensor tendon, 429–430, 429f–430f
flexor tendon, 419–421, 420f–421f
vascular tendon grafting in, 326–327
(See also Vascularized tendon transfer/graft)
Zone 2, 5f–6f
as “black box”, 129–130
extensor tendon injuries in, general
management of, 349, 350f
flexor tendon repair in
of flexor pollicis longus tendon, 186–187,
189t–190t
Mantero technique for, 203–207
Mayo Clinic experience, 133–136, 134f–135f
modified Paneva-Holevich technique,
307–313
Nantong experience, 138–143
(See also Nantong experience)
Omega pulley plasty, 104–110
pediatric, 184
secondary flexor tendon repairs, 279–284
single-stage free tendon grafting, 266–273
six-strand Lim/Tsai repair technique,
116–124
Standford experience, 158, 158f
tendon sheath and pulley enlargement in,
111–115
timing of, 83–84, 84f
venting of A2 and A4 pulleys in, 92–93,
99–101
as “no man’s land”, 104
history of term, 239–240
vincular anatomy and, 8
partial tendon laceration in, 172
pediatric injury in, 183
rehabilitation regimen for injury in
early active mobilization in, 408
early passive mobilization in, 406–407
extensor tendon, 429–430, 429f–430f
flexor tendon, 421–422, 423f
immobilization in, 405
tendon healing in, 17
vascular tendon grafting in, 326–327
(See also Vascularized tendon transfer/graft)
Zone 3, 5f–6f
FPL repair in, 285–286
general management of extensor tendon injuries
in, 349–350
microvideo observations of tendon structure in,
324–326
Nantong experience and methods, 143
rehabilitation regimen for injury in
extensor tendon, 430–432, 431f–432f
flexor tendon, 422–423
vascular tendon transfer from, 326
(See also Vascularized tendon transfer/graft)
Zone 4, 5f–6f
FPL repair in, 285–286
general management of extensor tendon injuries
in, 351
microvideo observations of tendon structure in,
324–326
rehabilitation regimen for injury in
extensor tendon, 432
flexor tendon, 423–424
vascular tendon transfer from, 326
(See also Vascularized tendon transfer/graft)
Zone 5
anatomy of, 6f
extensor tendon injury in, general management
of, 351–352, 351f
flexor tendon repair in, 194–202
clinical features, 194–195
of flexor digitorum superficialis, 195–196
outcomes, 200, 200f, 201t
outline, 194, 198–201
patients, 199, 199f
postoperative care, 199–200, 199f
summary, 200–201, 202f
surgical methods, 199
microvideo observations of tendon structure in,
324–326
rehabilitation regimen for injury in
extensor tendon, 432–434, 433f
flexor tendon, 424
skin deficiency exposing flexor tendons in, 303
vascular tendon transfer from, 326
(See also Vascularized tendon transfer/graft)
Zone 6, extensor tendon injuries in
general management of, 352
rehabilitation for, 432–434, 433f
Zone 7, extensor tendon injuries in
general management of, 352–353, 352f–353f
rehabilitation for, 434
Zone 8, extensor tendon injuries in
general management of, 352–353, 353f
rehabilitation for, 434
Zone 9, extensor tendon injuries in, 352–353
Zones
extensor tendon, rehabilitation and, 427, 428f,
429–434
flexor tendon, 6f, 81, 82f
rehabilitation for, 419–424
“safe” in rehabilitation, 410, 411f
Venting of pulleys (Continued)
Wrist (Continued)
Zone 2 (Continued)

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