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

438
Section 5:  Rehabilitation of Tendon Surgery
3. Hirai Y, Yoshida K, Yamanaka K, et al: An anatomic study of
the extensor tendons of the human hand, J Hand Surg (Am)
26:1009–1015, 2001.
4. Pinar Y, Bilge O, Govsa F, et al: Anatomo-histological analysis
of the juncturae and their relations to the extensor tendons
to the dorsum of the hand, Surg Radiol Anat 31:77–83, 2009.
5. Amadio PC: Friction of the gliding surface. implications for
tendon surgery and rehabilitation, J Hand Ther 18:112–119,
2005.
6. Newport ML: Extensor tendon injuries in the hand, J Am Acad
Orthop Surg 5:59–66, 1997.
7. Rosenthal EA, Stoddard CW: Questions hand therapists ask
about treatment of tendon injuries, J Hand Ther 18:313–318,
2005.
8. Lemmen MH, Schreuders TAR, Stam HJ, et al: Evaluation of
restoration of extensor pollicis function by transfer of the
extensor indicis, J Hand Surg (Br) 24:46–49, 1999.
9. Kapandji AI: Clinical evaluation of the thumb’s opposition,
J Hand Ther 5:102–106, 1992.
10. Handoll HH, Vaghela MV: Interventions for treating mallet
finger injuries, Cochrane Database Syst Rev CD004574, 2004.
11. Baratz ME, Schmidt CC, Hughes TB: Extensor Tendon Inju-
ries. In Wolfe SW, Hotchkiss RN, Pederson WC, et al, editors:
Green’s Operative Hand Surgery, ed 5, Philadelphia, 2005,
Elsevier Churchill Livingstone, pp 187–217.
12. Kalainov DM, Hoepfner PE, Hartigan BJ, et al: Nonsurgical
treatment of closed mallet finger fractures, J Hand Surg (Am)
30:580–586, 2005.
13. Pratt AL: Is eight weeks’ immobilisation of the distal inter-
phalangeal joint adequate treatment for acute closed mallet
finger injuries of the hand? A critical review of the literature,
Br J Hand Ther 9:4–10, 2004.
14. Schreuders TAR, Soeters JNM, Hovius SER, et al: A modifica-
tion of Elson’s test for the diagnosis of an acute extensor
central slip injury, Br J Hand Ther 11:111–113, 2006.
15. Elson RA: Rupture of the central slip of the extensor hood of
the finger. A test for early diagnosis, J Bone Joint Surg (Br)
68:229–231, 1986.
16. Smith PJ, Ross DA: The central slip tenodesis test for early
diagnosis of potential boutonniere deformities, J Hand Surg
(Br) 19:88–90, 1994.
17. Evans RB: Immediate active short arc motion following exten-
sor tendon repair, Hand Clin 11:483–512, 1995.
18. Crosby CA, Wehbe MA: Early protected motion after extensor
tendon repair, J Hand Surg (Am) 24:1061–1070, 1999.
19. Boscheinen-Morin J, Davey V, Conolly WB: The Hand Funda-
mentals of Therapy, Oxford, 1997, Butterworth-Heinemann.
20. Maddy LS, Meyerdierks EM: Dynamic extension assist splint-
ing of acute central slip lacerations, J Hand Ther 10:206–212,
1997.
21. O’Dwyer FG, Quinton DN: Early mobilisation of acute
middle slip injuries, J Hand Surg (Br) 15:404–406, 1990.
22. Walsh MT, Rinehimer W, Muntzer E, et al: Early controlled
motion with dynamic splinting versus static splinting for
zones III and IV extensor tendon lacerations: A preliminary
report, J Hand Ther 7:232–236, 1994.
23. Thomes LJ, Thomes BJ: Early mobilization method for surgi-
cally repaired zone III extensor tendons, J Hand Ther 8:195–
198, 1995.
24. Schreuders TAR, Soeters JNM, Augustijn WA, et al: Dynamic
extension splint: Rotterdam design, J Hand Ther 10:240–241,
1997.
25. Schreuders TAR, Soeters JNM, Augustijn WA, et al: Develop-
ment of extensor lag in treating boutonniere deformity [letter;
comment], J Hand Ther 9:415, 1996.
26. Evans RB, Thompson DE: The application of force to the
healing tendon, J Hand Ther 6:266–284, 1993.
27. Hung LK, Chan A, Chang J, et al: Early controlled active
mobilization with dynamic splintage for treatment of exten-
sor tendon injuries, J Hand Surg (Am) 15:251–257, 1990.
28. Saldana MJ, Choban S, Westerbeck P, et al: Results of acute
zone III extensor tendon injuries treated with dynamic exten-
sion splinting, J Hand Surg (Am) 16:1145–1150, 1991.
29. Newport ML: Zone I-V extensor tendon repair, Tech Hand Up
Extrem Surg 2:50–55, 1998.
30. Howell JW, Merritt WH, Robinson SJ: Immediate controlled
active motion following zone 4–7 extensor tendon repair,
J Hand Ther 18:182–190, 2005.
31. Sylaidis P, Youatt M, Logan A: Early active mobilization for
extensor tendon injuries. The Norwich regimen, J Hand Surg
(Br) 22:594–596, 1997.
32. Bulstrode NW, Burr N, Pratt AL, et al: Extensor tendon reha-
bilitation a prospective trial comparing three rehabilitation
regimes, J Hand Surg (Br) 30:175–179, 2005.
33. Chester DL, Beale S, Beveridge L, et al: A prospective, con-
trolled, randomized trial comparing early active extension
with passive extension using a dynamic splint in the rehabili-
tation of repaired extensor tendons, J Hand Surg (Br) 27:283–
288, 2002.
34. Khandwala AR, Webb J, Harris SB, et al: A comparison of
dynamic extension splinting and controlled active mobiliza-
tion of complete divisions of extensor tendons in zones 5 and
6, J Hand Surg (Br) 25:140–146, 2000.
35. Russell RC, Jones M, Grobbelaar A: Extensor tendon repair:
mobilise or splint? Chir Main 22:19–23, 2003.
36. Ip WY, Chow SP: Results of dynamic splintage following
extensor tendon repair, J Hand Surg (Br) 22:283–287, 1997.
37. Kerr CD, Burczak JR: Dynamic traction after extensor tendon
repair in zones 6, 7, and 8: A retrospective study, J Hand Surg
(Br) 14:21–22, 1989.
38. Newport ML, Blair WF, Steyers CM Jr: Long-term results
of extensor tendon repair, J Hand Surg (Am) 15:961–966,
1990.
39. Blair WF, Steyers CM: Extensor tendon injuries, Orthop Clin
North Am 23:141–148, 1992.
40. Slater RR Jr, Bynum DK: Simplified functional splinting
after extensor tenorrhaphy, J Hand Surg (Am) 22:445–451,
1997.
41. Stuart D, Zambia L: Duration of splinting after repair of
extensor tendons in the hand, J Bone Joint Surg (Br) 47:72–79,
1965.
42. Dargan EL: Management of extensor tendon injuries of the
hand, Surg Gynecol Obstet 128:1269–1273, 1969.
43. Soni P, Stern CA, Foreman KB, et al: Advances in extensor
tendon diagnosis and therapy, Plast Reconstr Surg 123:727–
728, 2009.
44. Josty IC, MacQuillan AH, Murison MS: Functional outcomes
following surgical repair of wrist extensor tendons, Br J Plast
Surg 56:120–124, 2003.
45. Mowlavi A, Burns M, Brown RE: Dynamic versus static splint-
ing of simple zone V and zone VI extensor tendon repairs: A
prospective, randomized, controlled study, Plast Reconstr Surg
115:482–487, 2005.
46. Elliot D, Southgate CM: New concepts in managing the long
tendons of the thumb after primary repair, J Hand Ther
18:141–156, 2005.
47. Browne EZ Jr, Ribik CA: Early dynamic splinting for extensor
tendon injuries, J Hand Surg (Am) 14:72–76, 1989.
48. Chinchalkar SJ: Dynamic splinting for the repair of the first
extensor compartment tendons, J Hand Ther 21:292–296,
2008.
49. Talsma E, de Haart M, Beelen A, et al: The effect of mobiliza-
tion on repaired extensor tendon injuries of the hand: A sys-
tematic review, Arch Phys Med Rehabil 89:2366–2372, 2008.

438.e1
Therapy Protocols After Extensor Tendon
Repairs: St Andrew’s Centre for Plastic
Surgery, Broomfield Hospital, Chelmsford,
Essex, UK
Appendix 1 
EXTENSOR TENDON REPAIRS
OF THE FINGERS
(i) Zones 5–8
(ii) Zone 9 with good strong repair of the intramuscu-
lar tendon.
1. Theatre
POP Palmar (volar) splint applied after tendon
repair(s)—
Wrist
−30°
MCPs
+40°
PIP
0°
DIP
0°
2. 0–5 days (Week 1)
Rest in POP splint for 5 days. (Week 1)
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
3. 6–13 Days (Weeks 1 and 2)
Day 6—Fabricate thermoplastic splint with same
joint angle of the MCP (+40°) but with splint only
extending distally to just proximal to the PIP
joints.
X10 hourly—extend to MCP 0°+PIP 0° +DIP 0°,
passively extend fingers to MCP 0°+PIP 0° +DIP
0° if there is extension lag,
then actively flex MCPs back to +40°,
then actively fully flex the PIP and DIP joints to
full flexion of both over the end of the splint.
Continue to elevate hand above elbow at all times.
Continue shoulder and elbow exercises 5×5 per day
(5 exercises 5 times per day).
X5
hourly—full
thumb
active
flexion
and
extension.
X5 hourly—full forearm active supination and
pronation.
Adjust pain control as necessary to allow this regime.
Hygiene and splint check at 7 days and 14 days.
4. 14–28 Days (Weeks 3 and 4)
Day 14—Remold splint so MCP +70°.
X10 hourly—extend to MCP 0°+PIP 0° +DIP 0°,
(passively extend fingers to MCP 0°+PIP 0° +DIP
0° if there is lag, and,
if lag persisting, fabricate splint for night wear at
MCP 0°+PIP 0° +DIP 0°),
then actively flex MCPs back to +70°,
then actively fully flex the PIP and DIP joints to
full flexion of both over the end of the splint.
Continue to elevate hand above elbow at all times.
Continue shoulder and elbow exercises 5×5 per day
(5 exercises 5 times per day).
Continue X5 hourly—full thumb active flexion and
extension.
Continue X5 hourly—full forearm active supination
and pronation.
Hygiene and splint check at 21 and 28 days.
Ultrasound if necessary from week 3.
5. 28+ Days (4–8 weeks)
X10 hourly—full active flexion and extension of all
joints of fingers without splint.
X10 hourly—active wrist flexion and extension
exercises with the fingers relaxed (fingers in the
position of the fingers in the wrist tenodesis maneu-
ver—wrist flexion with fingers loosely extended and
wrist flexion with fingers loosely flexed).
Also start active radial and ulnar wrist movements.
Passive extension of wrist and fingers to neutral.
Gradually increase active combined wrist and finger
extension as comfortable.
Add active combined wrist and digit flexion exercises
at 6 weeks post-op if needed.
MCPs +70° splint worn at night and in busy places
to 8 weeks.

438.e2
Section 5:  Rehabilitation of Tendon Surgery
Continue shoulder and elbow exercises 5×5 per day
(5 exercises 5 times per day).
Continue X5 hourly – full thumb active flexion and
extension + add active thumb abduction/adduc-
tion/opposition.
Continue X5 hourly – full forearm active supination
and pronation
From 4 weeks – light hand use but not lifting any-
thing more than 150 gm (6oz) = a full yogurt pot
6. 8 weeks onwards
Continue all exercises as above.
Passive finger flexion if required.
Dynamic flexion splinting if required.
From 8 weeks – return to light work and driving.
From 12 weeks – return to heavy work and contact
sports.
If there is extensor tendon tethering – forced passive
flexion exercises + massage dorsal skin of digit and
dorsum of hand with finger held in flexion +
ultrasound.
In Theatre
Days 0–5 Week 1
Days 6–13 Weeks 1–2
Days 14 -28 Weeks 3–4
Day 28+ Weeks 4–8
POP
Palmar Splint
Rest in POP splint
Thermoplastic  
Splint to PIP level
Made day 6
Thermoplastic  
Splint to PIP level
adjusted day 14
Thermoplastic + 70°
Splint to PIP level as
weeks 3/4
Wrist  −30°
MCPs  +40°
PIP 0°  DIP 0°
Wrist  −30°
MCPs  +40°
PIP 0°  DIP 0°
Wrist  −30°
MCPs  +40°
PIP 0°  DIP 0°
Wrist  −30°
MCPs  +70°
PIP 0°  DIP 0°
Splint only worn
at night and in busy
places
Fingers—
No movement
Fingers—
No movement
X10 hourly
Full active extn.
x 3 joints then
MCP flexn. + 40°
PIP/DIP flexn. full
X10 hourly
Full active extn.
x 3 joints then
MCP flexn. + 70°
PIP/DIP flexn. full
X10 hourly—full active
flexion and extension of
all joints of fingers
without splint
Passively extend joints
to neutral if necessary
Passively extend joints to
neutral if necessary
X10 hourly—full active
wrist flexn. and
extension exercises with
the fingers relaxed
If lag persists, fit night
splint with all joints
straight
From 4 weeks light hand
use—less than 150 gm
(full yogurt pot)
Elevate hand
above elbow
Elevate hand above
elbow
Elevate hand above
elbow
From 8 weeks—light
work/driving
Shoulder exercises
5x5 times per day
Shoulder exercises 5x5
times per day
Shoulder exercises 5x5
times per day
From 12 weeks—heavy
work/contact sports.
Elbow exercises
5x5 times per day
Elbow exercises 5x5
times per day
Elbow exercises 5x5
times per day
X5 hourly—full thumb
active flexion/extension
X5 hourly—full thumb
active flexion/extension
X5 hourly—full forearm
active supin./pronation
X5 hourly—full forearm
active supin./pronation
Adjust pain control as
necessary
Adjust pain control as
necessary
Hygiene and splint
checks—7 & 14 days
Hygiene and splint
checks—21 & 28 days
Ultrasound if necessary
from week 3

438.e3
Appendix 2 
Therapy Protocols After Extensor Tendon
Repair of the Thumb: St Andrew’s Centre
for Plastic Surgery, Broomfield Hospital,
Chelmsford, Essex,
UK
Zones 1–4
1. Theatre
POP Palmar (volar) splint applied after tendon
repair(s)—
Wrist
−30°
MCP
0°
IP
0°
2. 0–5 days (Week 1)
Rest in POP palmar (volar) splint for 5 days. (Week 1)
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
3. 5–7 Days (Week 1)
Day 6—Fabricate thermoplastic dorsal dynamic
extension splint with same joint angle of the wrist
and thumb MCP and with the splint lifting off the
thumb at the mid-proximal phalangeal level so
that a sling can be attached around the distal pha-
langeal palmar (volar) surface.
When resting, the sling remains around the distal
phalanx.
X5 hourly, slide sling back under the proximal
phalanx and actively flex and extend the IP joint
alone.
X5 hourly, actively flex and extend the MCP joint
alone, with the sling under the distal phalanx and
the base of the thumb supported with the other
hand. Aim thumb tip for the base of the middle
finger during this maneuver.
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active pronation and supination of the forearm
5×5 per day.
Full active flexion and extension of all fingers 5×5 per
day.
Adjust pain control as necessary to allow this regime.
4. 7–14 Days (Week 2)
When resting, the sling remains around the distal
phalanx.
X5 hourly, slide sling back under the proximal
phalanx and actively flex and extend both MCP
and IP joints together, aiming for the base of the
ring finger ×10 hourly (may need to support the
base of the thumb).
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active pronation and supination of the forearm
5×5 per day.
Full active flexion and extension of all fingers 5×5 per
day.
Adjust pain control as necessary to allow this regime.
Hygiene and splint check at 7 days and 14 days.
5. 14–28 Days (2–4 Weeks)
Active combined MCP and IP flexion/opposition,
aiming for the base of the little finger ×10 hourly
(may need to support the base of the thumb).
Ultrasound from week 3 if needed.
Elevate hand above elbow at all times.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active pronation and supination of the forearm
5×5 per day.
Full active flexion and extension of all fingers 5x5 per
day.
Adjust pain control as necessary to allow this regime.
Hygiene and splint check at 21 days and 28 days.
6. 28+ Days (4–8 Weeks)

438.e4
Section 5:  Rehabilitation of Tendon Surgery
Continue X10 hourly—active combined MCP and IP
flexion/opposition, aiming for the base of the little
finger x10 hourly (may need to support the base of
the thumb)
+
add
active
thumb
abduction/adduction/
opposition.
X10 hourly—active wrist flexion and extension exer-
cises with the fingers relaxed (fingers in the posi-
tion of the fingers in the wrist tenodesis
manoeuvre—wrist flexion with fingers loosely
extended and wrist flexion with fingers loosely
flexed).
Also start active radial and ulnar wrist movements.
Passive extension of wrist and fingers to neutral.
Gradually increase active combined wrist and finger
extension as comfortable.
Add active combined wrist and digit flexion exercises
at 6 weeks post-op if needed.
Thumb splint worn at night and in busy places to 8
weeks.
Shoulder and elbow exercises 5×5 per day (5 exer-
cises 5 times per day).
Full active flexion and extension of fingers 5×5 per day.
Full forearm active supination and pronation 5×5 per
day.
From 4 weeks – light hand use but not lifting any-
thing more than 150 gm (6oz) = a full yogurt pot.
7. 8 weeks onwards
Continue all exercises as above.
Passive finger flexion if required.
Dynamic flexion splinting if required.
From 8 weeks – return to light work and driving.
From 12 weeks – return to heavy work and contact
sports.
In Theatre
Days 0–5
Week 1
Days 5–7
Weeks 1–2
Days 7–14
Weeks 1–2
Days 15–28
Weeks 3–4
Day 28+ Weeks 4–8
POP
Palmar Splint
Rest in POP
Splint
Thermoplastic
Splint fitted on
day 6*
Thermoplastic
Splint worn at
all times
Thermoplastic
Splint worn at
all times
Splint only worn at night/in
busy places
Wrist  −30°
MCP  0°
IP  0°
Wrist  −30°
MCP  0°
IP  0°
Wrist  −30°
MCP  0°
IP  0°
Wrist  −30°
MCP  0°
IP  0°
Wrist  −30°
MCP  0°
IP  0°
Wrist  −30°
MCP  0°
IP  0°
X5 per hr
Thumb
Exercises**
X5 per hr
Thumb
Exercises***
X10 per hr
Thumb
Exercises****
X10 per hr
Thumb Exercises****
Ultrasound from
week 3 as nec.
+ add active abd/add/opp.
Elevate hand
above elbow
Elevate hand
above elbow
Elevate hand
above elbow
Elevate hand
above elbow
Elevate hand above elbow
Adjust pain
control as nec.
Finger
Exercises
immediately
Finger
Shoulder
Elbow
Forearm
exercises
5x5 times daily
Finger
Shoulder
Elbow
Forearm
Exercises
5x5 times daily
Finger
Shoulder
Elbow
Forearm
Exercises
5x5 times daily
Finger
Shoulder
Elbow
Forearm
Exercises
5x5 times daily
Finger
Shoulder
Elbow
Forearm
Exercises
5x5 times daily
X10 hourly—full active wrist
movements with fingers relaxed
Hygiene/Splint
Checks–7&14d
Hygiene/Splint
Checks-21&28d
Increased Activity*****
*The Thermoplastic Dorsal Dynamic Extension Splint is made with the same joint angles of the wrist and thumb MCP and with the splint
lifting off the thumb at the mid-proximal phalangeal level so that a sling can be attached around the distal phalangeal palmar (volar)
surface. When resting, the sling remains around the distal phalanx.
**Five times hourly, the sling is slid proximally, under the proximal phalanx, and the IP joint alone actively flexed and extended. Five times
hourly, the MCP joint alone is actively flexed and extended, with the sling under the distal phalanx and the base of the thumb supported
with the other hand. The thumb tip is aimed for the base of the middle finger during this maneuver.
***Five times hourly, the sling is slid proximally, under the proximal phalanx, and both the MCP and the IP joint are actively flexed and
extended, with the thumb tip aimed for the base of the ring finger.
****Ten times hourly, the sling is slid proximally, under the proximal phalanx, and both the MCP and the IP joint are actively flexed and
extended, with the thumb tip aimed for the base of the little finger. After 28 days, the same exercises are continued without the splint.
*****From 4 weeks light hand use—less than 150 gm (full yogurt pot).
From 8 weeks—light work/driving.
From 12 weeks—heavy work/contact sports.

438.e5
Appendix 3 
Therapy Protocols After Extensor Tendon
Repairs of Fingers: Mid Essex Hospital
If there is extensor tendon tethering – forced passive flexion exercises + massage dorsal skin of digit and dorsum
of hand with finger held in flexion + ultrasound.
ST ANDREW’S CENTRE – HAND THERAPY
EXTENSOR TENDON REPAIRS – FINGERS
Instruction to Patients Weeks One to Four
This splint is to reduce the risk of the tendon(s) rupturing.
Weeks 1-4. A plastic splint will be made approximately 5 – 7 days after surgery. It is worn
continuously (24 hours) until 4 weeks after your surgery during which time you must
exercise your hand as instructed by your therapist. Do not use your hand, even unaffected
finger(s) and thumb.
Weeks 4-8. The splint is then worn for a further 4 weeks at night and when you are in
crowded places (e.g., shopping, using public transport). Do not drive until 8 weeks following
surgery. Your tendons are not strong enough and your insurance is invalid because of
your hand injury.
At 4 weeks after surgery you can begin to use your hand for very light activities only, not
lifting anything heavier than 6oz (150 grams) (e.g., yogurt pot).
At 8 weeks after surgery you can return to light work and driving.
From week 12 onwards you can return to heavy work after advice from your the surgeon
and the therapist.
EXERCISES FOR THE FIRST WEEK
You are required, as part of your treatment, to exercise as directed by your therapist
within the splint.
By gently exercising your hand, as instructed, these tendons will heal and are less likely to
become stuck or tightly caught in the scar.
1. Elbow and shoulder exercises – see separate sheet.
2. Straighten your thumb fully then bend it across your palm.
Repeat slowly 10 x each hour.

438.e6
Section 5:  Rehabilitation of Tendon Surgery
3. Bend your fingers at all joints over the edge of the splint.
DO NOT push with other hand.
Then fully straighten your fingers.
The therapist may ask you to assist by straightening your fingers with your other hand.
Repeat slowly 10 x each hour.
•
DO NOT bend or grip strongly with your fingers/thumb.
•
DO NOT try to pick anything up with your injured hand.
•
DO NOT let your hand hang down.
•
DO NOT remove any of the splint or bandages. If you take the splint off against our
advice and it is lost or left at home, it will not be replaced!
You should ring us if:
• You feel pain, swelling, or discomfort
• The splint feels loose or is not fitting well
• You have any worries
Make sure you bring the splint with you to every appointment.
If any problems do occur please telephone the Hand Therapy Department at
01245 516009 between 8:30 a.m. and 2:00 p.m. Monday to Friday, ask for _____________.
It is very important that your hand and splint are checked by your therapist regularly.
It is your responsibility to attend your appointment.
Please telephone to cancel or change appointments.

438.e7
Chapter 40:  State of the Art of Extensor Tendon Rehabilitation
ST ANDREW’S CENTRE – HAND THERAPY
EXTENSOR TENDON REPAIRS – FINGERS
Instruction to Patients Weeks Four to Eight
You must continue to use your splint for protection (i.e., at night, outside the house, and at
times when your hand may get accidentally knocked) (e.g. by dogs, cats, and young
children).
Light activities can be started, you can lift 6 oz/150grams (e.g., a small yogurt pot), but
avoid straining (e.g., tying shoe laces, pulling on tight clothing/belts, tight taps, tops of
bottles, door handles).
EXERCISES
1. Continue all your hand exercises hourly, out of the splint (as advised by your
therapist).
2. Gently bend your wrist forwards with your fingers relaxed and straight. Hold for 5
seconds.
Gently bend your wrist backwards, keeping your fingers relaxed and slightly bent.
DO NOT push. Hold for 5 seconds.
Repeat slowly 10x each hour.
Make sure you bring the splint with you to every appointment.
If any problems do occur please telephone the Hand Therapy Department at
01245 516009 between 8:30 a.m. and 2:00 p.m. Monday to Friday, ask for _____________.
It is very important that your hand and splint are checked by your therapist regularly.
It is your responsibility to attend your appointment.
Please telephone to cancel or change appointments.

438.e8
Andrew’s Centre-Hand Therapy, Essex, UK
Appendix 4 
Services, St
Timing
Regimen
Zone 1 tendon avulsion, tear, avulsion-fracture, zone 1–2 surgical repair
Week 1
• Apply thermoplastic splint to immobilize DIP joint in full extension or slight hyperextension to be worn
full time.
• No active or passive DIP joint motion.
• Monitor regularly and ensure skin hygiene and compliance.
Week 6
• Following surgical repairs and avulsion fractures wean from splint at 6 weeks slowly over 2 weeks and
commence active DIP joint flexion and extension exercises.
Week 8
• After tendon avulsion and substance tears wean from splint at 8 weeks slowly over 2 weeks and
commence active DIP joint flexion and extension exercises if good active extension.
Week 12
• Continue to wear splint at night until 12 weeks.
• Commence passive flexion stretch at 12 weeks if flexion slow to recover.
Zone 3 and distal zone 4 surgical repair
Week 1
• Apply thermoplastic cylinder or gutter splint to immobilize DIP and PIP joint in full extension.
Week 2
• If lateral bands are uninjured shorten splint to allow active and passive DIP joint flexion and extension
exercises.
• No PIP joint flexion until 3 weeks.
Week 3
• Continue with splint but remove to commence 0°–30° active PIP joint flexion and extension exercises.
10 repetitions hourly progressing to 20 repetitions when comfortable.
• Continue DIP joint exercises in splint.
Week 4
• Progress to 0°–40° active PIP joint flexion if there is no loss of active extension. 20 repetitions every 2
hours replacing cylinder splint between exercise periods.
• Continue DIP joint exercises.
Week 5
• Progress to 0°–50° active PIP joint flexion. Continue with splint.
Week 6
• Remove splint and commence light functional activity and free active PIP and DIP joint flexion and
extension exercises.
• Continue with cylinder splint at night in presence of extensor lag.
• Commence passive flexion stretching.
Week 12
• Return to normal activity.
Zone 4 (proximal), 5, and 6 surgical repair
Week 1
• Apply 2 part thermoplastic forearm based splint. Wrist in 45° extension, MCP joints 0°, IP joints in full
extension. Include only affected digits but in Zone 6 include adjacent digit if tendon linked by juncturae.
Removable digital plate allows IP joint flexion and extension exercises (Figures 40-10 and 40-11).
• Commence active IP joint flexion and extension exercises. 10 repetitions hourly. Digital plate to be
replaced between exercises periods.

438.e9
Chapter 40:  State of the Art of Extensor Tendon Rehabilitation
Timing
Regimen
Week 3–6
• Remove splint every 2 hours and commence active wrist flexion and extension exercises with digits
relaxed. Commence active MCP joint flexion and extension with wrist in flexion and IP joints extended.
Continue active IP joint flexion and extension exercises with MCP joints at 0°. 10 repetitions each
exercise. No composite flexion until 6 weeks.
Week 6
• Remove splint and commence composite flexion and extension exercises. Commence composite passive
flexion stretching. Allow light functional activity.
• Continue to wear splint at night in cases of extension loss.
• Return to normal activity once composite flexion regained.
Zone 7
Week 1
• Apply 2 part thermoplastic forearm based splint. Wrist in 21° extension, MCP joints 0°, IP joints in full
extension. Removable digital plate allows IP joint flexion and extension exercises.
• During weeks 1 and 2 IP joint flexion and extension exercises performed. 10 repetitions hourly.
Week 3–6
• Remove splint every 2 hours and commence gentle wrist motion with digits relaxed. No forced wrist
flexion.
• Commence active MCP joint flexion and extension with wrist at 0°.
• Continue IP joint active flexion and extension with MCP joints at 0°. 10 repetitions each exercise. No
composite flexion until 6 weeks.
Week 6
• Remove splint and commence composite flexion and extension exercises.
• Commence composite passive flexion stretching.
• Commence light functional activity.
• Continue to splint at night in presence of extensor lag.
Week 12
• Return to normal activity.
Zone 8
Week 1
• In combination tendon and muscle belly injuries or muscle bellies only apply high forearm based
thermoplastic splint. Wrist 45° extension. MCP joints 0°. IP joints in full extension. Immobilize for  
3 weeks.
Week 3
• For muscle bellies only remove splint and commence slow return to composite flexion.
• In cases of concomitant wrist tendon injury at 3 weeks reduce splint to allow unimpeded active MCP
and IP joint flexion and extension exercises. Remove splint 2 hourly for careful active wrist flexion and
extension exercises. 10 repetitions hourly.
Week 6
• Remove splint and commence composite active flexion and extension exercises.
• Commence composite passive flexion stretching.
Week 12
• Return to normal activity.
The Manchester Regimen for the Postoperative Rehabilitation Following Surgical Repair of Extensor Pollicis
Longus: Manchester, UK
Timing
Regimen
Zone T—1 surgical repair, avulsion fracture, and substance tear if treated conservatively
Week 1
• Apply thermoplastic splint to immobilize the IP joint only in full extension. To be worn full time for  
6 weeks for avulsion fracture and post surgical repair and 8 weeks for substance tear.
• No active IP joint flexion or extension.
• Monitor regularly and ensure skin hygiene and compliance.
Week 6
• Following surgical repairs or avulsion fracture with large fragment wean from splint slowly over 2
weeks and commence 0°–30° active IP joint flexion and extension exercises. Gradually increase
range of active IP joint flexion if there is no loss of active extension.
• No passive flexion stretch.
• In avulsion or substance tear continue with splint.

438.e10
Section 5:  Rehabilitation of Tendon Surgery
Timing
Regimen
Week 8
• Following avulsion or substance tear wean from splint slowly over 2 weeks and commence active IP
joint flexion and extension exercises. Gradually increase range of IP joint flexion if there is no loss of
active extension.
• No passive flexion stretch.
• All types to continue with splint at night in presence of extensor lag.
Week 12
• All types commence passive flexion stretch if required.
• All types return to normal activity.
Zone T—2 post surgical repair
Week 1
• Apply thermoplastic splint forearm splint with MP and IP joint in 0°. Thumb comfortably abducted
and extended.
Week 3
• Modify splint adding removable plate to commence 0°–30° active IP joint flexion and extension
exercises. 10 repetitions hourly.
Week 3–5
• Splint to be worn full time.
• Progress active IP joint flexion exercises increasing slowly 0°–60°.
Week 5
• Remove splint and commence light function. Increase active flexion and extension exercises.
• Continue with splint at night in presence of extensor lag.
Week 6
• Commence passive flexion stretch if required.
Weeks 10–12
• Return to normal activity.
Zones T—3–5 post surgical repair
Week 1
• Apply 2 part forearm based thermoplastic splint with wrist at 30°, MCP and IP joint at 0°. Thumb
comfortably abducted and extended. Removable plate to allow 0°–60° IP joint flexion and extension
exercises (Figs. 40-4, 40-5, and 40-6).
• Commence IP joint active flexion and extension exercises progressing to 60° flexion during the first  
3 weeks.
• No passive flexion stretch.
• Splint to be worn full time and immobilize at night.
Week 3
• Remove splint to perform careful wrist flexion and extension with thumb relaxed to encourage
tenodesis action and promote tendon glide especially in Zone T5 where there is risk of adhesions
under retinaculum.
Week 5
• Remove splint continue with active IP joint flexion and extension exercises.
• Commence composite active MCP and IP joint motion to restore opposition.
• Continue to wear splint at night in presence of extensor lag.
Week 6
• Commence passive flexion stretch if slow to regain flexion.
Weeks 10–12
• Return to normal activity.

438.e11
Regimen for Postoperative Rehabilitation
After Finger Extensor Tendon Repairs,
Manchester, UK
The Manchester
Appendix 5 
Day
Rehabilitation Program
Day 0
Extensor tendon injury rehabilitation program
Operation
Day 2
Dressing changed
Extension dynamic splint (Fig. 2) applied in occupational therapy department
Position: wrist 30° extension. MPJ and PIPJ full extension
Exercise program by physiotherapists
a. passive extension of MPJ and IPJ
b. active flexion of MPJ to 30°. IPJ to full flexion 1 against resistance of dynamic bands (with broad finger
straps at middle phalanx) 10 times hourly
c. no active extension
Discharged from hospital to hand class for alternate day treatment
Day 7
Splint adjusted to allow MPJ active flexion to 45° against traction system
Day 14
Splint adjusted to allow MPJ active flexion 1 to 60° against traction system
Sutures removed
Day 21
Splint adjusted to allow full active flexion of MPJ
Day 28
Should be able to regain full grip within splint
Day 35
Off splint
Exercise program
a. free active flexion and extension of fingers
b. gentle passive flexion of fingers
c. strong passive extension of fingers
d. wrist mobilization
Week 7
Active flexion and extension of finger against resistance
Passive flexion and extension of fingers
Gradual simultaneous active finger and wrist flexion
Week 8
Strengthening exercise

Date
*D1 1/52
*D8 2/52
*D15 3/52
*D22 4/52
*D29 5/52
*D36 6/52
*D43 7/52
*D50 8/52
Splintage
Wrist 30° ext.
MCP 15°–30°
+ outrigger
(dynamic band
at MP level, IP
fully ext)
Wrist 30°
ext.
MCP
15°–45°
+ outrigger
Wrist 30°
ext.
MCP
15°–60°
+ outrigger
Wrist 30°
ext.
MCP 0°
- full
+ outrigger
Wrist 30° ext.
*Off outrigger
Off splint for wrist mobilization
Active
Movement
Extension
No active fingers extension is allowed
Free active fingers
extension within
cock up splint
Free active
fingers
extension
Gentle
resistive
extension→
Strong resistive
extension
Flexion
Active fingers flexion within splint & outrigger 10 times
hourly
Free active fingers
flexion within
cock up splint
Free active
fingers
flexion
Resistive
fingers
flexion→
Strong resistive
flexion
Passive
Movement
Extension
Passive extension of MCP & IPJs within the splint
Strong passive extension of fingers
Flexion
No passion flexion of fingers is allowed
Gentle
passive
flexion of
fingers
Strong
passive
flexion of
fingers
Allow simultaneous
passive flexion of
fingers & wrist
Remarks
D14 Off
Stitches
Pressure Glove for scar as
indicated
Work rehab in Occ
Therapy as indicated
of Hong Kong, Hong
After Repair
of Extensor Tendon Injuries,
Queen Mary Hospital, The University
Protocols of Exercise

438.e13
Therapy Protocols After Extensor Tendon
Repair, Springfield, Mass, USA
Appendix 7 
Zone of
Injury
Immobilization
Passive Mobilization
Active Mobilization
1–2
• 6–8 weeks full-time DIP
extension cylinder cast or
splint if not pinned.
• Gradually wean out of splint
(first for exercise only, then for
increasing time) and initiate
active flexion and extension.
—
—
3–4
• 3 weeks in IP extension if
referred too late for early
mobilization.
• Wean out of splint as above
and initiate AROM.
• Focus on full extension and
initiate passive flexion
cautiously after 7 weeks.
• Prefer not to use – if patient
can perform, can probably
also do well with Short Arc
Motion (SAM) (Evans, 1992).
• See Active Mobilization.
• 4 weeks Short Arc Motion (SAM)
with resting splint full extension,
exercise template splint allowing
30° PIP flexion (Evans, 1992).
• Modify exercise splint to increase
allowed PIP flexion weekly, and
discontinue at 4 weeks.
5–6
• 3 weeks in wrist and IP
extension, 15–20° MP flexion.
May leave IPs free for Zone 6.
• Wean out of splint as above
and initiate AROM. Focus on
attaining full extension while
increasing MP and composite
flexion.
• 3 weeks in dynamic
extension splint with wrist at
40–45° and active flexion
without block to flexion
(similar to Evans and
Burkhalter, 1986).
• Wean out of splint and
initiate AROM.
• Prefer Immediate Controlled
Active Mobilization (ICAM)
(see Active Mobilization)
when a border digit not
involved.
• Except for border digits, Immediate
Controlled Active Mobilization
(ICAM) (Howell et al, 2005).
• 1st 3 weeks: Yoke splint holding
MP(s) of involved finger(s) in
15–20° greater extension relative
to adjacent uninjured fingers.
Worn with separate 20–25° wrist
extension splint. Full motion as
allowed by splints.
• From 3–5 weeks wean out of wrist
splint and initiate wrist ROM
slowly.
• 5–7 weeks, yoke splint only.
Discontinue by 7 weeks.
7
• 3 weeks wrist extension and
15–20° MP flexion.
• Wean out of splint and initiate
active ROM. Focus on
differential glide between
extensors.
• None for wrist extensors.
• Dynamic extension as for
Zones 5–6.
• None for wrist extensors. For
digits, have considered but not
tried Evans (2002) combination of
dynamic extension with protected
short arc active extension in
therapy only.

438.e14
Section 5:  Rehabilitation of Tendon Surgery
References
Zone of
Injury
Immobilization
Passive Mobilization
Active Mobilization
T-1
• As for Zones 1–2 (IP extension
fulltime 6–8 weeks). Wean out
of splint slowly and initiate
AROM.
• 3–5 weeks dynamic thumb
extension with MP extension
block, outrigger cuff at DIP
joint (Elliot, 2005).
• Blocked MP and IP flexion
first week.
• Thumb opposition to middle
finger tip second week.
• Full opposition third week.
Wean out of splint thereafter
as indicated.
—
T-2 to
5
• 3 weeks in wrist extension,
thumb in extension and
abduction as determined by
structures repaired.
• Dynamic thumb extension
with MP extension block
(Elliot, 2005). Protocol above
—
Elliot D, Southgate CM: New concepts in managing the long
tendons of the thumb after primary repair. J Hand Ther 18:
141–156, 2005.
Evans R, Thompson D: An analysis of factors that support early
active short arc motion of the repaired central slip. J Hand Ther
5:187–201, 1992.
Evans RB: Clinical management of extensor tendon injuries. Reha-
bilitation of the Hand and Upper Extremity. E. J. Mackin, A. D.
Callahan, T. M. Skirven, L. H. Schneider and A. L. Osterman.
St. Louis, C.V. Mosby. 1: 542–582, 2002.
Evans RB, Burkhalter WE: A study of the dynamic anatomy of
extensor tendons and implications for treatment. J Hand Surg
(Am) 11:774–779, 1986.
Howell JW, Merritt WH, Robinson SJ: Immediate controlled active
motion following zone 4–7 extensor tendon repair. J Hand
Ther 18:182–190, 2005.

438.e15
Protocols of Sydney Hand Therapy &
Rehabilitation Centre, Sydney, Australia
Appendix 8 
Zone
Protocol Type
Splint
Exercises in Splint
Exercises Out
of Splint
Time in
Therapy
3–4
SAM
Splint position: Full extension,
template splints or other
devices to limit flexion
initially to 30 degrees.
Some cases (e.g., crush
injuries) may switch to
Capener at 2 or 4 weeks.
Splint stays on for: 6 weeks,
splinting may be longer  
if there is a lag and the
splint may be changed to
Capener or neoprene in the
day and static digit at night
Immediately start
exercises following
SAM protocol as
described by Evans.
Avoid stress on repair
for 6 weeks.
However if the
joint is stiff and
thick and glide
poor more vigorous
exercises may be
commenced at 4
weeks.
Generally this is
started at 6
weeks, but may be
sooner at 4 weeks
if the joint is stiff,
always monitoring
to ensure
extension to 0 is
maintained.
Graded resisted
exercises are
commenced  
week 6.
Total time in
therapy is
about 3
months, if
difficulties
maybe 4
months.
Comments
We use a “custom made” Capener that has very low tension (less than 300 g) that can be adjusted and
measured in order to facilitate the therapy program for Zone 3 PIP joint level injuries. Sometimes this works
better than taking splints on and off, but not always. An OFF the shelf Capener is ENTIRELY NOT appropriate
as they are all too strong (600 g plus). It is good to have some different options for different or difficult
situations.
Zone 5–6
Merrit or
Norwich
(Depending on
referring
surgeon)
Merrit:
Wrist extension splint in 45
deg
plus hand piece with involved
digit 15 deg more
extension than adjacent
digits
Norwich:
POSI type splint with wrist 45
deg ext
MP 45 deg flexion and IPs in
full ext
The splint stays on for 6
weeks and then 2 wks at
night and for travel
Exercises as
described in
original articles
As described in the
original articles,
graded resisted
exercise is
commenced at 6
weeks
Total time in
therapy
3–4
months
Comments
The protocols used are generally reported but are sometimes changed depending on the healing of the
tissues, the patients scar and the mobility of the joint(s), and also what the surgeon found at the time of the
repair eg was it tight or was the tendon really mashed up. Also other factors like patient compliance, other
injuries to other structures in the hand can influence the protocol.
Zone 7
Immobilization
Wrist in 40 degrees extension
Splinting is for 6 weeks then
weaned over 2–4 weeks
Active exercises start
at 3 weeks
More vigorous active
exercises started
at 6 weeks
Total time in
therapy 3
months

438.e16
Therapy Protocols from Royal Free
Hampstead NHS Trust, London, UK
Appendix 9 
Zone
Protocol Type
Splint and Positions
Exercises in Splint
Exercises Out
of Splint
Total Time
in Therapy
3–4
Immobilization for
the first 3
weeks then
controlled
mobilization
Cylinder splint for PIP
joint which is
extended, DIP free
unless lateral bands
repaired
MCP joint free
2–3 weeks full time
until edema
controlled and some
extension central
slip control visible
From 3–6 weeks  
splint full time in
extension coming
out for gentle PIP
joint exercises. Splint
stopped 6 weeks
unless complications
Active MCP/DIP
joint flexion/
extension from
day 1
PIP joint motion
commenced at
2–3 weeks as
long as central
slip can extend
back to neutral
4–6 weeks increase
range of PIP joint
flexion as long as
extension good
Passive flexion and
commence some
gripping after 6
weeks
6–8 weeks unless
complications
Comments
We delay PIP active mobilization protocol slightly especially if the PIP joint is swollen or the wound infected.
Zone 5-6
Active–Norwich
Position:
Wrist joint 20
extension
MP 30 flexion unless
extension lag noted:
MCP in extension
IP neutral
Splint full time 4 weeks
with exercises within
splint
Splint for protection
4-8 weeks as
required depending
on age/occupation/
hand dominance, etc.
Splint week 4–8
reducing gradually
Stop splinting at 8 wks
First appointment
start passive ext
from splint
Active ext from
splint
Active ext fingers
from splint and if
extension good
then gentle
flexion of fingers
towards splint
NB patient must be
able to maintain
extension MCP
joints before
flexion is allowed
4 wks post op:
exercises out
of splint and
start moving
wrist joint
Increase flexion
fingers
towards
palm as long
as extension
good
Light activities
with hand
allowed
8–10 weeks on
average

439
SECTION
6
CURRENT STATUS
AND FUTURE

This page intentionally left blank

441
CHAPTER
41 
CURRENT STATUS AND FUTURE
Peter C. Amadio, MD
A
Current Status and Future of
Flexor Tendon Surgery
for many of them, joint contractures and loss of motion
are unsightly at best, and functionally awkward for
many. In short, while the current state of tendon surgery
is better than it has ever been, it is not nearly as good
as those with injured tendons want it to be.
THE FUTURE OF FLEXOR TENDON SURGERY
What does the future hold for tendon surgery? A good
place to start is current research. These focus on two
general areas—accelerating the pace of tendon healing
and reducing adhesion formation. Along the way,
researchers in both areas must address a common
pitfall—too much load, too soon, will result in tendon
rupture, and a need for the patient to start all over again.
Speeding up tendon healing has already run down
one blind alley: once a tendon is moving, there is no
evidence that more load on a repair speeds healing or
reduces adhesions—all it can do is break the repair.
Thus, the only reason to create ever stronger repairs is
to permit a bit more of a margin of safety for early
mobilization, while at the same time not creating so
much bulk as to impede healing or gliding. In my
opinion, there is little more we can practically do in this
regard—current repairs are “good enough.”
What is needed to shorten tendon healing time? Two
things—cells, and matrix, and these are interrelated,
because making matrix requires cells—specifically,
fibroblasts initially, and then tenocytes. Tendons are not
very cellular, and the cells that are there are often trapped
in a dense collagen matrix. Adding cells from outside
the tendon should help, and there are several studies
now underway in animal models that should be trans­
latable to humans soon, delivering differentiated cells
or stem cells, either via a cell-seeded patch of some sort
between the cut tendon ends, or by literally attaching
the cells to the tendon suture. Add in the right mix of
cytokines, or perhaps even platelet-rich plasma, and we
should be able to develop a cocktail that can cut down
total healing time, and even better, accelerate the early
CURRENT STATUS OF FLEXOR
TENDON SURGERY
Tendon surgery has certainly advanced over the past
century. Our repairs are stronger and more reproduc­
ible; most surgeons who deal with these injuries have
had some sort of training in the management of tendon
injuries, and within the past 60 years hand surgery has
developed as a specialty, while within the past 30 years
hand therapy has joined it as a recognized field of spe­
cialization. There are hand surgeons in nearly every
country on the planet; in the larger and more developed
countries, there are literally thousands of trained hand
surgeons and therapists.
One might think that, with all this progress, tendon
injuries would be a solved problem. But, despite our
best efforts, this is not the case. The average result after
surgery restores perhaps 80% of normal finger motion
when both tendons are cut in zone 2, and that assumes
a sharp laceration and a cooperative patient. Ragged
cuts, multiple injuries, and patients who are not able or
willing to cooperate with an early mobilization rehabili­
tation program still frequently end up with adhesions,
ruptures, infections, contractures, and other forms of
unsatisfactory results.
Why is this? Primarily because while our under­
standing of tendon healing, biomechanics, and physiol­
ogy has grown dramatically, our ability to improve
upon Mother Nature remains where it was in Sterling
Bunnell’s day—or, for that matter, Galen’s. We may
sometimes be able to avoid slowing down the healing
process, by better techniques, but we have not yet found
a method to speed things up. And we must face reality—
tendon injuries are most common in those who can
least afford time away from work for rehabilitation and
protection—mostly adolescents and young adults,
mostly male, and mostly in occupations where heavy
use of both hands is an expectation. And, while our
patients are often satisfied with less than normal motion,

442
Section 6:  Current Status and Future
cause? Here, tissue engineering may help. While build­
ing a tendon from scratch is daunting, it may be pos­
sible to manipulate allograft tissue, seeding it with host
cells, and specialized surfaces in the middle for gliding,
and at the ends for attachment to tendon, muscle, or
bone. Such work is already proceeding.
In short, I think that the future for tendon surgery is
bright. With a decade, or two at the most, we should
have solved the remaining vexing problems of healing
and function and have begun to apply those solutions
clinically. The best is yet to come.
healing phase, so that repair strength grows faster in the
first few weeks, when the repair is in greatest jeopardy.
Reducing adhesions has always been possible, but at
a price—aggressive mobilization may result in tendon
rupture, and adhesion barriers are usually also healing
barriers. New research into more permeable barrier,
and ones that biodegrade over the critical first week
or two, when most adhesions begin to form, may do
the trick.
Finally, what to do when no tendon is available,
due to extensive injury, tumor resection, or some other
Robert Savage, MB, FRCS, FRCS Ed Orth, MS
B
Current Status and Future
overrated (or underrated) and that cyclic load tests
would give more reliable information. Further con­
trolled studies comparing static and cyclic load testing
are indicated, and perhaps we should adopt cyclic load
tests for all laboratory studies.
Recent studies have shown that different mammalian
tendons have different physical characteristics. The com­
monly used and readily available pig flexor tendon
appears to be less like human flexor tendon than, for
example, sheep flexor tendon. The wide use of pig flexor
tendon could have produced some inaccurate informa­
tion and it may be better to use sheep tendon in
preference.
Many other technical problems in medicine and
surgery have been resolved by a gadget using the special
properties of a physical material and clever engineering.
The tendon repair would seem ripe for such a develop­
ment but currently we only have some relatively crude
barbed suture techniques and screw devices. Further
development of these ideas on a more refined scale
might yield something practical and strong.
Developments in post surgical rehabilitation may be
found, which combined with improved repair quality,
could lead to less restrictive and shorter splintage regi­
mens. As a parallel there are other aspects of trauma
surgery in which multipoint fixation; for example, distal
radius fractures, has enabled mobilization of the wrist
before the fracture has healed. We have not reached a
A reasonable starting point for considering the future
for tendon surgery would be to consolidate what we
know of best practice today, and to ensure that this
knowledge is as widely known as possible. Other chap­
ters in this book cover this in detail and as previously
reported in surgical history practitioners will choose
which bits of advice are most believable and applicable.
There now appears to be very strong evidence that mul­
tistrand tendon repairs give a more reliable outcome to
acute tendon division. Hopefully, the use of two-strand
core sutures is diminishing for it appears important that
at least a four-strand core suture should be used. This
should be combined with, at least, a simple peripheral
suture but a crossed or interlocked peripheral suture
adds further strength and gap resistance. A six-strand
core suture further improves repair strength, but it is
debatable whether addition of a crossed or interlocked
peripheral suture is beneficial. All these elements give a
repair that is, in the main, sufficiently robust to with­
stand the controlled active motion program and to
reduce the chance of rupture in the healing phase.
In laboratory testing, traditionally single static tests
have been used to describe the quality of a tendon
repair, but they do not mimic real life where a repair is
subject to repeated loads. Single static load tests are rela­
tively straightforward to perform in a laboratory and
clearly give a reasonable evaluation of a repair’s quali­
ties, but it is possible that tendon repairs have been

443
Chapter 41C:  Future of Tendon Surgery of the Hand
point where repair strength is sufficient to discard the
splint immediately after surgery, although possibly this
could come about, but presumably another means of
restricting finger activity would be required. A theoreti­
cal idea for reducing power to one finger could be devel­
oped: the injured finger would be held slightly more
flexed than the neighboring fingers reducing the tension
within the flexor tendons of the injured finger yet allow­
ing it to move.
Other ideas will emerge!
Biological research may identify methods of acceler­
ating tendon healing and reducing adhesion. Current
tried techniques include grafts and locally applied
agents.
Jin Bo Tang, MD
C
Future of Tendon Surgery
of the Hand
involving serious damages to multiple structures (such
as fractures or soft tissue defects), though not related to
the quality of tendon repair only, frequently result in
distinct loss of function. In many such cases, extensive
adhesions form; arduous staged reconstruction is neces­
sary. There is still no guarantee of functional recovery to
the level desired by both patients and surgeons. Fortu­
nately, the number of such cases declined drastically
after the inception of primary tendon repair in the
digital sheath area. Though relevant to surgery of the
tendon per se only partly, tendon transfers do not
restore full, or sometimes, major hand function after
nerve palsies.
It is difficult to precisely or inclusively predict future
developments in a field. Scientific and technical innova­
tions are by their nature unpredictable. Nevertheless, we
can summarize those areas where work is under way and
those that await answers and continuing efforts.
We will probably see the following changes in the
near future:
1. More widespread use of stronger surgical repairs.
We already see a trend towards use of stronger
surgical repairs. However, the speed of change
varies with the resources of the hospital and with
geographic region. I expect that strong surgical
repairs will become the method of choice for the
vast majority, if not all, of surgeons, particularly in
digital areas and for flexor tendons.
The repair of injured tendons is a fascinating field that
has attracted the particular attention of hand surgeons
over the past century. In the early 1970s, Verdan wrote
a classic review: “Half a century of flexor-tendon surgery.
Current status and changing philosophies” (J Bone
Joint Surg [Am] 52:472–491, 1972). In 1987, Hunter,
Schneider, and Mackin edited the book Tendon Surgery
in the Hand to summarize the progress.
The authors of the current book and our predecessors
have witnessed major paradigm shifts in both funda­
mental concepts and the practice of tendon repair. The
content of this book reflects the growing body of knowl­
edge and advances over the past 25 years. After almost a
century of efforts by basic scientists and surgeons, our
accumulated knowledge of basic scientific knowledge
offers both useful and meticulous guidance for clinical
practice, making it much more feasible to restore the
function of the hand. Principles of primary repair and
secondary reconstruction have been established; surgical
and postoperative care methods have been developed.
Armed with current guidelines for surgical repair and
postoperative care, well-trained hand surgeons can
expect to restore near-normal function of the hand and
digits after repair of injuries chiefly involving the tendons.
It appears that major scientific and technical obstacles
on the path to nearly optimal primary tendon repair
have been eliminated, except in a few specific instances.
Nevertheless, tendon injuries with delayed presenta­
tion, injuries in a complex wound setting, and injuries

444
Section 6:  Current Status and Future
2. Early combined passive-active motion. It is clear
to me that combined passive-active motion is an
ideal way to rehabilitate repaired fingers. However,
regimens incorporating this principle can vary
enormously. I believe that rubber band traction
should be abandoned in digital flexor tendon
rehabilitation and that passive-only motion
reserved for patients who fail to comply with
active motion regimens. Generally, in each exer­
cise session, passive motion should precede active
motion to lessen resistance to tendon gliding.
3. Simplification of motion protocols. We currently
see a variety of protocols in different units, and
some are quite complex. The variation in proto­
cols that produce comparable clinical outcomes
indicates that some protocol details are of second­
ary importance. We should be cognizant that
current protocols are largely experience-based and
in fact constitute “expert opinions.” My opinion is
that workload of patients and therapists may be
reduced, without lowering rate of success. For
example, hourly exercise of repaired tendons
may not be necessary; four or five sessions of exer­
cise in a day would probably suffice. The number
of repetitions is increased in each session. This
would relieve the patients from hourly exercise
of the repaired fingers. In addition, it appears
unnecessary to actively move the finger through a
full range of motion, particularly in the initial 1
to 2 weeks. It is vital to keep in mind that the most
extreme portion of active finger flexion carries the
greatest risk of disrupting the repair. Partial active
finger flexion not only reduces the chance of over­
loading the tendon, but also diminishes pain and
discomfort. Nevertheless, passive finger motion
does need to be executed over the entire range.
4. Loosely controlled postoperative motion. In
patients whose tendon has been repaired with a
strong method, and after proper measures (such
as pulley release) have been taken to diminish
tendon gliding resistance, the finger can be
expected to actively move under less stringent pro­
tection or a substantially simplified protocol, pro­
vided such motion is not against resistance.
Employment of such hand motion perhaps will be
a major advance in the future.
The following changes may not occur in the near future,
but are likely in the years or decades to follow:
1. Biological approaches to increase intrinsic
tendon healing. Recent years have seen growing
realization of the impact of molecular biotechnol­
ogy on medicine. Molecular therapy catches public
imagination of future medicine, and offers thera­
peutic promise to regulating tendon healing. In
the future, efforts to accelerate tissue healing and
repair will find the tendon a perfect test ground
for transferring some basic scientific concepts to
the clinic, because tendons are composed mainly
of uniform collagen building blocks with aston­
ishingly little vascularization. Compared with
tissues rich in vasculature, enhancement of tissue
repair in tendons may be more attainable. We
expect that injection or implantation of bioactive
agents will fortify weak tendon healing capacity.
Currently, approaches with such potentials include
gene therapy, controlled release systems, or coated
surgical sutures; certainly novel methods would
emerge and will bring us even closer to this goal.
2. Reducing adhesion formation. Reducing adhe­
sions has been a constant theme in tendon surgery
and imputes for investigations. Limiting adhe­
sions is important not only for primarily repaired
tendon, but also after secondary tendon grafting
or tenolysis. Broadly, avoiding adhesion or scar is
desirable after all surgical interventions, but it is
particularly necessary for tendons, which glide
within a restrictive sheath. Surface modifications
of tendons, which have been the goal of Peter
Amadio and his colleagues for a decade, are impor­
tant to reduce not only gliding resistance but
adhesions as well. Such efforts likely offer great
potential for decreasing adhesions arising from
the tendon surface. Another fertile research area is
molecular methods to regulate tendon healing
and inhibit key mediators of scar formation.
However, we must be prepared to understand the
complex nature and interactions of molecular
events, and recognize the complexity of interven­
tions at the molecular level. Such approaches may
not prove easy and straightforward, particularly
when aimed at simultaneously maintaining
healing strength.
3. Engineered tendons for reconstruction of tendon
defects. This is certainly a worthwhile future direc­
tion. The work of researchers in James Chang’s lab
leads me to expect that decellularized allogenic
tendons will serve as a good scaffold clinically,
providing structural supports for cell seeding in
vitro before implantation or cellular ingrowths
from surrounding tissues in vivo. These tendons
bypass the major obstacle in generating scaffolds
that mimic the flexibility and loading capacity of
intrasynovial tendons. In contrast, it is hard to
speculate whether or how soon a “tendon” made
of biomaterials incorporated with cells in vitro or
in vivo will be used to replace a tendon graft; there
is a long road ahead of us. There is the open ques­
tion of whether we can ever produce materials
with the superb mechanical properties of natural
intrasynovial tendons. If we ever do reach that

445
Chapter 41C:  Future of Tendon Surgery of the Hand
goal, I expect it to happen in the quite distant
future.
4. Novel materials and methods to promote tendon
healing or a manufactured tendon substitute.
Basic scientific developments always offer novel
tools to battle against frustrating problems. Lately
emergent options constantly replace old ones,
though only very few among these may offer actual
solutions. Each innovation creates energy and
enthusiasm for tackling the problem. I expect that
novel materials and methods will be used to
produce tendon substitutes (or enhancing the
healing process). Nevertheless, tendons have many
unique requirements as a viable biologic tissue—
bearing both compressive and pulling forces
during motion, being firm enough to sustain com­
pression and flexible enough to accommodate
angular motion, while surrounded by a restrictive
sheath in some parts. The tendon should not be
bulky, but smooth and free of restraining adhe­
sion. Any manufactured tendon substitute must
possess these biological and mechanical qualities.
The following issues are unlikely to be overcome in
foreseeable future, and will thus continue to affect out­
comes: (1) less-qualified surgeons still repair a propor­
tion of cases; (2) particular injuries, such as those in the
little finger, will continue to be a problem; (3) severe
injuries involving multiple structures, whose outcomes
do not chiefly depend on treatment of tendon injuries,
limit the extent of recovery, and (4) socioeconomic con­
ditions limit the availability and affordability of surgery
and postoperative rehabilitation.
Finally, future development of our field includes the
education of qualified hand surgeons. This remains a
great concern and is also a pressing task. Scientific
advances have cleared the major obstacles encountered
50 years ago in repairing injured tendons. Nevertheless,
close-to-ideal outcomes are expectable only when sur­
geons have been well-trained in tendon repair and abide
by up-to-date surgical and postsurgical care guidelines.
Unfortunately, tendon injuries may have disastrous
clinical results if treated by unqualified surgeons.
In most regions of the world, it is not the current state
of scientific and technical knowledge that limits return of
clinically acceptable function after tendon injury; rather, it
is the lack of both trained surgeons and adequate rehabilita­
tion systems that prevents functional restoration of the injured
hand (Injury 37:1036–1042, 2006).
Therefore, in countries where hand surgery is not
fully recognized as an established surgical subspecialty,
surgeons should be encouraged to become specialists in
the hand. It should be realized that, development of
techniques and expansion of knowledge on treating
hand disorders make a general orthopedic or plastic
surgeon less likely to treat a tendon injury in the hand
proficiently. Poor mastery of surgical techniques and
lack of sufficiently precise knowledge of anatomy jeop­
ardize treatment outcomes. Ideal repair of lacerated
tendons is based on understanding of hand anatomy
and biomechanics, possession of fine surgical skills, and
knowledge of hand rehabilitation or cooperation with
hand therapists. Improving education and training is
one of the most momentous tasks among all that we
will have in the future.

e1
CHAPTER
42 
CHEMICAL MODIFICATION OF
TENDON GLIDING SURFACE
Yu-Long Sun, PhD, and Peter C. Amadio, MD
Phospholipase C selectively removes certain types of
phospholipids, such as phosphatidylcholine, without
destroying the extracellular matrix network.14 The
increase in friction after treatment with phospholipase
C suggests that phospholipids are present on the surface
of the FDP tendon, and that phospholipids help to
lubricate FDP tendon (see Figure 42-1). This conclusion
was further confirmed by the increase in friction after
treatment with lipid solvent. The increased effect of
lipid solvent compared to phospholipase C suggests
that phospholipids other than phosphatidylcholine
may also affect tendon lubrication.
Trypsin can digest lubricin as well as other extracel­
lular matrix proteins except collagen, the principal
protein in tendon. Trypsin digestion resulted in a sig­
nificant increase of friction of the FDP tendon (see
Figure 42-1). Although the increase of friction could
contribute to phospholipids, which could be carried by
lubricin and/or other extracellular matrix proteins, it
was found that the friction of the FDP tendons could
be further increased with trypsin after the elimination
of phospholipids with lipid solvent (see Figure 42-1).
Hence, the effect on friction could be due to a removal
of protein components, especially lubricin, a glycopro­
tein both known to have lubricating ability, although it
cannot exclude an effect from other proteins on the
tendon surface.
Many factors appear to contribute to the lubrication
mechanism of the FDP tendon. The research findings
are strongly suggestive of the presence of, and a role for,
proteins, HA, and phospholipids in tendon lubrication.
Phospholipids, HA and lubricin, may serve as boundary
lubricants in FDP tendon lubrication.
CHEMICAL SURFACE MODIFICATION
OF TENDON IN VITRO
Tendons attach muscle to bone and transfer the power
of the muscle to bone over a distance. The structure of
tendon is directly related its physical and physiological
function. The surface of tendons well adapts to their
mechanical environments.15 Tendons are characterized
based on their anatomic location as either intrasynovial
or extrasynovial.16-18 The intrasynovial tendons, such as
the FDP tendon, have parietal and visceral synovial
TENDON LUBRICANTS
The flexor digitorum profundus (FDP) tendon glides
within tendon sheath, which consists of annular liga­
ments or pulleys, during the movement of fingers. This
tendon-pulley system has a low coefficient of friction
(0.04), which is similar to that of articular cartilage
(0.014).1
Lubrication mechanism of articular cartilage has been
widely investigated.2,3 Hyaluronic acid (HA), lubricin,
and phospholipids are thought to be involved in the
lubrication of the cartilage–cartilage interface, acting
alone or in combination. HA is a polyanionic polysac­
charide, present in the intercellular matrix of most ver­
tebrate connective tissues, especially in synovial fluid.
The unique properties of HA result in a molecular
network that, in highly hydrated conditions, is extremely
viscoelastic and pseudoplastic, favorable rheological
properties for a potential lubricant. Lubricin, also known
as superficial zone protein and proteoglycan 4, is a gly­
coprotein which has been identified in synovial fluid4,5
and the superficial zone of articular cartilage.6 It has
been noted to lubricate articular cartilage with the same
lubricating properties as normal synovial fluid. Lubricin
is widely considered to be the principal lubricant in
joints.3,7 Furthermore, phospholipids, the major compo­
nent of all biological membranes, are known to contrib­
ute to joint lubrication and to lubricate other gliding
surfaces as well.8,9
HA and lubricin have been identified on the surface
of the FDP tendon.10-12 While phospholipids have not
been sought in tendon, it is reasonable to assume that
some are present, as phospholipids are found in all
living tissues. To assess the effect of HA, lubricin, and
phospholipids on tendon lubrication, the enzymatic
and chemical treatments were applied to remove them
from the surface of canine FDP tendons.13
Hyaluronidase can effectively digest HA. The effect of
the hyaluronidase digestion on the friction between
FDP tendon and its associated pulley was measured. The
friction between the FDP tendon and its pulley increases
after the FDP tendon is treated with hyaluronidase
(Figure 42-1).10,13 Therefore, HA has been assumed to
play a role in lubricating the surface of the FDP tendon.
This chapter does not appear in the print edition.

e2
Chapter 42:  Chemical Modification of Tendon Gliding Surface
disaccharide that consists of N-acetyl-D-glucosamine
and D-glucuronic acid linked by a β1–4 glycosidic bond
(Figure 42-2).25 The disaccharides are linked by β1–3
bonds to form the HA chain. Each disaccharide has one
carboxyl group, which can be activated by carbodi­
imides at physiological condition to form an amine-
reactive O-acylisourea intermediate that quickly reacts
with an amino group to form an amide bond and
release an isourea. As amino group universally exists in
the protein components, such as collagen, the major
extracellular matrix in tendon, with the activation of
carbodiimides, HA could cross-link paratenon and
tendon and keep paratenon resist abrasion. Further­
more, HA is a lubricant of tendon. The chemical reac­
tion can tightly bind HA on the surface of tendon and
play a role in lubrication (Figure 42-3).
We performed a study to evaluate HA and carbodi­
imide derivatized HA (cd-HA) on the gliding of canine
PL tendon, an extrasynovial tendon.26 We found that
the gliding resistance of normal PL increased with the
increase of cycle of repetitive motion (Figure 42-4).
The administration of exogenous HA (1%) resulted in
the nonchange of gliding resistance in the first cycle of
motion after the administration. However, the gliding
resistance of PL treated with HA increased significantly
over five cycles of repetitive motion than normal PL did.
The quick discharge of the lubricating ability of exoge­
nous HA indicates the weak attachment of HA on the
sheaths that form a closed compartment that contains
synovial fluid for lubrication and nutrition. In extrasy­
novial tendons, such as the peroneus longus (PL)
tendon, there is a peritendinous sheet of loose fibrillar
tissue, the paratenon, which functions as an elastic
sleeve, permitting limited movement of the tendon
against the surrounding tissue. The extrasynovial auto­
graft, intrasynovial allograft, and the repaired flexor
tendon are the accepted procedures in flexor tendon
surgery. The chemical surface modification of these
tendons is described later.
Extrasynovial Autograft
Tendon graft plays an important role in reconstruction
to restore finger function in the cases of severe flexor
tendon damage, adhesion formation, and primary
tenorrhaphy rupture. As the potential sources of intra­
synovial tendons available for use as tendon autografts
are limited, the most donor tendons, such as palmaris
longus tendon, plantaris tendon, and long extensor
tendon, come from extrasynovial tendon sources in
clinical settings. Extrasynovial tendons have rougher
surfaces than intrasynovial tendons.19,20 The coating of
paratenon on the surface of extrasynovial tendon is
extremely susceptible to damage as the tendon repeti­
tively glides against the pulley. Extrasynovial tendons
create higher friction against a pulley compared to intra­
synovial tendons, particularly after multiple repetitive
motion.20-22 Animal models have shown that extrasyno­
vial tendon grafts are associated with more adhesions
to the surrounding tissue than intrasynovial tendon
grafts.19,23,24 Therefore, outcomes of extrasynovial grafts
may be improved by keeping paratenon intact as well
as low friction of the grafts.
HA is a linear, unbranched polysaccharide with a
high molecular weight. It is composed of a repeating
Figure 42-1  The friction of FDP tendons treated with
control solution (Control), hyaluronidase (HAase),
phospholipase C (PLC), lipid solvent (LipSol), trypsin, and the
combination of lipid solvent and trypsin (LipSol-Try).
Control
HAase
PLC
LipSol
Trypsin
LipSol-
Try
Treatment
*
*
*
*
Friction (N)
0.15
0.12
0.09
0.06
0.03
0
Figure 42-2  The chemical structure of hyaluronic acid.
OH
OH
O
O
O
O
NH
O
n
O
HO
HO
OH
Figure 42-3  Chemical surface modification of
extrasynovial tendon with cd-HA. EDC is 1-ethyl-3-
(3-dimethylaminopropyl)carbodiimide.
Tendon
HA
EDC
Paratenon
HOOC
COOH
COOH
NH2
NH2
NH2
COOH
COOH
COOH
CONH
CONH
CONH
HOOC

e3
Chapter 42:  Chemical Modification of Tendon Gliding Surface
between the PL tendon treated with cd-gelatin and the
PL tendon treated with cd-HA–gelatin (p < 0.05), with
the latter group having a lower gliding resistance at
comparable cycles of simulated flexion/extension. At
the 500th cycle, the increase in gliding resistance of
the cd-HA–gelatin treated PL tendons was roughly 4
times that of the FDP tendon, compared to a 20-fold
difference for the saline treated PL tendon. The gliding
of the PL tendon treated with cd-HA–gelatin almost
approached that of the FDP tendon. The chemical mod­
ification of the surface of the PL tendon with cd-HA–
gelatin also significantly improved its resistance to
abrasion. After 500 flexion/extension cycles, the sur­face
of untreated PL tendons was roughened, and the col­
lagen fibers covering the PL tendon surface were twisted
into large strands. In contrast, the surface of the PL
tendon treated with cd-HA–gelatin was still smooth
after 500 cycles of repetitive motion, and the normal
collagen fibers on the PL tendon surface remained
intact, similar to the FDP tendon.
The formula of cd-HA–gelatin and the curing time
were further optimized to improve the surface gliding
of extrasynovial tendon grafts.28,29 cd-HA–gelatin with
1% HA, 10% gelatin, 1% EDC, and 1% NHS showed
the best improvement of gliding of extrasynovial tendon
grafts. Meanwhile, it was found the curing time could
be as short as 5 minutes for this formula of
cd-HA–gelatin.
In addition to HA, lubricin also is believed a lubri­
cant of tendon. Can lubricin improve the gliding of
extrasynovial tendon grafts by itself or a chemical
approach? A study compared the lubricating ability of
surface of the tendon. cd-HA, which is composed of
1% HA with 1% 1-ethyl-3-(3-dimethylaminopropyl)
carbodiimide hydrochloride (EDC) and 1% N-
hydroxysuccinimide (NHS), significantly decreased the
gliding resistance of the PL tendon compared with that
of normal PL tendon or the PL tendon treated with HA
only, at each corresponding cycle of repetitive motion.
This finding indicates the chemical modification
improves the attachment of HA and/or paratenon on
the surface of the PL tendon.
Although cd-HA improves the gliding of the PL
tendon, the gliding resistance decreased significantly
only in the first cycle of motion after the administration
and increased over 20 cycles of repetitive motion.
Gelatin, which serves as a carrier of HA and a cross-
linker and a cross-linker, was introduced to further
improve the gliding of the PL tendon. It was found that
all PL tendons treated with saline, 10% gelatin, or cd-HA
(1% HA, 0.25% EDC, and 0.25% NHS) showed similar
trends up to 500 cycles of repetitive motion22,27 (Figure
42-5). Over the first 200 cycles, the gliding resistance
increased linearly and then reached a plateau. There was
no significant difference in gliding resistance between
the saline-, gelatin-, and cd-HA–treated PL tendons for
any given number cycles of motion. For the PL tendon
treated with cd-gelatin (10% gelatin, 0.25% EDC, and
0.25% NHS) and cd-HA–gelatin (1% HA, 10% gelatin,
0.25% EDC, and 0.25% NHS), the gliding resistance
increased at a much more gradual rate over the 500
cycles. Beginning at 100 cycles of simulated flexion/
extension, the gliding resistance of tendons treated with
cd-HA–gelatin was significantly lower than that of the
saline-treated tendons. Starting at 200 cycles, the gliding
resistance of tendons treated with cd-gelatin was also
significantly lower than that of the saline-, gelatin-, and
cd-HA–treated PL tendons. Starting at 300 cycles, there
was also a significant difference in the gliding resistance
Figure 42-4  Gliding resistance of PL tendon treated with
saline, exogenous HA, or cd-HA over 100 cycles of repetitive
motion against pulley.
1.2
1
0.8
0.6
0.4
0.2
0
Normal
1
5
10
20
Cycles
50
100
Gliding resistance (N)
Saline
HA
cd-HA
Figure 42-5  Gliding resistance of FDP tendons and PL
tendons treated with saline, gelatin, cd-HA, cd-gelatin, or
cd-HA–gelatin at different cycles of simulated motion.
1.4
1.2
1
0.8
0.6
0.4
0.2
0
0
200
300
400
100
500
Cycles
Gliding resistance (N)
FDP
Saline
Gelatin
cd-HA
cd-gelatin
cd-HA-gelatin

e4
Chapter 42:  Chemical Modification of Tendon Gliding Surface
significantly lower than that of the saline-treated control
after 1000 cycles (Figure 42-7). The gliding resistance
in these treatment groups decreased within the first 50
cycles and then increased at a much more gradual rate
over the 1000 cycles, with the cd-HA–gelatin plus lubri­
cin group being most stable. The results indicate that
the chemical modification can be applied in a variety of
extrasynovial tendons.
HA, lubricin, and phospholipids exist in native syno­
vial fluid and also are found to play the role of tendon
lubrication. Instead of using purified HA and lubricin,
native synovial fluid may serve as a lubricating material
to improve the gliding of extrasynovial tendon. Canine
PL tendons were treated with either saline, 1% EDC/1%
NHS, cd-gelatin, synovial fluid, synovial fluid plus 1%
EDC/1% NHS, or cd-gelatin–synovial fluid. The gliding
resistance was measured for 1000 cycles of simulated
flexion/extension motion. Same as HA and lubricin
only, synovial fluid alone did not improve the gliding
of the tendon (Figure 42-8). The gliding resistance of
the tendons treated with synovial fluid plus 1% EDC/1%
NHS, cd-gelatin, or cd-gelatin–synovial fluid was signifi­
cantly lower than the control group after 1000 cycles of
tendon motion. The gliding resistance of the tendon
treated with cd-gelatin–synovial fluid was significantly
lower than that of the tendon either treated with syno­
vial fluid plus 1% EDC/1% NHS or cd-gelatin. No sig­
nificant difference was found in the gliding resistance
between first cycle and 1000 cycles for the gliding resis­
tance of the tendon treated with cd-gelatin–synovial
canine PL tendons that were treated with saline, bovine
lubricin (260 µg/mL), cd-gelatin (10% gelatin, 1% EDC,
and 1% NHS), cd-HA–gelatin (1% HA, 10% gelatin, 1%
EDC, and 1% NHS), or cd-gelatin plus lubricin (260 µg/
mL lubricin was applied after cd-gelatin treatment).30
There was no significant difference in the gliding resis­
tance between the tendons treated with saline solution
and those treated with lubricin alone or between the
tendons treated with cd-HA–gelatin and those treated
with cd-gelatin plus lubricin (Figure 42-6). However,
the gliding resistance of the tendons treated with
cd-gelatin plus lubricin was significantly lower than that
of the tendons treated with saline solution, lubricin
alone, or cd-gelatin alone. The results indicate that
lubricin does have an important effect on tendon lubri­
cation. Like HA, lubricin may preferentially adhere to
tendon surface pretreated with cd-gelatin and when so
fixed in place.
The gliding of the canine PL tendon can be improved
with the chemical treatment of cd-gelatin, cd-HA–
gelatin, and cd-gelatin plus lubricin. The feasibility of
these approaches was tested with human ipsilateral
palmaris longus tendon, an extrasynovial tendon often
used for tendon grafting clinically. Human palmaris
longus tendons were treated with either saline, cd-HA–
gelatin, cd-gelatin plus lubricin, or cd-HA–gelatin plus
lubricin. After treatment, tendon gliding resistance
was measured during up to 1000 cycles of simulated
flexion and extension motion.31 The gliding resistance
of the PL tendons in the cd-HA–gelatin, cd-gelatin plus
lubricin, and cd-HA–gelatin plus lubricin groups was
Figure 42-6  Gliding resistance of PL tendons treated with
saline, lubricin, cd-gelatin, cd-HA–gelatin, or cd-gelatin/
lubricin at different cycles of tendon motion.
1.2
1.0
0.8
0.6
0.4
0.2
0.0
0
400
600
800
200
1000
Cycles
Gliding resistance (N)
Saline
Lubricin
cd-gelatin
cd-HA-gelatin
cd-gelatin
+ lubricin
Figure 42-7  Gliding resistance of PL tendons treated with
saline, cd-HA–gelatin, cd-gelatin/lubricin, or cd-HA–gelatin/
lubricin at different cycles of tendon motion.
0.5
0.6
0.7
0.8
0.9
0.4
0.2
0.3
0.1
0.0
0
400
600
800
200
1000
Cycles
Saline
cd-HA-
gelatin
cd-
gelatin +
lubricin
cd-HA-
gelatin +
lubricin

e5
Chapter 42:  Chemical Modification of Tendon Gliding Surface
fluid. The results indicate that synovial fluid can be
applied by chemical approach to improve the gliding of
extrasynovial tendon.
Intrasynovial Allograft
Intrasynovial tendon autografts may have better out­
comes than extrasynovial autografts do. The autologous
intrasynovial tendons are rarely available for tendon
grafts. However, intrasynovial tendon allografts are
more available and can be potentially used as flexor
tendon graft. In order to reduce immunogenicity and to
facilitate storage, allografts may be subjected to repeti­
tive freeze/thaw cycles and lyophilization.32 We found
that frictional force of the flexor digitorum profundus
tendon, which was lyophilized and rehydrated in a
saline solution, was significantly increased in compari­
son with that of the normal FDP tendon (Figure 42-9).
With the surface modification of FDP tendon allograft
with cd-HA–gelatin (1% HA, 10% gelatin, 1% EDC,
“and 1% NHS), the frictional force of the lyophilized
FDP tendon was significantly decreased in comparison
with the untreated lyophilized tendon even after 1000
cycles of repetitive motion in vitro (see Figure 42-9).
The results indicate that tendon surface modification
Figure 42-8  Gliding resistance of PL tendons treated with saline, cd-HA–gelatin, cd-gelatin/lubricin, or cd-HA–gelatin/
lubricin at different cycles of tendon motion.
1.00
0.80
0.60
0.40
0.20
0.00
0
400
300
600
500
800
700
900
200
100
1000
Gliding times
Gliding resistance (N)
cd-SF-gelatin
cd-gelatin
Control
EDCNHS
cd-SF
SF
Figure 42-9  The gliding resistance for the groups of
normal tendons, untreated lyophilized tendons, and
lyophilized tendons treated with cd-HA–gelatin.
First cycle
† ‡
†
‡
1000 cycles
*
**
*
*
*
Cycle
Before
Lyophilized
After cd-HA
*, **; p <0.05
†, ‡; p <0.05
Friction (N)
0.6
0.5
0.4
0.3
0.2
0.1
0

e6
Chapter 42:  Chemical Modification of Tendon Gliding Surface
at much more gradual rate over the 1000 cycles (Figure
42-10). In these groups, the mean and peak gliding
resistance after 1000 cycles was still lower than the
initial gliding resistance before treatment, while the
gliding resistance in the saline control tendons increased
significantly over the 1000 cycles of testing. The repaired
tendons treated with cd-HA–gelatin plus lubricin had
the lowest gliding resistance comparing the tendons in
other three groups at same cycle of repetitive motion.
The surfaces of the repaired tendons appeared smooth
after 1000 cycles of tendon motion for the tendons
treated with cd-HA–gelatin, cd-gelatin plus lubricin,
and cd-HA–gelatin plus lubricin, while that of the saline
control appeared roughened. These results suggest that
tendon surface modification can improve tendon gliding
ability, with a trend suggesting that lubricin fixed on the
repaired tendon may provide additional improvement
over that provided by HA and gelatin alone.
EVALUATION OF CHEMICAL MODIFICATION
IN ANIMAL MODELS
The chemical surface modification succeeded in improv­
ing the gliding ability of extrasynovial tendon, intrasy­
novial tendon allograft, and the repaired flexor tendon
in vitro. It was also applied to improve digit function in
the canine models in vivo.42-45
with cd-HA–gelatin can improve the gliding ability of
lyophilized flexor tendons and therefore may improve
the utility of lyophilized tendon allografts as a tendon
graft substitute.
Flexor Tendon Primary Repair
With the development of surgical techniques and post­
operative controlled mobilization, the primary repair
after injury has been the mainstream in flexor tendon
surgery. Stronger repairs have been advocated to permit
early active mobilization and to reduce adhesion forma­
tion,33 but tendon adhesions and tendon repair rupture
remain a problem even with stronger repairs.34 The role
of friction as a source of adhesions has been investi­
gated. The data suggest that many strong repairs also
have higher friction35-37 and that this higher friction is
associated with poorer results in an animal model.38
The repair constantly increases the gliding resistance
of the flexor tendon.39 A number of suture techniques
were investigated to repair FDP tendon.35-37 The modi­
fied Kessler and modified Pennington techniques are
satisfied with relatively high breaking strength and low
gliding resistance. However, gliding resistance of the
FDP tendon repaired with these two techniques is sig­
nificantly higher than the intact FDP tendon.
The effects of chemical surface modification on
gliding and repair integrity were investigated during
simulated repetitive motion of a repaired tendon in
vitro.40 The gliding resistance between the FDP and the
proximal pulley was measured before laceration. After
the repair with modified Kessler technique, the tendons
were treated with saline, 1% HA, or cd-HA–gelatin (1%
HA, 10% gelatin, 0.25% EDC, and 0.25% NHS). Then
the gliding resistance of the tendons was measured up
to 500 cycles of repetitive motion. The results showed,
from the first cycle to the 10th cycle, no significant dif­
ferences in gliding resistance between the three testing
groups. From the 50th cycle onward, the friction was
significantly lower in the cd-HA–gelatin group than
in the control group. Neither breaking strength, nor
tendon stiffness, nor resistance or gap formation of the
repairs, was significantly different with the treatment of
cd-HA–gelatin.
The effects of lubricin chemical modification on the
gliding of repaired FDP tendons were also investigated
in vitro.41 Canine FDP tendons were completely lacer­
ated, repaired with a modified Pennington technique,
and treated with one of the following solutions: saline,
cd-HA–gelatin (1% HA, 10% gelatin, 1% EDC, and 1%
NHS), cd-gelatin plus lubricin (260 µg/mL), or cd-HA–
gelatin plus lubricin. After treatment, the gliding resis­
tance was measured up to 1000 cycles of simulated
flexion/extension motion. The gliding resistance of the
repaired FDP tendons in the cd-HA–gelatin, cd-gelatin
plus lubricin, and cd-HA–gelatin plus lubricin groups
decreased within the first 50 cycles and then increased
Figure 42-10  Increase in average gliding resistance of
repaired FDP tendon in the four treatment groups at
different cycles of tendon motion.
0.40
0.30
0.20
0.10
–0.30
–0.20
–0.10
0.00
0
400
600
800
200
1000
Gliding cycles
Increase in average gliding resistance (N)
Saline
cd-gelatin
+ Lubricin
cd-HA-gelatin
cd-HA-gelatin
+ lubricin

e7
Chapter 42:  Chemical Modification of Tendon Gliding Surface
of flexion of the allografts treated with cd-HA–gelatin
were significantly less than those in the saline-solution
control group (Figure 42-12). This study indicates the
chemical modification with cd-HA–gelatin can improve
the digital function in flexor tendon allograft model
in vivo.
cd-HA–Gelatin: Extrasynovial
Tendon Autograft
The canine PL tendons were harvested and transplanted
to replace the FDP tendons in the second and fifth digits
of one forepaw.42,43 Prior to grafting, one of the PL
tendons was coated with cd-HA–gelatin (1% HA, 10%
gelatin, 0.25% EDC, and 0.25% NHS), while the other
was immersed in saline solution only. Adhesion and
digital normalized work of flexion were evaluated
after surgery at 1, 3, and 6 weeks. The adhesion score
of cd-HA–gelatin treated tendons was significantly
less than the saline treated tendons at all time points
(p < 0.05) (Table 42-1). All saline-treated graft digits at
6 weeks had severe adhesions at both the pulley and
tendon bed, including the entire zone 2 area. The adhe­
sion score at 1 week in both groups was significantly less
than at 3 and 6 weeks in their respective groups (treated
or control), with no significant difference between the
3- and 6-week results. In consistence with adhesion
score, the normalized work of flexion of the tendons
treated with cd-HA was significantly lower than that of
the saline-solution-treated controls at each time point
(Figure 42-11). In addition, the gliding resistance of the
cd-HA group was significantly lower than that of the
saline-solution group at 3 and 6 weeks. The chemical
surface modification of an extrasynovial tendon auto­
graft with cd-HA–gelatin decreases adhesion formation
and improves the digital function in flexor tendon auto­
graft model in vivo.
cd-HA–Gelatin: Intrasynovial
Tendon Allograft
A primary repair failure model was first created by lac­
erating and repairing the FDP tendons in zone 2 from
the second and fifth digits of dogs.44 The dogs were
allowed free active motion postoperatively. Six weeks
later, the tendons were reconstructed with use of FDP
allografts. In each dog, one allograft was treated with
cd-HA–gelatin (1% HA, 10% gelatin, 1% EDC, and 1%
NHS) and the other was treated with saline solution, as
a control. The dogs were restricted from free active
motion, but daily therapy was performed beginning on
postoperative day 5 and continued until 6 weeks after
the operation. The gliding resistance and mean work
Figure 42-11  The gliding resistance (A) and normalized
work (B) of flexion in the normal, cd-HA–gelatin–treated,
and saline-solution–treated groups at 1, 3, and 6 weeks. A
difference in symbols denotes a significant difference
between values (p < 0.05), with the triangle being
significantly less than the circle.
1-week
A
3-week
Normal
cd-HA
Saline
GLIDING RESISTANCE OF TENDON GRAFT
6-week
Resistance (N)
0.6
0.5
0.4
0.3
0.2
0.1
0
1-week
B
3-week
Normal
cd-HA
Saline
NORMALIZED WORK OF FLEXION (nWOF)
6-week
nWOF (N-mm/degree)
7
6
5
4
3
2
1
0
Table 42-1  Adhesion Scores in Extrasynovial Tendon Autografts
1 W
3 W
6 W
Adhesion Score
Saline
Modified
Saline
Modified
Saline
Modified
0
1
7
0
1
0
0
1
2
1
0
5
0
5
2
5
0
2
2
0
2
3
0
0
6
0
8
1

e8
Chapter 42:  Chemical Modification of Tendon Gliding Surface
((260 µg/mL). Passive synergistic motion therapy was
started on the fifth postoperative day and continued
until the dogs were killed on day 10, day 21, or day 42.
The prevalence of severe adhesions was decreased in the
tendon treated with cd-HA–gelatin plus lubricin (Table
42-2). The normalized work of flexion of the repaired
tendons treated with cd-HA–gelatin plus lubricin was
significantly lower than that of the nontreated repaired
tendons at all time points (Figure 42-13). The results
indicate treatment with cd-HA–gelatin plus lubricin
appears to be an effective means of decreasing postop­
erative adhesions after flexor tendon repair.
SUMMARY
Flexor tendon injuries are a frequent clinical problem.
Restoration of tendon function after flexor tendon lac­
eration especially in zones 1 and 2 has been difficult.
The introduction of chemical surface modification and
the development of carbodiimide-derivatized gelatin
cd-HA–Gelatin/Lubricin: Tendon Repair
In this study, dogs were randomly assigned to either a
chemical treatment group or an untreated control
group.45 The second and fifth FDP tendons from each
dog were lacerated fully at the zone 2 area and then
repaired. Following repair, the tendons in the chemical
treatment group were treated with cd-HA–gelatin (1%
HA, 10% gelatin, 1% EDC, and 1% NHS) plus lubricin
Figure 42-12  The gliding resistance (A) and normalized
work (B) of flexion in the normal, cd-HA–gelatin–treated,
and saline-solution-treated groups at 10, 21, and 42 days.
CHG, cd-HA-gelatin.
Normal
n = 18
*
*
n = 8
n = 10
A
CHG
GLIDING RESISTANCE
Saline
Force (N)
0.5
0.4
0.3
0.2
0.1
0
Normal
n = 18
*
*
n = 8
n = 10
B
CHG
NORMALIZED WORK OF FLEXION
Saline
nWOF (N-mm/degree)
1.6
1.4
1.2
1
0.8
0.6
0.4
0.2
0
Figure 42-13  The work of flexion normalized by the
proximal interphalangeal and distal interphalangeal angle
(nWOF) of repaired FDP tendons with or without cd-HA-
gelatin plus lubricin (CHL) treatment and of the normal,
contralateral digit at days 10, 21, and 42.
D-10
D-21
D-42
*
*
*
*
*
*
*
*
*
*
*
*
*
*
*
Normal FDP
CHL
Repair-control
nWOF (N-mm/degree)
5
4
3
2
1
0
Table 42-2  Adhesion Scores in the Repaired FDP Tendon
10 Day
21 Day
42 Day
Adhesion Score
Saline
Modified
Saline
Modified
Saline
Modified
0
10
11
9
12
5
9
1
3
5
3
0
4
3
2
4
0
2
2
4
3
3
1
0
3
1
7
2

e9
Chapter 42:  Chemical Modification of Tendon Gliding Surface
digital function after flexor tendon autograft, allograft,
and direct end-to-end tendon repair in vivo. Chemical
surface modification with cd-HA–gelatin derivatives is
likely able to provide hand surgeons a new and useful
method to improve the quality of flexor tendon surgery.
incorporation of HA and lubricin successfully improved
the gliding ability of the extrasynovial tendon, intrasy­
novial tendon allograft, and the repaired flexor tendon
in vitro. The methods of chemical surface modification
also reduced adhesion formation and improved the
References
1. Uchiyama S, Coert JH, Berglund L, et al: Method for the
measurement of friction between tendon and pulley, J Orthop
Res 13:83–89, 1995.
2. Hills BA, Monds MK: Enzymatic identification of the load-
bearing boundary lubricant in the joint, Br J Rheum 37:137–
142, 1998.
3. Jay GD, Haberstroh K, Cha CJ: Comparison of the boundary-
lubricating ability of bovine synovial fluid, lubricin, and
Healon, J Biomed Mater Res 40:414–418, 1998.
4. Swann DA, Silver FH, Slayter HS, et al: The molecular
structure and lubricating activity of lubricin isolated from
bovine and human synovial fluids, Biochem J 225:195–201,
1985.
5. Jay GD: Characterization of a bovine synovial fluid lubricat­
ing factor. I. Chemical, surface activity and lubricating prop­
erties, Connect Tissue Res 28:71–88, 1992.
6. Schumacher BL, Block JA, Schmid TM, et al: A novel proteo­
glycan synthesized and secreted by chondrocytes of the super­
ficial zone of articular cartilage, Arch Biochem Biophys 311:
144–152, 1994.
7. Swann DA, Slayter HS, Silver FH: The molecular structure of
lubricating glycoprotein-I, the boundary lubricant for articu­
lar cartilage, J Biol Chem 256:5921–5925, 1981.
8. Hills BA: Oligolamellar lubrication of joints by surface active
phospholipid, J Rheumatol 16:82–91, 1989.
9. Hills BA: Surface-active phospholipid: a Pandora’s box of
clinical applications. Part II. Barrier and lubricting properties,
Inter Med J 32:242–251, 2002.
10. Uchiyama S, Amadio PC, Ishikawa J, et al: Boundary lubrica­
tion between the tendon and the pulley in the finger, J Bone
Joint Surg (Am) 79:213–218, 1997.
11. Rees SG, Davies JR, Tudor D, et al: Immunolocalisation and
expression of proteoglycan 4 (cartilage superficial zone pro­
teoglycan) in tendon, Matrix Biol 21:593–602, 2002.
12. Sun Y, Berger EJ, Zhao C, et al: Expression and mapping of
lubricin in canine flexor tendon, J Orthop Res 24:1861–1868,
2006.
13. Sun Y, Chen MY, Zhao C, et al: The effect of hyaluronidase,
phospholipase, lipid solvent and trypsin on the lubrication
of canine flexor digitorum profundus tendon, J Orthop Res
26:1225–1229, 2008.
14. Moreau H, Pieroni G, Jolivet-Reynaud C, et al: A new kinetic
approach for studying phospholipase C (Clostridium perfrin­
gens alfa toxin) activity on phospholipid monolayers, Bio­
chemistry 27:2319–2323, 1988.
15. Okuda Y, Gorski JP, An KN, et al: Biochemical, histological,
and biomechanical analyses of canine tendon, J Orthop Res
5:60–68, 1987.
16. Cohen MJ, Kaplan L: Histology and ultrastructure of the
human flexor tendon sheath, J Hand Surg (Am) 12:25–29,
1987.
17. Jozsa LG, Kannus P: Human tendons: anatomy, physiology and
pathology, Champaign, IL, 1997, Human Kinetics, pp 46–51.
18. Kannus P: Structure of the tendon connective tissue, Scand J
Med Sci Sports 10:312–320, 2000.
19. Seiler JG 3rd, Chu CR, Amiel D, et al: The Marshall R. Urist
Young Investigator Award. Autogenous flexor tendon grafts.
Biologic mechanisms for incorporation, Clin Ortho Relat Res
345:239–247, 1997.
20. Uchiyama S, Amadio PC, Coert JH, et al: Gliding resistance
of extrasynovial and intrasynovial tendons through the A2
pulley, J Bone Joint Surg (Am) 79:219–224, 1997.
21. Momose T, Amadio PC, Zobitz ME, et al: Effect of paratenon
and repetitive motion on the gliding resistance of tendon of
extrasynovial origin, Clin Anat 15:199–205, 2002.
22. Sun YL, Zhao C, An KN, et al: Biomimetic modification of
gliding surface of extrasynovial tendon, J Mater Res 21:2079–
2083, 2006.
23. Gelberman RH, Seiler JG 3rd, Rosenberg AE, et al: Intercalary
flexor tendon grafts: a morphological study of intrasynovial
and extrasynovial donor tendons, Scand J Plast Reconstr Surg
Hand Surg 26:257–264, 1992.
24. Seiler JG, Uchiyama S, Ellis F, et al: Reconstruction of the flexor
pulley. The effect of the tension and source of the graft in an
in vitro dog model, J Bone Joint Surg (Am) 80:699–703, 1998.
25. Lapcik L Jr, Lapcik L, De Smedt S, et al: Hyaluronan: prepara­
tion, structure, properties, and applications, Chem Rev 98:
2663–2684, 1998.
26. Momose T, Amadio PC, Sun YL, et al: Surface modification
of extrasynovial tendon by chemically modified hyaluronic
acid coating, J Biomed Mater Res 59:219–224, 2002.
27. Sun YL, Yang C, Amadio PC, et al: Reducing friction by chemi­
cally modifying the surface of extrasynovial tendon grafts,
J Ortho Res 22:984–989, 2004.
28. Tanaka T, Sun YL, Zhao C, et al: Optimization of surface
modifications of extrasynovial tendon to improve its gliding
ability in a canine model in vitro, J Orthop Res 24:1555–1561,
2006.
29. Tanaka T, Sun YL, Zhao C, et al: Effect of curing time and
concentration for a chemical treatment that improves surface
gliding for extrasynovial tendon grafts in vitro, J Biomed Mater
Res A 79:451–455, 2006.
30. Taguchi M, Sun YL, Zhao C, et al: Lubricin surface modifica­
tion improves extrasynovial tendon gliding in a canine model
in vitro, J Bone Joint Surg (Am) 90:129–135, 2008.
31. Taguchi M, Zhao C, Sun YL, et al: The effect of surface treat­
ment using hyaluronic acid and lubricin on the gliding resis­
tance of human extrasynovial tendons in vitro, J Hand Surg
(Am) 34:1276–1281, 2009.
32. Ikeda J, Zhao C, Sun YL, et al: Carbodiimide-derivatized hyal­
uronic acid surface modification of lyophilized flexor tendon:
A biomechanical study in a canine in vitro model, J Bone Joint
Surg (Am) 92:388–395, 2010.
33. Winters SC, Gelberman RH, Woo SL, et al: The effects of
multiple-strand suture methods on the strength and excur­
sion of repaired intrasynovial flexor tendons: A biomechani­
cal study in dogs, J Hand Surg (Am) 23:97–104, 1998.
34. Peck FH, Bucher CA, Watson JS, et al: A comparative study of
two methods of controlled mobilization of flexor tendon
repairs in zone 2, J Hand Surg (Br) 23:41–45, 1998.
35. Momose T, Amadio PC, Zhao C, et al: Suture techniques with
high breaking strength and low gliding resistance: Experi­
ments in the dog flexor digitorum profundus tendon, Acta
Orthop Scand 72:635–641, 2001.

e10
Chapter 42:  Chemical Modification of Tendon Gliding Surface
36. Zhao C, Amadio PC, Zobitz ME, et al: Gliding resistance after
repair of partially lacerated human flexor digitorum profun­
dus tendon in vitro, Clin Biomech (Bristol, Avon) 16:696–701,
2001.
37. Zhao C, Amadio PC, Zobitz ME, et al: Gliding characteristics
of tendon repair in canine flexor digtorum profundus
tendons, J Orthop Res 19:580–586, 2001.
38. Zhao C, Amadio PC, Momose T, et al: The effect of suture
technique on adhesion formation after flexor tendon repair
for partial lacerations in a canine model, J Trauma 51:917–
921, 2001.
39. Coert JH, Uchiyama S, Amadio PC, et al: Flexor tendon-
pulley interaction after tendon repair. A biomechanical study,
J Hand Surg (Br) 20:573–577, 1995.
40. Yang C, Amadio PC, Sun YL, et al: Tendon surface modifica­
tion by chemically modified HA coating after flexor digito­
rum profundus tendon repair, J Biomed Mater Res B Appl
Biomater 68:15–20, 2004.
41. Taguchi M, Sun YL, Zhao C, et al: Lubricin surface modifica­
tion improves tendon gliding after tendon repair in a canine
model in vitro, J Orthop Res 27:257–263, 2009.
42. Zhao C, Sun YL, Amadio PC, et al: Surface treatment of flexor
tendon autografts with carbodiimide-derivatized hyaluronic
Acid. An in vivo canine model, J Bone Joint Surg (Am) 88:
2181–2191, 2006.
43. Tanaka T, Zhao C, Sun YL, et al: The effect of carbodiimide-
derivatized hyaluronic acid and gelatin surface modification
on peroneus longus tendon graft in a short-term canine
model in vivo, J Hand Surg (Am) 32:876–881, 2007.
44. Zhao C, Sun YL, Ikeda J, et al: Improvement of flexor tendon
reconstruction with carbodiimide-derivatized hyaluronic acid
and gelatin-modified intrasynovial allografts, J Bone Joint Surg
(Am) 92:2817–2828, 2010.
45. Zhao C, Sun YL, Kirk RL, et al: Effects of a lubricin-containing
compound on the results of flexor tendon repair in a canine
model in vivo, J Bone Joint Surg (Am) 92:1453–1461, 2010.

e11
CHAPTER
43 
TENDON GLIDING: THE ROLE
AND MECHANICAL BEHAVIOR
OF CONNECTIVE TISSUES
Jean Claude Guimberteau, MD
hypodermis, the vessels, the aponeurosis, and the
muscles. Present everywhere are structures that allow
sliding to take place.
We present a view of physiology of tendon sliding in
human tissues, based on microanatomical observations
that we made with the aid of video recording and analy­
sis. We present new hypotheses concerning the organi­
zation of these subcutaneous tissues.
MATERIALS AND METHODS
In Vitro Study of the Paratenon
This study was carried out on 30 human upper limb
biopsies of flexor digitorum superficialis (FDS) and pro­
fundus (FDP) with their surrounding sheaths, and 26
animal samples including the flexor carpi radialis from
cattle where the organization is very similar to that of
the human flexor profundus (Figure 43-2).
The preparation was treated with potassium bichro­
mate, placed in formalin, and finally in caustic soda,
allowing for a softer and more complete hydrolysis
(Prof. J. P. Delage, INSERM Laboratories, Bordeaux,
France). It was then frozen and freeze-dried under stan­
dard conditions for dehydration. Afterward, it was dis­
sected under a binocular loupe at ×3.5 magnification.
Samples were taken, given a gold-metallic finish, and
then observed under the electron microscope. The
INSERM Laboratories (Prof. Herbage, Lyon, France)
helped us to analyze the chemical components of this
connective tissue.
In Vivo Study of Digital Zones 3, 4, and 5 by
Microanatomical Video Endoscopic
Observation
The tendon gliding system was observed and recorded
on video in 65 cases of tendon revascularization in
Kleinert’s zones 3, 4, and 5 after releasing the
tourniquet.
All of the patients gave their consent before surgery.
Of the 65 cases, 57 procedures were forearm island
reverse flaps. The remaining eight procedures were
OUTLINE
The work and experiments of the author and his col­
leagues, including surgeons, histophysiologists, and
biomechanical engineers, have convinced them that
current understanding about tendon physiology is to
be moved ahead. After carrying out in vivo dissections
and video-recording of the tissues existing between
the skin and tendons in carpal tunnel and forearm
areas, the author and his colleagues questioned some
basic mechanics of the tendon sliding. This chapter
presents a new approach of morphological studies,
and the author attempts to explain the existence of the
multimicrovacuolar collagenous dynamic absorbing
system. This system enables easy and extensive sliding
of the tendons without interference from surrounding
tissues, facilitating tissue interdependence. The multi­
microvacuolar collagenous dynamic absorbing system,
which initially seems chaotic and complex, is based
on the vacuolar concept, which is found in many parts
of the human body, and is structurally composed of
multiple interconnected fibrous tissues organized to
facilitate functional adaptation of the tendon during
movement.
For many years, the scientific explanations concerning
the natural mechanism of flexor tendon mobility in the
fingers were limited to the notion of a virtual space or
the existence of loose connective tissue organized in
layers, but the biomechanical foundations for these
theories were vague.1-3
The biomechanical characteristics and histological
findings of the structures around the tendons are some­
times confusing, and the roles and the definitions of the
paratenon, mesotendon, peritendon, and sheaths and
have largely varied among authors and their described
surgical procedures4-9 (Figure 43-1).
When surgical dissection is performed in vivo, visual
magnification demonstrates the presence of a varied
arrangement of tissue connections; a histological con­
tinuum with no clear separation between the skin, the
This chapter does not appear in the print edition.

e12
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
It is also clear from observing the behavior of the
vessels of the common carpal sheath after revasculariza­
tion and during flexion and extension, that there is
apparent disorder and irregularity of shape of the micro­
vascular network. There are surprisingly complex forms
of vascular distribution, a finesse to the microvascular
network, which is much more complex than a simplistic
mechanistic distribution.10-14
When we observed the area around the tendon, we
noted an apparently circular longitudinal and periph­
eral vascularization, which seemed to represent a real
continuity between the sheath and the tendon, and
which was not interrupted despite the excursion and
distension occurring during sliding and subsequent
return to the original position.
At first sight, this is not incompatible with classical
anatomical descriptions.
Ten-Fold Microscopic Examination
However, during flexion and extension of the tendon,
tenfold microscopic examination of zones 3, 4, and 5
enabled us to observe vascular patterns in different
planes of excursion and with different speeds of vessel
progression due to modifications in the capillary
network and depending on variations in tendon
movements (Figure 43-3). Small vessels are subjected
to deformation during movement but do not follow
any logical or rational sequence. Some vessels pro-
gress quickly, while others move more slowly, and
some overtake other vessels. The diameter of the vessel
seems to be of no importance in this process. There
is dynamic progression with no apparent order or
proportionality.
Very little research has been done to study this
mechanical phenomenon, since the issue was consid­
ered by many to have been solved by the concept of a
virtual space (i.e., the tendon slides in the carpal sheath
like a bullet in a gun barrel without touching the sides,
or rather, it slides in membranous or visceral layers or
by stratification of different coaxial layers).
In vivo observation has rendered this concept unac­
ceptable partly because it is surgically impossible to
define a clear field of dissection between the paratenon
and the tendon (Figure 43-4).
At 10-fold microscopic examination (Figure 43-5),
video observation at rest showed an inaccessible micro­
anatomical arrangement, a tissue-continuity, and a gel-
like tissue surrounding the tendon. We saw a glossy
structure stretching across the tendon. Within this
tissue, collagen fibers can be seen framing the vessels
in a random fashion. We were confronted with the
notion of global dynamics and continuous matter
between the tendon and the surrounding tissue, radi­
cally opposing the classical descriptions of sliding struc­
tures based on the notion of tissue stratification and
a virtual space between the tissue layers. Instead, we
axillary flaps. Static and dynamic observations were
carried out using an endoscope with an attached camera
Tri CCD-HD-Image 1 22220055 Karl Storz endoscopy
fiber optic camera and Xenon Nova 201315 light source
at ×25 magnification.
Continuous sequences were captured on video during
flexion of the digital flexors to allow for subsequent
analysis.
RESULTS
In Vivo Observations
Macroscopic Observations
When the flexor tendon moves, its movement is barely
discernible in the palm. There is no dynamic repercus­
sion of the movement on the skin surface. However, the
flexor tendon excursion is at least 2 cm, without any
hindrance and without displacing any of the neighbor­
ing tissues in the palmar area or along the common
carpal sheath.
This suggests the existence of some sort of shock-
absorbing system.
Figure 43-1  When the tendon moves, the movement is
barely discernible. There is an absorbing system surrounding
the tendon. The capillary network around the tendon
changes as the tendon moves. Vascular network observed
during flexion (A), and during extension (B).
A
B

e13
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-2  MVCAS shown under electron microscope. A, The flexor carpi radialis of cattle was harvested for observation.
B, Preparation frozen-dried samples. C, Appearance of the sliding structure, MVCAS, under the electron microscope (×5).
D, Findings under a higher power magnification. Tissues surrounding the tendon are made of microvacuoles (×25).
A
B
C
D

e14
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
found total histological continuity. It therefore became
necessary to investigate this tissue further in order to
gain better knowledge of its properties and its different
roles.
At 25-Fold Magnification
At 25-fold magnification, this glossy system consists of
loose connective tissue situated between the tendon and
its neighboring tissue, and is composed of intertwining
multidirectional filaments creating partitions that form
a new type of vacuole: three-dimensional, structured
microvacuolar volumes (Figure 43-6). Apart from some
adipocytes and fibroblasts, there are few cells in this
multifibrillar network.
We called it the MultimicroVacuolar Collagenous
dynamic Absorbing System (MVCAS), to emphasize its
functional and architectural impact.15-17
This tissue network is a continuous structure com­
posed of billions of microvacuolar components that
must be considered as a three-dimensional network.
The basic component of this sliding framework is the
microvacuole.
The microvacuoles measure from a few microns to a
few hundred microns and are organized in a dispersed
branching fractal pattern. They have a pseudo-geometric
shape forming a basic polyhedron.
A microvacuole can be considered as a microvolume
(Figure 43-7); however, the organization differs accord­
ing to dynamic role—The greater the distance that the
structure must travel, the smaller and denser are the
vacuoles; when stimulated, the structures can move
freely without anything else moving around them; and
under physical constraints, the structure is resistant,
adapting, and yet able to maintain shape. Its apparent
major role is to ensure the dynamics of movement and
absorb the shocks that this creates. The structure also
has a memory, so it returns to its initial position, pre­
serving its form and volume. Slight traction on this
microvacuolar system reveals mini air explosions that
prove the existence of a tissular pressure, which is dif­
ferent from atmospheric pressure.
As well as providing efficient movement, shape, form,
and filling space, this microvacuolar tissue plays two
other essential roles18 (Figures 43-8 and 43-9).
As an essential structural element, fibrils serve as a sup­
porting frame for the network of the blood supply,
which accounts for the huge variety of blood supply
shapes. This frame constitutes the continuum of tissues
between the mobile tendon and the neighboring tissues,
ensuring the collagenous, vascular, lymphatic, and
nervous continuity between the tendon, epitenon, and
paratenon. Tissue continuum is total.
As a biomechanical and dynamic system, it has a
mixed role of combined transmission and absorption
of the stress. Thanks to this dynamical behavior, the
microvacuolar system permits the transmission and
Figure 43-3  A, Cold light variable magnification
endoscope and 3 CCD camera. B, Intriguing vascular
patterns that change in the capillary network depending
on the direction of tendon movements during flexion and
extension. C, Vessels are not all going at the same speed
and are in different planes.
A
B
C
1
3
3
2
2
4
4
1

Figure 43-4  A, Traction on the paratendon during surgery. B, Searching for a space over the tendon surface. C, Network
between the tendon and the surrounding tissues: the MVCAS. D, The movable, elastic sliding tissues, MVCAS.
A
B
C
D
Figure 43-5  A, Peritendinous sliding system. B, Tissue continuity between tendon and microvacuolar distribution. C, 3D
MicroVacuola. D, Apparent fibrillar distribution in the dispersed branching pattern.
A
B
C
D

Figure 43-6  A, Fibrils composed of collagen and elastin
delimit the microvacuoles. B, Magnification MVCAS under
the electron microscope. C, A microvacuola with a hexagonal
shape. D, Diagram of the basic building brick of the MVCAS:
the microvacuola filled with GAG and the frame contains
collagen types I, III, and IV.
A
B
Collagen I
Collagen I
Collagen I
Collagen VI
Network of glycolicans
Polysaccharides, hyaluronan
Network of glycolicans
Network of glycolicans
Collagen I
C
D
Figure 43-7  A, Diagrams showing the microvacuoles
inside the MVCAS. B, Real microvacuole with a hexagonal
shape at the beginning of dissection. C, Microvacuole
hyperpressure after atmospheric pression exposure filled
with GAG and the collagen type I, III, and IV framework.
A
B
C

e17
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-8  Collagen frameworks along with fibrils provide
support and nutrition.
Figure 43-9  Chaotic dynamic system showing a tendency
of pseudo-geometric arrangement.
absorption of the constraint across the tissue while at
the same time the surrounding tissues are not affected.
During progressive traction (2 N/cm2) (Figure 43-10),
the fibers rearrange themselves in response to the local
stress. As the stress increases, the fibers become more
aligned in the direction of the stress. All of the compo­
nent parts then turn so as to be oriented as much as
possible in the direction of the applied force. However,
this set of movements is difficult to analyze, so certain
fibers have to be selected for analysis on an arbitrary
basis. We therefore stained some fibers yellow and
observed their behavior.
Other internal factors need also be taken into account:
The fibrillar struts behave in a very peculiar manner.
First, in response to stretching a fibril becomes longer
by resembling a wormlike chain or a spring, which
means that it is capable of molecular rearrangement and
can recover its initial form by returning to its initial
position (Figure 43-11). This mechanism seems to be
involved in minor forms of tension.
Second, the fibers undergoing mechanical stimula­
tion can divide in space into several other fibrils, which
enables an immediate dispersion and distribution of
the forces across the tissue space (Figure 43-12).
Third, the fibers are able to glide past each other
around a mobile focal point along the entire length of
both fibers (Figure 43-13). Because classic linear models
based on straight lines cannot account for these move­
ments, we are required to use fractal and nonlinear
mathematics to explain them.
These three dynamic abilities always coexist, which
allows the structure to move in three-dimensional space
and to respond optimally no matter what direction in
which it is stretched (Figure 43-14).

e18
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-10  A 200-fold magnification of fibrillary movements during traction. Time span between photographs A and F is
2 seconds. Diameter of fibrils = 10 µm. Two-dimensional analysis of what actually occurs in three dimensions. The fibrils
become oriented in the direction of traction but in a less-organized manner than the rules of linearity would have it.
A
B
C
D
E
F
Figure 43-11  Distention-retraction of a fiber.

e19
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-12  Division of a fiber into several fibrils that diffuse the stress three-dimensionally.
Figure 43-13  Fiber moves freely along axis of another fiber.

e20
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
incorporated into this network and are connected with
it on their superior and inferior aspects, thereby increas­
ing the shock-absorbing properties of the tissue and
allowing the structures to move interdependently.
Whether it is in the abdominal, thoracic, dorsal, or ante­
brachial regions or in the scalp, this tissue network is
omnipresent (Figure 43-17).
Indeed, there is no space within the body where it is
not found. This fibrillar tissue network surrounds even
structures subject to relatively little movement—such as
nerves and the periosteum—although in these cases,
there are differences in the network itself and in the size
of the vacuoles. Indeed, it would seem that the MVCAS
occurs everywhere in the body.
The notion of tissue continuity provided by the mul­
timicrovacuolar collagenic absorbing system, MVCAS.
All of our observations support this tissue continuity
and the microvacuolar and fibrillar architecture. In tra­
ditional observations of this tissue, the concept of
sliding was thought to be due to several coaxial con­
joined layers with progressively decreasing diameters
framing the vascular structures, or to a virtual space
between visceral and membranous layers.
The layer closest to the tendon would move the
fastest, while the one farther away would move more
slowly. This concept of annular layers sliding between
each other based on the theoretical concept of virtual
space and a hierarchical tissular distribution seems
to be incorrect (see Figure 43-5). For this reason, we
have developed the concept of a tissue continuum. This
concept supposes that there is an association between
the way tissues are organized and how they behave.
We have frequently observed glycosaminoglycan
(GAG) gel movements inside the fibers, the sliding
of drops along the fibrils, together with dilaceration,
absorption, and reconstitution. It is impossible to ignore
the role of GAG in response to traction (Figures 43-15
and 43-16).
In Vitro Observations
The sides of the intertwined microvacuoles are com­
posed of collagen fibers (75%, mostly type I, some type
III, IV, and VI collagens) and 20% elastin. Type I collagen
makes up 23% of the microvacuolar unit. Their diameter
ranges from a few to several dozen microns and they
vary in length, thus giving an overall disorganized
chaotic aspect. These microvacuoles contain a highly
hydrated proteoglycan gel (70%), which can change
shape during movement but whose volume remains
constant. Their lipid content (4%) is high. A major issue
in this system is the presence of water, which is omni­
present as soon as the skin is penetrated (Prof. Herbage,
INSERM Laboratories, Lyon, France). For this reason, no
biomechanical explanation for the sliding of subcutane­
ous structures can disregard the dynamics of the fluids
present (e.g., osmotic pressure and superficial tension).
DISCUSSION
This sliding tissue with its basic polyhedric shaped units
is to be found in every nook and cranny of our organ­
ism. The tissue, which used to be referred to as connec­
tive or areolar tissue, is totally continuous throughout
the fibers and their prolongations. Even the intermedi­
ary structures such as the deep premuscular fascia are
Figure 43-14  Variation of fibrillar movements in the three dimensions of space opens a lot of dynamical opportunities. The
chaotic, pseudo-geometric distribution of the structures in vivo and the different ways in which the fibrils behave require a
specific vision of the system.

e21
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
This sliding system and its multifibrillar organization
participating simultaneously in movement, restitution,
and the transfer of energy seem to be composed of ele­
ments developed from within this tissue rather than a
superposition of different tissues. We get the impression
of elements united to compose one sole tissue with
genuine continuity between the tendon, the sliding
tissue, and all surrounding tissues. The notion of layers
is replaced by a greater or lesser densification of the
MVCAS with a more or less specific cellularization. In
vivo observation has rendered the notion of tissue layers
unacceptable. This means that we need a new way of
thinking—a way of posing the problem in terms of
global dynamics and continuous matter and a theory
involving the concept of a tissue continuum. This is in
total contradiction with the traditional view of sliding
structures, tissue stratification, and virtual space between
tissue layers.
The microvacuole as the basic structural unit enables
the MCVAS to perform its function of filling space and
preserving form.19-23 This multimicrovacuolar collagenic
absorbing system is made of microvolumes and micro­
fibrils and is focused around the microvacuole, which
we can consider to be the basic framework unit. This
enables us to explain the very notion of form and the
fact that this form adapts to its environment but does
not change. We need to move to three dimensions to
really understand this.
It would seem that the existing polyhedron shape of
the microvacuole is the optimal shape for occupying
space with the most minimal arrangement. It is essential
to grasp that to fill space, living structures tend to adapt
geometrically simple forms such as polygons, spirals, or
cylinders.
By accumulation and superposition, these multimi­
crovacuolar polyhedric patterns under internal tension
will build an elaborate form. The concept of the micro­
vacuole explains the ability of the tissues to resist com­
pression and expansion while maintaining a stable
volume.
Efficient Dynamic Behavior
MVCAS is highly dynamic, and its components have
efficient dynamic behavior. Although the arrangement
of the structures is chaotic, with a dispersed pattern of
distribution, this flexible, polyhedric architecture is able
to assume many shapes, thereby providing stability and
efficient sliding.
We are now confronted with the dilemma of chaotic
architecture and optimal efficiency. Because of the exis­
tence of this sliding system, called the paratenon or
areolar or subsynovial connective tissue (SSCT)5 by
other investigators, the tendon displays optimal sliding
and can move smoothly and quickly without any hin­
drance and without disturbing anything around it,
It is important to highlight that, due to the dispersed
pattern of the fibrils and the cohesive nature of the
extracellular matrix, the sliding system forms a continu­
ous deformable framework performing three major
mechanical roles:
 Responding to any kind of mechanical stimulus in
a highly adaptable and energy-saving manner,
ensuring the complete movement of the tendon
 Preserving peripheral tissue stability, structures,
and shapes; providing information during action
and springing back to its original shape
 Ensuring the interdependence and autonomy of
the various functional units
Figure 43-15  Three-dimensional sketch showing potential
for interfibrillar movement involving the three dynamic
capacities of the system.

e22
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-16  The multimicrovacuolar system during peritendinous sliding.
Figure 43-17  The sliding system in different sites. A, Forearm subcutaneous area. B, Thoracic wall. C, Thigh region.
D, Abdominal wall.
A
B
C
D

e23
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
thus allowing the tendon to move freely without trans­
ferring the movement to the surrounding structures.
This accounts for the absence of any dynamic repercus­
sions of the movement on the skin surface.
The essential function of the network is to ensure its
own efficient movement. Every structure component in
this network must permit movement while at the same
time ensuring shock absorption, which is indispensable
to avoid rupture of the mechanical elements within
the network. The question of how the microvacuolar
network behaves as a shock absorber, including the fact
that the closest vacuole to the moving structure under­
goes maximal deformation while those farthest away
hardly change shape, remains to be explained. These
two apparently conflicting roles must also be accompa­
nied by the spring-back memory function. It appears to
be a very elastic system that accommodates tendon
movement but does not disrupt the stretched collagen
fibers within the normal range of motion of tendon
motion.
These highly flexible, stressed or loaded fibrils take
various shapes during tendon sliding and movement
of extremities. The changes of interlacing, intertwining
fibrillar structures are created by the repetition of move­
ments, including distention, retraction, and compres­
sion during extremity movement. The system seems to
function optimally dynamically. The fibril movement
is highly organized and nicely coordinated, without
abnormal force distribution within the system, and the
motion of the tendon and other tissues is smooth and
efficient.
Due to the natural arrangement of the fibrils in their
seemingly chaotic or dispersed pattern and due to the
hydrophilic nature of the GAG in the extracellular
matrix, the microvacuole (which is a microvolume) is
able to adapt, change form, and return to its original
form. The MVCAS therefore displays chaotic patterns
and multiadaptive efficiency.
A Global System
This internal multifibrillar and microvacuolar architec­
ture is too repetitive not to be taken into account. Seen
in these terms, the whole structure of the body may
be considered as an immense collagen network. Going
from the macroscopic to the limits of the microscopic,
this network can be seen to stretch continuously from
the peritendinous surface to the finest multimicro­
vacuolar organization, the ultimate boundary of the
mesosphere, before entering the realm of molecular
dynamics. The entire dynamic and structural continuum
may thus be explained and represented (Figure 43-18).
It may even be that this fundamental system obeys
dynamic and biomechanical principles that are subject
to influences other than gravity.
Anatomical Features
In order to transmit forces, this complex sliding system
must be resistant and able to adapt to environmental
and mechanical requirements. It must be able to con­
serve its mobility while maintaining its architecture and
adapting to the mechanical demands imposed on it. As
the function of different regions differ, its structures
therefore vary by anatomical sites according to changing
functional needs.
This type of microvacuolar sliding that we described
within a multimicrovacuolar framework has been seen
in zones 3, 4, and 5 of the flexor tendons. In the digital
fibrous sheath area, an efficient change in the subcuta­
neous tissue is observed. The digital sheath and the
sheath in the carpal tunnel area share some mechanical
characteristics, but each has its own specific morphologic
features and function.
CONCLUSION
The notion of virtual space between the sheath in the
carpal tunnel area and the flexor tendons or the absence
of any connecting tissue and especially vascular tissue
must be reconsidered. The vision described here has
resulted from anatomical observations performed on
fresh or formalin-treated cadavers. A different view of
the sliding system is therefore required. Based upon our
in vivo studies, a new sliding system can now be pro­
posed. The basic framework of this sliding tissue system
is the nonlinear, interconnecting, multimicrovacuolar
network, which seems chaotic and complex and yet
simultaneously shows graceful simplicity with one final
objective: to promote and facilitate sliding adaptation
and mobility. Future research in biology and chemistry
must examine the behavior of these basic structures,
which have long been neglected due to their apparently
self-evident nature.

e24
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
Figure 43-18  Progressive 50-fold enlargement of peritendinous area from the macroscopic to the pre-molecular conveys an
idea of the total tissue continuity of the sliding system with tendon. (Magnification: A, ×0; B, ×2, C, ×5, D, ×20, E, ×50.)
A
B
C
D
E

e25
Chapter 43:  Tendon Gliding: The Role and Mechanical Behavior of Connective Tissues
References
1. Potenza AD: Critical evaluation of flexor-tendon healing and
adhesion formation within artificial digital sheaths, J Bone
Joint Surg (Am) 45:1217–1233, 1963.
2. Lundborg G, Holm S, Myrhage R: The role of the synovial
fluid and tendon sheath for flexor tendon nutrition. An exper­
imental tracer study on diffusional pathways in dogs, Scand
J Plast Reconstr Surg 14:99–107, 1980.
3. Littler JW: Free tendon grafts in secondary flexor tendon
repair, Am J Surg 74:315–321, 1947.
4. Verdan CE: Half a century of flexor-tendon surgery. Current
status and changing philosophies, J Bone Joint Surg (Am)
54:472–491, 1972.
5. Strickland JW, Glogovac SV: Digital function following flexor
tendon repair in Zone II: a comparison of immobilization
and controlled passive motion techniques, J Hand Surg (Am)
5:537–543, 1980.
6. Strickland JW: Results of flexor tendon surgery in zone II,
Hand Clin 1:167–179, 1985.
7. Hunter JM: Tendon salvage and the active tendon implant: A
perspective, Hand Clin 1:181–186, 1985.
8. Paneva-Holevith E: Résultats du traitement des lésions mul­
tiples des tendons fléchisseurs des doigts par greffe effectuée
en deux temps, Rev Chir Orthop Reparatrice Appar Mot 58:481–
487, 1972.
9. Boyes JH: Flexor-tendon grafts in the fingers and thumb: An
evaluation of end results, J Bone Joint Surg (Am) 32:489–499,
1950.
10. Colville J, Callison JR, White WL: Role of mesotenon in
tendon blood supply, Plast Reconstr Surg 43:53–60, 1969.
11. Lundborg G, Myrhage R, Rydevik B: The vascularization of
human flexor tendons within the digital synovial sheath
region—structureal and functional aspects, J Hand Surg (Am)
2:417–427, 1977.
12. Schatzker J, Brånemark PI: Intravital observations on the
microvascular anatomy and microcirculation of the tendon,
Acta Orthop Scand Suppl 126:1–23, 1969.
13. Smith JW, Ellinger CG: La vascularisation des tendons. In
Tubiana IR, editor: Traité de la Chirurgie de la Main, Paris,
1986, Masson, pp 375–380.
14. Zbrodowski A: Vascularization of the flexor tendons in
the fingers, Chir Narzadow Ruchu Ortop Pol 39:265–270,
1974.
15. Guimberteau JC: Journey to the tendon and satellite sheath
areas. In vivo anatomical observations of flexor tendon vascu­
larization and surrounding sheaths. Brussels International
Symposium Tendon Lesions, Injuries and Repair: Genval-
Brussels; 1999.
16. Guimberteau JC: New Ideas in Hand Surgery; Island Vascular­
ized Flexor Tendon Transfers, the Sliding System, France, 2001,
Aquitaine Domaine Forestier, pp 210.
17. Guimberteau JC, Panconi B, Boileau R: Mesovascularized
island flexor tendon: new concepts and techniques for flexor
tendon salvage surgery, Plast Reconstr Surg 92:888–903, 1993.
18. Zhao C, Amadio PC, Zobitz ME, et al: Gliding characteristics
of tendon repair in canine flexor digitorum profundus
tendons, J Orthop Res 19:580–586, 2001.
19. Guimberteau JC, Bakhach J: Subcutaneous tissue function:
the multimicrovacuolar absorbing sliding system in hand and
plastic surgery. In Siemonov MZ, editor: Tissue Surgery. New
York, 2006, Springer, pp 41–54.
20. Guimberteau JC, Sentucq-Rigall J, Panconi B, et al; Introduc­
tion to the knowledge of subcutaneous sliding system in
humans, Ann Chir Plast Esthet 50:19–34, 2005.
21. Ingber DE: Cellular tensegrity: defining new rules of biologi­
cal design that govern the cytoskeleton, J Cell Sci 104:613–
627, 1993.
22. Levin SM: Continuous tension, discontinuous compression.
a model for biomechanical support of the body. Available at

23. Thompson D: On Growth and Form, Cambridge, 1992, Cam­
bridge University Press.