You are on page 1of 6


JHT Read for Credit Article #002

Recent Progress in Flexor Tendon Healing
The Modulation of Tendon Healing with Rehabilitation
Martin I. Boyer, MD
Charles A. Goldfarb, MD
Richard H. Gelberman, MD
Department of Orthopaedic Surgery
Orthopaedic Hand Surgery Service
Saint Louis, Missouri

In the 1960s, the first reports demonstrated that
flexor tendon lacerations within the confines of the
fibro-osseous flexor digital sheath could be repaired
primarily, and rehabilitation be carried out successfully, without excision of the lacerated tendons followed by primary tendon grafting.1,2 Major advances
in the understanding of intrasynovial flexor tendon
biology have been made since that time. The concept
of adhesion-free tendon healing has been validated
both in experimental and in clinical studies since that
time,3–6 lending support to efforts which attempt to
achieve a reliable technique of primary flexor tendon
repair and digital rehabilitation without the inevitable
need for later tenolysis because of ingrowth of restrictive adhesions from the surrounding sheath.
Despite advances in the repair and rehabilitation of
injured flexor tendons within the fibroosseous digital
sheath, the results, measured experimentally as
Correspondence and reprint requests to Martin I. Boyer, MD, MSc,
FRCS (C), Department of Orthopaedic Surgery, Orthopaedic Hand
Surgery Service, Suite 11300, West Pavilion, One Barnes
Hospital Plaza, Saint Louis, MO 63110; e-mail: <boyerm@msnotes.>.



ABSTRACT: Until recently, attempts to optimize the postoperative regimen following intrasynovial flexor tendon repair had been
essentially empirical, in that both the time and graduation of the
exercise regimen have lacked clear conceptual guidelines. The
magnitude of load applied in previous studies had not been clearly
controlled, and similarly, the effects of increased repair site
excursion and gap formation had not been evaluated in clinically
relevant models. Recent experimental in vivo data on the
application of force and excursion as independent variables by
the authors and other investigators have helped to clarify the
respective roles of these two variables. The goal of surgical
treatment of intrasynovial flexor tendon lacerations is the
achievement of a primary tendon repair of tensile strength
sufficient to allow early controlled motion after surgery. The
implementation of an appropriate postoperative rehabilitation
protocol will, based on the experimental data discussed in this
article, decrease the formation of intrasynovial adhesions, facilitate
the restoration of the gliding surface, and stimulate the accrual of
strength at the repair site.
J HAND THER. 2005;18:80–85.

tendon excursion and clinically as digital range of
motion, continue to be unpredictable. Historically,
several factors contributing to the formation of
adhesions (tendon suture, sheath injury, and postoperative immobilization) have been considered to
be unavoidable components of the injury and the
repair process.7 A number of scientific and prospective clinical studies have shown that it is possible to
obtain adhesion-free (so-called primary) tendon healing with the timely application of protected passive
motion rehabilitation.8–10 Duran et al.11,12 suggested
that as little as 3 mm intrasynovial excursion is
sufficient to prevent the formation of restrictive
adhesions and the firm adherence of the repaired
tendon within the digital sheath. Other investigators
have also demonstrated both experimentally and
clinically, that protected motion can effectively restore the tendon’s gliding surface, leading to improved repair site strength and excursion.13–17
There has been considerable concern, however,
about whether the early application of motion postoperatively would invariably lead to repair site
failure. In 1941, Mason and Allen18 described the
site of an immature tendon repair as a gelatinous
exudate between the two tendon stumps that, between five and nine days after repair, underwent

considerable softening and loss of tensile strength. In
1960, Lindsay et al.19 explored the causes of gap
formation at the intrasynovial repair site in chickens.
Inadequate immobilization was associated with increased adhesion formation and increased tendon
callus size, and was thought to be a major cause of
significant repair site elongation. Ketchum et al.20,21
observed that gaps as small as 1 mm were associated
with increased formation of adhesions, and were
detrimental to tendon function. Seradge22 concurred,
demonstrating that the formation of repair site gaps
correlated directly with poor clinical outcomes. To
minimize the formation of repair site gaps, Lindsay
et al. advocated increasing the length of immobilization—a concept supported clinically by Potenza,
Peacock, and others.23–26 Invocations that the application of ‘‘excessive’’ stress to an immature repair site
would lead to gap formation and poor clinical results
created a formidable challenge for those seeking to
improve the rehabilitation of these injuries.
Realizing that the greater the rehabilitation force
applied to the repair site, the greater the risk of gap
formation and repair site failure, modern suture
techniques that attempt to improve the time-zero
(time of tendon repair) and early postoperative biomechanical characteristics of the repair site have been
developed.27–32 These suture techniques demonstrate
improved time-zero tensile properties, and have
shown in experimental studies to minimize the
formation of repair site gaps and adhesions. Ex vivo
and in vivo investigations in linear, in situ, and other
models have suggested that core suture configurations with the greatest tensile strength are those in
which there are multiple sites of tendon suture
interaction. Although the Kessler1,33 or modified
Kessler techniques still enjoy widespread acceptance,
newer techniques such as Tajima,34 Strickland,35–37
Cruciate,38 Becker,39 and Savage30 configurations all
offer greater suture hold on the tendon that is independent of the suture knot. These modern methods
of core suture technique have been shown to offer
not only greater time-zero repair site tensile strength,
but also improved strength up to and including
six weeks postoperatively.28
Although substantial advances had been made in
core suture technique, attempts to optimize the postoperative regimen following intrasynovial flexor
tendon repair had been essentially empirical, in that
both the time and graduation of the exercise regimen
have lacked clear conceptual guidelines. The magnitude of load applied in previous studies had not
been clearly controlled, and similarly, the effects of
increased repair site excursion and gap formation
have not been evaluated in clinically relevant
The goal of the surgical treatment of intrasynovial
flexor tendon lacerations is the achievement of
a primary tendon repair of tensile strength sufficient

to allow the application of a postoperative motion
rehabilitation protocol to inhibit the formation of
intrasynovial adhesions, facilitate restoration of the
gliding surface, and stimulate the accrual of strength
at the repair site.

Over the past 50 years, details about the response
of fibroblasts to mechanical load have been provided.15,40–44 Becker et al.45 applied static loads to
chicken tendons in vitro and noted increased fibroblast migration, increased collagen deposition, and
improved alignment of cells along the axis of applied
tension compared to unloaded controls. Slack et al.43
cultured digital flexor tendons on an apparatus
designed to apply controlled mechanical loads. They
noted an increase in synthetic capability, with higher
levels of DNA, protein, and glycosaminoglycans in
tendons loaded for 48 to 72 hours. Almekinders et al.46
designed an in vitro model to study the effects of
repetitive motion on human fibroblasts. Cells that
underwent cyclic deformation showed significantly
increased levels of prostaglandin E2 production. Mass
et al.42 studied the effects of constant mechanical load
on rabbit flexor tendon in vitro. The tendons showed
increased strength by three weeks (during scar
maturation), confirming the ability to heal through
intrinsic mechanisms independent of adhesion formation. Importantly, the investigators noted greater
extensibility in unloaded tendons and surmised that
the effect resulted from a more random orientation of
collagen fibers in those tendons producing a deformable meshwork.
The concept that an increase in stress alone,
without a significant increase in tendon excursion,
improves the quality of the repair response and
decreases adhesion formation has been addressed
in several clinically relevant experimental studies.
Hitchcock et al.,17 focusing on the loss of repair site
tensile strength (‘‘softening’’) seen characteristically
in the first postoperative week, studied the effects of
immediate constrained digital motion on the strength
of flexor tendon repairs in chickens. They found that
early controlled motion diminished profoundly the
adhesion response and obviated the softening of
tendon seen frequently with postoperative immobilization. Tendons of the mobilized digits showed
early and progressive strength gains. Strickland and
Glogovac,15 in a clinical study, demonstrated that
digits mobilized with early passive motion demonstrated an increased total active motion compared
to nonmobilized digits. Specifically, the percentage
of good results improved by over 40% with the
utilization of early controlled passive motion compared to immobilization. Feehan and Beauchene47
April–June 2005


demonstrated a significant increase in repair site
stiffness and ultimate stress in tendons that were
mobilized compared to their immobilized counterparts. Taken together, these experimental and clinical
studies lent support to the concept that stress applied
to the repair site in the immediate postoperative
period markedly improved healing efficiency.
Although the clinical and experimental results
seen with the application of low levels of postoperative force were promising, some authors advocated
increasing the levels in vivo applied force during
rehabilitation. In a clinical study, Small et al.48 reported 77% good and excellent results in a series of 98
patients treated with controlled active motion rehabilitation. The investigators noted that the necessity of secondary reconstructive procedures such as
tenolysis decreased by 75% with the use of an active
motion program. They did, however, report a rupture
rate of 9%. This high level of repair site failure is
cautionary, because loads applied to the repair site
with active motion rehabilitation protocols may lack
suitable control and therefore may exceed the repair
site’s ultimate load capacity during the first postoperative weeks.
In an effort to define the in vivo forces seen
clinically during passive and active range of motion
activities, Schuind et al.49 applied buckle transducers
to the flexor tendons of patients undergoing open
carpal tunnel surgery. They found a large variation in
the in vivo force from between 1 N and 34 N for
passive single digit flexion and active tip pinch. Mean
values for passive digital flexion were approximately
3 to 5 N, whereas values for passive digital flexion
with extension were between 15 to 20 N. Lieber
et al.50,51 demonstrated subsequently in a canine
model that significant differences in intrasynovial
tendon gliding and in vivo tendon force could be
demonstrated by applying rehabilitation regimens
differing in the extent of applied digital and wrist
flexion and extension movements. The smallest
amounts of intrasynovial flexor tendon excursion
and the lowest levels of applied in vivo force
occurred with passive digital flexion-extension carries out with the wrist held in flexion. Mean loads of
less than 5 N and excursions of 1.7 mm were achieved
on the canine flexor digitorum profundus tendon.
Passive digital flexion and extension with the wrist
held in extension increased significantly both the
levels of force (average 17 N) and the levels of
intrasynovial excursion (3.5 mm). Passive digital
flexion and extension with synergistic wrist extension and flexion likewise increased tendon excursion,
but minimized applied load. By application of these
rehabilitation regimens, it has been possible to isolate
both repair site excursion and applied musculotendinous load as independent variables in the investigation of their individual effects in a clinically
relevant model of flexor tendon rehabilitation whose


measured values of force and excursion replicate
directly those achieved during rehabilitation in humans. The importance of these three studies cannot
be overstated.

In recent experimental trials, clinical investigators
have focused on increasing the magnitude of tendon
excursion in contrast to in vivo force.16,17,52–55 In an
effort to increase the magnitude of tendon excursion
and reduce in vivo force clinically, Silfverskiold
et al.56 recommended a modification of the technique
in which digits are mobilized. They believed that
a tethering effect occurred when digits were flexed
and extended individually, and recommended that
four-finger flexion rehabilitation be used to achieve
increased intrasynovial repair site excursion. The
investigators posited that an increase in excursion
of between 6 to 9 mm constituted the threshold
needed to demonstrate benefit. Horii et al.16 used
synergistic wrist motion to eliminate the tendons’
slackness in the palm, in an effort to increase
excursion without increasing applied load. Without
applied load, excursions of 5 mm were seen. With
applied loads of 3 or 4 N, intrasynovial excursion of
up to 13 mm were seen. When two traditional splints
were compared to a splint allowing synergistic wrist
motion, the authors noted several remarkable benefits: tendon crimping was reduced, excursion was
increased and buckling under the pulley system was
obviated. The conclusion was, however, that increased force application was required for the benefits of synergistic motion to be realized.
In a clinical study, Hagberg and Selvik53 demonstrated that methods of rehabilitation utilizing increased levels of both force and excursion (realized
by combining passive digital flexion with synergistic
wrist motion, along with active digital contraction)
resulted in improved repair site excursion. However,
considerable repair site elongation as measured by
intratendinous metallic markers was seen. Investigators
have, in the past, believed that repair site elongation
( gap formation) and the formation of intrasynovial
restrictive adhesions were related directly. In a study
using a clinically relevant canine model, it was
convincingly demonstrated that repair site gap formation during the first six postoperative weeks does
not correlate with loss of digital motion or with the
formation of intrasynovial adhesions.57 The effect of
gap formation seen during the first three postoperative weeks was only to obviate the time dependent
accrual of repair site strength seen between three and
six weeks postoperatively if the size of the gap
exceeded 3 mm in length.

Previous investigations have demonstrated that the
repair site during the early postoperative period is
active in the synthesis of compounds known to be
responsible for the transduction of extracellular matrix signals to the interior of the fibroblast, and for
compounds stimulating angiogenesis directly.58–61 In
addition, tendon cells and explants respond positively to applied mechanical stress.40–44 On the basis
of these studies, we hypothesized that intrasynovial
flexor tendons treated with protected passive motion
would be responsive to variations in applied in vivo
force during the first six weeks after repair.
Two-hundred and fourteen canine intrasynovial
flexor tendon repairs were assigned to one of four
groups based on the rehabilitation method (low force
[,5 N] or high force [17 N]) and the repair technique
( four-strand or eight-strand core suture). Animals
were killed at intervals between five and 42 days
postoperatively. Repair site structural properties
were determined by tensile testing, and digital range
of motion was assessed by a motion analysis system.
We found that the tensile properties did not differ
between the low- and the high-force rehabilitation
groups, irrespective of repair technique.62 By contrast, the tensile properties were affected significantly
by the repair technique with the tendons in the eightstrand group having a significantly higher ultimate
force than those in the four-strand group throughout
the postoperative period. As demonstrated in a previously published study, ultimate force did not
change significantly with time during the first 21
days.57 Of note, there was no evidence of tendon
softening in either of the rehabilitation groups. The
repair site ultimate strength increased significantly
from 21 to 42 days in all groups.
This study demonstrated that increasing the level
of clinically relevant applied musculotendinous
force from 5 to 17 N during the immediate postoperative period did not accelerate the timedependent accrual of repair site strength or stiffness.
Suture technique was of primary importance, however, in providing a strong and stiff repair site
throughout the early healing interval. These findings suggested that there be a re-evaluation of the
concept that increases in force provided by more
vigorous rehabilitation techniques are beneficial to
early tendon healing. Even in the context of modern
eight-strand suture repair techniques, increased
applied force might potentially increase the incidence of repair site dehiscence or gap formation,
and is not advocated at present.

The effects of increased in vivo tendon excursion
(independent of applied musculotendinous force) on
digital range of motion and tendon strength after
flexor digitorum profundus (FDP) tendon transection
and repair were evaluated as well.63 Ninety-six FDP
tendons were injured, repaired and treated by lowforce (5 N) passive mobilization rehabilitation protocols starting on the first postoperative day. The
protocols held the applied force constant but varied
the excursion achieved: 1.7 mm of intrasynovial
excursion for the low-excursion group, and 3.5 mm
for the high-excursion group. Rehabilitation for the
first group (low force/low excursion) consisted of
passive flexion and extension of the four digits with
the wrist maintained in the flexed position; for the
second group (low force/high excursion) the wrist
and digits flexed and extended simultaneously. Our
results indicated that the use of rehabilitation that
produced increased tendon excursion within the
context of low applied force did not influence
range-of-motion or tensile properties. Joint rotation
and tendon excursion in digits from the low-force/
low-excursion and low-force/high-excursion groups
were not significantly different ( p > 0.05), with both
groups not significantly different from unoperated
controls. Tensile structural properties (ultimate force,
rigidity, strain at 20 N, strain at failure) were not
significantly affected by increased excursion ( p > 0.05).
We conclude that a threshold of 1.7 mm of tendon
excursion is sufficient to inhibit adhesion formation
and to allow excellent recovery of functional properties following sharp transection of the canine FDP
tendon. Additional excursion, at the same low force
level, appeared to provide little added benefit. These
results contrast those recently reported by Zhao
et al.,64 who demonstrated in an in vivo canine model
of partial tendon laceration and repair that, based on
improvements in adhesion breaking strength and
decreased overall formation of adhesions, synergistic
wrist motion coupled with passive digital flexion was
beneficial to tendon healing and digital motion.
Although the model utilized was one of partial
tendon laceration and repair wherein the force required to rupture the repair site averaged a minimum
of 135 N (over seven times that force applied during
clinically relevant high-force rehabilitation), the implication is that increased tendon excursion within
the context of low applied force may be of benefit in
the minimization of the formation of intrasynovial

Based on presently available experimental and
clinical data, we conclude that primary repair of
a intrasynovial flexor tendon laceration65 using
a modern multistrand core and epitendinous suture
April–June 2005


technique27 should be able to withstand repair site
gap formation of 3 mm during the first three postoperative weeks.57 A passive motion rehabilitation
protocol that strives to emphasize intrasynovial repair site excursion,63 rather than increased application of musculotendinous force62 across the repair
site, should be utilized.66
We currently perform an eight-strand, locked repair using a synthetic, coated suture supplemented
by an epitendinous running repair within ten to 14
days of injury. Therapy begins on postoperative day 1
with a synergistic protocol. Early motion is protected
by a hinged splint, with wrist extension typically
blocked at 30 degrees and MP extension typically
blocked at 70 degrees. Early place and hold is also
utilized. Close coordination between the therapist
and surgeon helps to maximize outcome by modifying the rehabilitation protocol for the individual patient as necessary.

1. Kessler I, Nissim F. Primary repair without immobilization of
flexor tendon division within the digital sheath. An experimental and clinical study. Acta Orthop Scand. 1969;40:587–601.
2. Verdan C. Primary repair of flexor tendons. J Bone Joint Surg
Am. 1960;42:647–57.
3. Gelberman RH, Manske PR, Akeson WH, Woo SL, Lundborg
G, Amiel D. Flexor tendon repair. J Orthop Res. 1986;4:119–28.
4. Lundborg G. Experimental flexor tendon healing without
adhesion formation—a new concept of tendon nutrition and
intrinsic healing mechanisms. A preliminary report. Hand.
5. Lundborg G, Rank F. Experimental intrinsic healing of flexor
tendons based upon synovial fluid nutrition. J Hand Surg
[Am]. 1978;3:21–31.
6. Lundborg G, Rank F. Tendon healing: intrinsic mechanisms.
In: Hunter J, Schneider L, Mackin E (eds). Tendon Surgery in
the Hand. St. Louis: CV Mosby, 1987, pp 54–60.
7. Matthews P, Richards H. Factors in the adherence of flexor
tendon after repair: an experimental study in the rabbit. J Bone
Joint Surg Br. 1976;56:618–25.
8. Gelberman RH, Amifl D, Gonsalves M, Woo S, Akeson WH.
The influence of protected passive mobilization on the healing
of flexor tendons: a biochemical and microangiographic study.
Hand. 1981;13:120–8.
9. Gelberman RH, Woo SL, Lothringer K, Akeson WH, Amiel D.
Effects of early intermittent passive mobilization on healing
canine flexor tendons. J Hand Surg [Am]. 1982;7:170–5.
10. Woo SL, Gelberman RH, Cobb NG, Amiel D, Lothringer K,
Akeson WH. The importance of controlled passive mobilization on flexor tendon healing. A biomechanical study. Acta
Orthop Scand. 1981;52:615–22.
11. Duran R, Houser R, Coleman C, Postlewaite D. A preliminary
report in the use of controlled passive motion following flexor
tendon repair in zones II and III (abstract). J Hand Surg. 1976;
12. Duran RJ, Houser RG. Controlled passive motion following
flexor tendon repair in zones 2 and 3. In: AAOS Symposium on
Tendon Surgery in the Hand. St. Louis: CV Mosby, 1975, pp
13. Lister GD, Kleinert HE, Kutz JE, Atasoy E. Primary flexor
tendon repair followed by immediate controlled mobilization.
J Hand Surg [Am]. 1977;2:441–51.
14. Kleinert HE, Kutz JE, Atasoy E, Stormo A. Primary repair of
flexor tendons. Orthop Clin North Am. 1973;4:865–76.



15. 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]. 1980;
16. Horii E, Lin GT, Cooney WP, Linscheid RL, An KN.
Comparative flexor tendon excursion after passive mobilization: an in vitro study. J Hand Surg [Am]. 1992;17:559–66.
17. Hitchcock TF, Light TR, Bunch WH, et al. The effect of
immediate constrained digital motion on the strength of
flexor tendon repairs in chickens. J Hand Surg [Am]. 1987;12:
18. Mason ML, Allen HS. The rate of healing of tendons: an
experimental study of tensile strength. Ann Surg. 1941;113:
19. Lindsay W, Thompson H, Walker H. Digital flexor tendons:
an experimental study. Br J Plast Surg. 1960;13:1–9.
20. Ketchum LD. Primary tendon healing: a review. J Hand Surg.
21. Ketchum LD, Martin NL, Kappel DA. Experimental evaluation
of factors affecting the strength of tendon repairs. Plast
Reconstr Surg. 1977;59:708–19.
22. Seradge H. Elongation of the repair configuration following
flexor tendon repair. J Hand Surg [Am]. 1983;8:182–5.
23. Potenza A. Concepts of tendon healing and repair. In: AAOS
Symposium on Tendon Surgery in the Hand. St. Louis: CV
Mosby, 1975, pp 18–47.
24. Potenza A. Philosophy of flexor tendon surgery. Orthop Clin
North Am. 1986;17:349–52.
25. Peacock E. Fundamental aspect of wound healing relating to
the restoration of gliding function after tendon repair. Surg
Gynecol Obstet. 1964;119:241–50.
26. Peacock E. Biological principles in the healing of long tendons.
Surg Clin North Am. 1965;45:461–76.
27. Winters SC, Gelberman RH, Woo SL-Y, Chan SS, Grewal R,
Seiler JG. The effects of multiple-strand suture methods on the
strength and excursion of repaired intrasynovial flexor tendon:
a biomechanical study in dogs. J Hand Surg [Am]. 1998;23:
28. Winters SC, Seiler JG III, Woo SL, Gelberman RH. Suture
methods for flexor tendon repair. A biomechanical analysis
during the first six weeks following repair. Ann Chir Main
Memb Super. 1997;16:229–34.
29. Taras J, Skahen J, James R, Raphael J, Marzyk S, Bauerle W. The
double-grasping and cross-stitch for acute flexor tendon
repair: Applications with active motion. Atlas Hand Clin.
30. Savage R. In vitro studies of a new method of flexor tendon
repair. J Hand Surg [Br]. 1985;10:135–41.
31. Lin GT, An KN, Amadio PC. Cooney WP III. Biomechanical
studies of running suture for flexor tendon repair in dogs.
J Hand Surg [Am]. 1988;13:553–8.
32. Wagner WF Jr, Carroll Ct, Strickland JW, Heck DA, Toombs JP.
A biomechanical comparison of techniques of flexor tendon
repair. J Hand Surg [Am]. 1994;19:979–83.
33. Kessler I. The ‘‘grasping’’ technique for tendon repair. Hand.
34. Tajima T. History, current status, and aspects of hand surgery
in Japan. Clin Orthop. 1984;184:41–9.
35. Strickland JW. Flexor tendon repair. Hand Clin. 1985;1:55–68.
36. Strickland J. Flexor tendon repair: Indiana method. Indiana
Hand Center Newsletter. 1993;1:1–12.
37. Strickland JW. Flexor tendon injuries: II. Operative technique.
J Am Acad Orthop Surg. 1995;3:55–62.
38. McLarney E, Hoffman H, Wolfe SW. Biomechanical analysis of
the cruciate four-strand flexor tendon repair. J Hand Surg
[Am]. 1999;24:295–301.
39. Becker H. Primary repair of flexor tendons in the hand without
immobilization: preliminary report. Hand. 1978;10:37–47.
40. Harris E, Bass B, Walker L. Tensile strength and stress-strain
relationships in cadaveric human tendons [abstract]. Anat Rec.
41. Gillard GC, Reilly HC, Bell-Booth PG, Flint MH. The influence
of mechanical forces on the glycosaminoglycan content of the














rabbit flexor digitorum profundus tendon. Connect Tissue Res.
Mass DP, Tuel RJ, Labarbera M, Greenwald DP. Effects of
constant mechanical tension on the healing of rabbit flexor
tendons. Clin Orthop. 1993;296:301–6.
Slack CM, Flint MH, Thompson BM. The effect of tensional
load on isolated embryonic chick tendons in organ culture.
Connect Tissue Res. 1984;12:229–47.
Woo SL, Gomez MA, Amiel D, Ritter MA, Gelberman RH,
Akeson WH. The effects of exercise on the biomechanical and
biochemical properties of swine digital flexor tendons.
J Biomech Eng. 1981;103:51–6.
Becker H, Graham MF, Cohen IK, Diegelmann RF. Intrinsic
tendon cell proliferation in tissue culture. J Hand Surg [Am].
Almekinders L, Banes A, Ballenger C. Effects of repetitive
motion on human fibroblasts. Med Sci Sports Exer. 1993;25:
Feehan LM, Beauchene JG. Early tensile properties of healing
chicken flexor tendons: early controlled passive motion versus
postoperative immobilization. J Hand Surg [Am]. 1990;15:63–8.
Small JO, Brennen MD, Colville J. Early active mobilisation
following flexor tendon repair in zone 2. J Hand Surg [Br].
Schuind F, Garcia-Elias M, Cooney WP III, An KN. Flexor
tendon forces: in vivo measurements. J Hand Surg [Am]. 1992;
Lieber RL, Amiel D, Kaufman KR, Whitney J, Gelberman RH.
Relationship between joint motion and flexor tendon force in
the canine forelimb. J Hand Surg [Am]. 1996;21:957–62.
Lieber RL, Silva MJ, Amiel D, Gelberman RH. Wrist and digital
joint motion produce unique flexor tendon force and excursion
in the canine forelimb. J Biomech. 1999;32:175–81.
Cannon NM, Strickland JW. Therapy following flexor tendon
surgery. Hand Clin. 1985;1:147–65.
Hagberg L, Selvik G. Tendon excursion and dehiscence during
early controlled mobilization after flexor tendon repair in zone
II: an x-ray stereophotogrammetric analysis. J Hand Surg
[Am]. 1991;16:669–80.
Horibe S, Woo SL, Spiegelman JJ, Marcin JP, Gelberman RH.
Excursion of the flexor digitorum profundus tendon: a kinematic study of the human and canine digits. J Orthop Res. 1990;
May EJ, Silfverskiold KL. Rate of recovery after flexor tendon
repair in zone II. A prospective longitudinal study of 145
digits. Scand J Plast Reconstr Surg Hand Surg. 1993;27:89–94.

56. Silfverskiold KL, May EJ, Tornvall AH. Gap formation during
controlled motion after flexor tendon repair in zone II:
a prospective clinical study. J Hand Surg [Am]. 1992;17:
57. Gelberman RH, Boyer MI, Brodt MD, Winters SC, Silva MJ. The
effect of gap formation at the repair site on the strength and
excursion of intrasynovial flexor tendons. An experimental
study on the early stages of tendon-healing in dogs. J Bone
Joint Surg Am. 1999;81:975–82.
58. Harwood FL, Goomer RS, Gelberman RH, Silva MJ, Amiel D.
Regulation of alpha(v)beta3 and alpha5beta1 integrin receptors by basic fibroblast growth factor and platelet-derived
growth factor-BB in intrasynovial flexor tendon cells. Wound
Repair Regen. 1999;7:381–8.
59. Harwood FL, Monosov AZ, Goomer RS, et al. Integrin
expression is upregulated during early healing in a canine
intrasynovial flexor tendon repair and controlled passive
motion model. Connect Tissue Res. 1998;39:309–16.
60. Boyer MI, Watson JT, Lou J, Manske PR, Gelberman RH, Cai
SR. Quantitative variation in vascular endothelial growth
factor mRNA expression during early flexor tendon healing:
an investigation in a canine model. J Orthop Res. 2001;19:
61. Bidder M, Towler DA, Gelberman RH, Boyer MI. Expression
of mRNA for vascular endothelial growth factor at the repair
site of healing canine flexor tendon. J Orthop Res. 2000;18:
62. Boyer MI, Gelberman RH, Burns ME, Dinopoulos H, Hofem R,
Silva MJ. Intrasynovial flexor tendon repair. An experimental
study comparing low and high levels of in vivo force during
rehabilitation in canines. J Bone Joint Surg Am. 2001;83:891–9.
63. Silva MJ, Brodt MD, Boyer MI, et al. Effects of increased in vivo
excursion on digital range of motion and tendon strength
following flexor tendon repair. J Orthop Res. 1999;17:777–83.
64. Zhao C, Amadio PC, Momose T, Couvreur P, Zobitz ME, An
KN. Effect of synergistic wrist motion on adhesion formation
after repair of partial flexor digitorum profundus tendon
lacerations in a canine model in vivo. J Bone Joint Surg Am.
65. Gelberman RH, Siegel DB, Woo SL, Amiel D, Takai S, Lee D.
Healing of digital flexor tendons: importance of the interval
from injury to repair. A biomechanical, biochemical, and
morphological study in dogs. J Bone Joint Surg Am. 1991;73:
66. Silva MJ, Boyer MI, Gelberman RH. Recent progress in flexor
tendon healing. J Orthop Sci. 2002;7:508–14.

April–June 2005