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SCIENTIFIC/CLINICAL ARTICLES

JHT Read for Credit Article #002

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

BACKGROUND
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.
wustl.edu>.
doi:10.1197/j.jht.2005.01.009

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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
models.
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.

SCIENTIFIC AND CLINICAL BASIS
FOR APPLICATION OF FORCE
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
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81

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

SCIENTIFIC AND CLINICAL BASIS
FOR THE APPLICATION OF
EXCURSION
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.

THE EFFECT OF PROXIMAL
MUSCULOTENDINOUS FORCE AND
INTRASYNOVIAL REPAIR SITE
EXCURSION, AS INDEPENDENT
VARIABLES, ON REPAIR SITE
STRUCTURE AND FUNCTION
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
adhesions.

SUMMARY
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
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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.

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