Published online: 2021-07-15

211

Tendon: Principles of Healing and Repair

Christian Chartier, MD1 Hassan ElHawary, MD, MSc2 Aslan Baradaran, MD, MSc2
Joshua Vorstenbosch, MD, PhD, FRCSC2 Liqin Xu, MD, MSc, FRCSC2 Johnny Ionut Efanov, MD, PhD, FRCSC3

1 Faculty of Medicine, McGill University, Montreal, Quebec, Canada Address for correspondence Johnny Ionut Efanov, MD, PhD, FRCSC,
2 Division of Plastic and Reconstructive Surgery, McGill University Division of Plastic and Reconstructive Surgery, Centre hospitalier de
Health Centre, Montreal, Quebec, Canada l’Universite de Montreal, 1051 Rue Sanguinet, Montreal, Quebec,
3 Division of Plastic and Reconstructive Surgery, Centre Hospitalier de H2
3E4, Canada (e-mail: [email protected]).
l’Université de Montréal, Montreal, Quebec, Canada

Semin Plast Surg 2021;35:211–215.

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Abstract Tendon stores, releases, and dissipates energy to efficiently transmit contractile forces from
muscle to bone. Tendon injury is exceedingly common, with the spectrum ranging from
chronic tendinopathy to acute tendon rupture. Tendon generally develops according to
three main steps: collagen fibrillogenesis, linear growth, and lateral growth. In the setting
of injury, it also repairs and regenerates in three overlapping steps (inflammation,
proliferation, and remodeling) with tendon-specific durations. Acute injury to the flexor
and extensor tendons of the hand are of particular clinical importance to plastic surgeons,
Keywords with tendon-specific treatment guided by the general principle of minimum protective
► tendon healing immobilization followed by hand therapy to overcome potential adhesions. Thorough
► tendon repair knowledge of the underlying biomechanical principles of tendon healing is required to
► tendon inflammation provide optimal care to patients presenting with tendon injury.

Tendon has chiefly a mechanical part to play at the intersec- mature tendon is a highly hierarchical connective tissue
tion of muscle and bone, directly transmitting contractile composed of ensheathed fascicles of collagen (mainly type
forces while dissolving stress that would otherwise concen- I) fibrils aligned with intervening fibroblasts. The tendon’s
trate should muscle interface directly with bone.1,2 It stores, outermost capsule is the epitenon, while its individual
releases, and dissipates energy to efficiently maintain the fascicles are contained in the endotenon. Paratenon overlies
joint-loading cycle while protecting adjacent tissues.1 None- the epitenon in regions where no sheaths exist. All of these
theless, tendinous injuries are exceedingly common, with encapsulating structures are composed of connective tissue
50% of musculoskeletal injuries recorded in the United States and provide most of the tendon’s blood, nerve, and lymphatic
involving tendinous or ligamentous injury and 10% of people supply.5,6
(50% of runners) experiencing Achilles tendinopathy by age Macroscopically, a tendon should be conceptualized in
of 45.1,3 While tendon rupture usually corresponds to an thirds, each with different features and blood supply: the
acute incident, evidence suggests that chronic degenerative proximal myotendinous junction (MTJ), the distal osteoten-
changes are usually present and contribute to the rupture.4 dinous junction (OTJ), and the central third or belly. The MTJ
Thus, it is crucial to consider tendon healing in the context of consists of tendinous collagen fibrils interfacing with myo-
its development, regeneration, and of the histologic changes cyte processes and is most vulnerable to injury by tear. A
that reflect its long-term degeneration. tendon attaches to bone at the OTJ, which is segmented into
four zones: dense connective tissue, uncalcified fibrocarti-
lage, calcified fibrocartilage, and bone.7 Vascularization to
Tendon Anatomy and Classification
each third varies by tendon type. The OTJ and MTJ are largely
A firm grasp of hand and tendon anatomy is the backbone of a supplied by an intrinsic system, with periosteal vessels and
productive hand surgery practice. Mechanically, a functional, vessels from the muscle extending into the tendon fibrils.

published online Issue Theme Healing, Inflammation, © 2021. Thieme. All rights reserved. DOI https://doi.org/
July 15, 2021 and Fibrosis; Guest Editor: Joshua Thieme Medical Publishers, Inc., 10.1055/s-0041-1731632.
Vorstenbosch, MD, PhD, FRCSC 333 Seventh Avenue, 18th Floor, ISSN 1535-2188.
New York, NY 10001, USA
212 Tendon: Principles of Healing and Repair Chartier et al.

The extrinsic system supplies blood through the paratenon tendon injuries) and of injuries to the index finger has been
or through the synovial sheath via vincula, which are con- reported compared with other digits.17 Importantly, flexor
nective tissue bands bridging tendon to bone and containing tendon injury occurs most frequently in Zone 2 with the
tiny blood vessels.8 profundus tendon to the small finger identified as the most
Muscular, cutaneous, and peritendinous nerve trunks common flexor tendon injured.17,20
innervate tendon, though few nerve fibers actually enter
tendon proper, instead terminating on its surface as nerve
Development and Structure of Healthy
endings.8 Golgi tendon bodies are myelinated fiber nerve
Tendon
endings functioning as mechanoreceptors capable of detect-
ing changes in tension or pressure—stretch receptors. They While tissue-specific checkpoints govern fibrillogenesis
occur most frequently at the MTJ.9 Unmyelinated parasym- throughout the body, tendon generally develops according to
pathetic and sympathetic nerve fiber endings function as three main steps: (1) tendon collagen fibrillogenesis, (2) linear
nociceptors capable of transmitting and sensing pain.10 growth, and (3) lateral growth.1,21,22 The first step consists of
Three to seven vincula supply each flexor tendon (flexor immature fibril formation by extracellular assembly of colla-

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digitorum superficialis [FDS] and flexor digitorum profundus gen molecules. In the second step, the fibril intermediates
[FDP]) in the human hand.11 There are two triangular fibrous attach end-to-end and attain mechanical/lengthwise maturi-
bands called vincula brevia in each finger, one connecting the ty. Large diameter fibrils spawn in the third step as a result of
FDS tendon to the proximal interphalangeal joint/P1 head side-to-side attachment of multiple long fibrils.22 Though
and one connecting the FDP tendon to the distal interpha- tendon in its mature form is approximately 70% collagen I,
langeal (DIP) joint/P2 head. There are two longer and more other regulatory molecules are essential as they underpin
slender bands in each finger called vincula longa, one con- tissue-specific fibrillogenesis. For example, it is known from
necting the FDS tendon to the base of P1 and one connecting animal models that prominent expression of collagen III may
the FDP and FDS tendons distal to Camper’s chiasm.11 be related to smaller fibril diameter and suppressed lateral
Tension, friction, and compression can compromise tendon growth of collagen I. The opposite is thought to be true about
vascularity, which also decreases with age.12 dermatan sulfate or chondroitin proteoglycan side chains,
Both flexor and extensor tendon lacerations are described which are thought to be associated with larger diameter
by anatomical location. Anatomically, flexor tendon injuries fibrils.23–25
can be classified by affected zone, with zones labeled one to
five, distal to proximal. Zone 1 extends from FDP insertion to
Acute and Chronic Changes in Tendon Injury
FDS insertion—FDP avulsion injuries, also known as jersey
finger, in this zone are described using the Leddy–Packer While extreme exercise, concomitant loading, aging, and
classification.13,14 Zone 2 spans the FDS insertion to the A1 oxidative stress are recognized as physical and biological
pulley. Zone 3 is from the distal palmar crease to the carpal factors that engender tendinopathy, the exact pathogenesis
tunnel. The carpal tunnel constitutes Zone 4, while Zone 5 of tendinopathy is poorly defined. For years, the accepted
spans the wrist to the forearm. Extensor injuries are similarly model of tendinopathy was one of tendinitis, or inflamma-
categorized by affected zone, ranging from Zone 1 at the DIP, tion. More recent histopathological studies have identified
the disruption of which causes mallet fingers, to Zone 9 tendinosis (chronic degeneration), as the culprit in most
encompassing most of the upper forearm.15 cases of tendinopathy.26–30 It is responsible for the symp-
toms of pain, decreased strength, and impairment in activi-
ties of daily living commonly attributed to tendinitis. The
Epidemiology of Tendon Injury
affected region in tendinosis exhibits structural and cellular
The dramatic increase in tendon injuries in recent decades is changes relative to unaffected tissue. While healthy tendon is
attributable in large part to a population-level shift toward characterized by parallel, wavy, clearly defined bundles of
active living. Interestingly, despite being the strongest ten- collagen, diseased tissue is recognizable by its lack of align-
don in the human body, the Achilles tendon is injured more ment or demarcation between neighboring bundles and its
frequently than any other, succumbing to tensional forces increased diameter.31 On a cellular level, tendinosis is char-
created by repetitive movements in strenuous sporting activi- acterized by neovascularization, hypercellularity, and atypi-
ty.16 Of particular interest to plastic surgeons, hand injuries cal fibroblast proliferation.32 Tenocytes capable of producing
represent up to 20% of all injuries treated in emergency collagen change shape, with their nuclei exhibiting signs of
departments, with 55 and 93% of patients, respectively, treated fibrocartilaginous metaplasia.33,34 Biomechanically, tendi-
for short-superficial or short-deep hand lacerations experienc- nosis predisposes tendon to rupture.4
ing concomitant tendon injury. For reference, tendinous hand Similar features have been observed in senescent tendon.
injury was found to be 23 times more common than scaphoid Aging decreases tenoblast volume and plasmalemmal sur-
fractures.6,17 face density, increases the nucleus-to-cytoplasm ratio, and
A higher propensity for tendinous hand injury has been suppresses protein synthesis.1 Collectively, these features
reported in men as compared with women—a finding largely contribute to decreased collagen turnover, characterized
attributed to gender-related activities.17–19 A higher inci- by thicker collagen fibers with greater variability in fiber
dence of extensor tendon injuries (as compared with flexor diameter. The activity of lysol oxidase, an enzyme essential

Seminars in Plastic Surgery Vol. 35 No. 3/2021 © 2021. Thieme. All rights reserved.
 Tendon: Principles of Healing and Repair Chartier et al. 213

for collagen production, decreases, which in turn increases delayed, sometimes for days. This difference is attributable to
nonreducible collagen cross-linking.1,35 Biomechanically, the synovium’s enhanced inflammatory and proliferative
this impedes capacity to withstand loading and increases capacity as compared with the tendon proper.36 Importantly,
stiffness.1 extrinsic-predominant healing is associated with larger ten-
In the setting of acute intrasynovial flexor tendon injury, don diameter, increased collagen disorganization, and con-
disruption of the tissue surrounding the lacerated tendon sequently a propensity to adhere to peritendinous tissue
compound the severity of injury. Leakage of synovial fluid (tendon adhesions). On the other hand, intrinsic healing
from within the digital sheath causes tendon starvation, constitutes the basis upon which early active range of motion
slowing the repair process. This occurs through absolute protocols are made possible. Thus, through a mix of meticu-
synovial fluid loss, but also through disruption of the pres- lous surgical technique and early rehabilitation, treatment
sure distribution crucial to the process of imbibition by teams seek to activate the intrinsic pathway rather than the
which tendon gets most of its nutrients.36 It follows logically extrinsic pathway. In practice, the goal of treatment is to
that injury to the tendon blood supply itself also hinders identify the minimum amount of motion to avoid scarring
tendon healing in the acute setting. Importantly, as surgical and tethering to nearby tissue while avoiding jeopardizing

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apposition of the two ends of an injured tendon remains the the repair site.
gold standard for tendon injury treatment, one must be From a surgical repair standpoint, it is generally accepted
mindful to limit intraoperative trauma, which is additive that repair strength is proportionate to the number of
to the severity of the original injury. strands spanning the repair site, with traditional repair
A common nontraumatic pathology of hand tendons is techniques including Tajima and Kessler (two sutures across
proliferative extensor tenosynovitis of the wrist, a condition the repair site) becoming less popular in favor of techniques
well-documented in patients diagnosed with rheumatoid with four to eight strands across the repair site and a running
arthritis. It is characterized by pain and limited range of epitenon stitch.1 While there is controversy on the use of
motion localizing to the fourth extensor compartment and braided sutures over monofilament in certain repairs such as
can lead to tendon rupture.37 In the context of rheumatoid rotator cuff repairs, monofilament is preferred in the flexor
arthritis, the proliferation is due to synovial tissue hypertro- tendons of the hand as it generates less friction and tendon
phy, inflammation, and fluid production. Histologically, the deformity than braided sutures.41–44
pathology infiltrates the tendon proper and exhibits fibri- Other factors that affect tenorrhaphy strength include
nous adhesions, a feature also observed in tendon healing suture caliber, position (“locked” vs. “grasping”), material,
from acute or chronic traumatic injury.37 and degree of gap formation across the apposition site.45
While surgeons largely opt for 3–0 over 4–0 suture in tendon
repair due to its tensile strength, this preference comes at the
Repair and Regeneration
cost of a more traumatic repair process that may further
Similar to fibrillogenesis, tendon regeneration can be dis- delay healing.45 Further, while locked sutures confer the
tilled down to three overlapping steps: (1) inflammation, (2) added benefit of better mechanical load distribution (as
proliferation, and (3) remodeling.1 The inflammatory stage compared with grasping sutures), the position of the knot
lasts approximately 48 hours and consists of erythrocyte, relative to the repair site has been shown to have little impact
leukocyte, endothelial chemoattractant, and platelet infiltra- on repair strength.45 Knots external to the repair site may
tion. At this point, the role of macrophages is to consume the interfere with adjacent structures while knots on the repair
necrotic tissue. The proliferative stage is characterized by site increase the overall diameter of the repair.45 Regardless,
macrophage and tenocyte-directed synthesis of new, less it is important to note that circumferential sutures have
durable collagen III, the predominant tendon tissue. The proven to be mainly useful as additive—for orientation
tenocytes in this second stage primarily proliferate in the purposes—to core tendon suture.
epitenon. The proliferative phase occurs for a period of 7 to
21 days. The third stage begins months after the initial injury,
Practical Approach for Surgeons
can last longer than 12 months, and involves extracellular
matrix alignment and collagen I synthesis replacing the For surgeons to achieve an optimal tendon repair, an appro-
collagen III. Collagen fibers undergo maturation and reorient priate balance between durable tendon repair against exces-
themselves parallel to the direction of mechanical stress. sive adhesion formation must be achieved. Careful selection
However, the regenerated tissue has a scar-like appearance of the appropriate repair technique and timely rehabilitation
and is biomechanically inferior to the original healthy has the potential to significantly improve treatment
tendon.38–40 outcomes.
The three phases of tendon healing occur through a As mentioned previously, tendon repair strength is de-
combination of extrinsic and intrinsic mechanisms.36 The rived from the number of strands crossing the repair site and
extrinsic mechanism involves inflammatory cells and fibro- from the suture caliber.46 Further, locked and epitendinous
blasts infiltrating from surrounding tissue, whereas in the sutures provide more biomechanical leverage. In flexor
intrinsic mechanism, these cells originate from the tendon tendon injury repair, the A2 and A4 pulleys can be vented
and epitenon. The extrinsic mechanism predominates earlier to ease gliding across the system—this has been associated
in the healing process while the intrinsic mechanism can be with better functional recovery.47 Due to the fact that

Seminars in Plastic Surgery Vol. 35 No. 3/2021 © 2021. Thieme. All rights reserved.
214 Tendon: Principles of Healing and Repair Chartier et al.

prolonged tendon immobilization has been associated with 11 Armenta E, Lehrman A. The vincula to the flexor tendons of the
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