Injury location affects ligament healing: A morphologic and mechanical study of the healing rabbit medial collateral ligament

Based on the heterogeneity of the rabbit medial collateral ligament (MCL) along its length, we tested the hypothesis that injury location would affect its healing response. The right MCL of 80 skeletally mature New Zealand white rabbits was sectioned adjacent to bone at the femoral end (40 rabbits) or the tibial end (40 rabbits) and reapposed with sutures. Animals were killed after 3, 6, 14, or 40 weeks of healing to examine wounds histologically (2 rabbits per healing interval) and mechanically (8 rabbits per healing interval). Results of the mechanical tests were compared to midsubstance MCL repairs (24 rabbits) and to uninjured normal MCLs (20 rabbits). The morphology of the near-insertion repairs was characterized by abnormal callus-like formation and patchy bone resorption, particularly at the tibial insertion. Mechanically, insertional injuries remodeled towards normal MCL low-load, viscoelastic and failure properties more slowly than midsubstance injuries at the early healing intervals. After 40 weeks of healing, few injury-specific differences persisted. All injured ligaments had ultimate strengths 15-35 percent short of normal at 40 weeks and the femo-rally-injured ligaments were weaker than normal at this time. These results suggest that rabbit MCLs, injured near either end, heal more slowly that those injured in their midsubstance and develop abnormal insertion morphology.     

Denervation impairs healing of the rabbit medial collateral ligament.

Little is known about the contribution of innervation to ligament healing after traumatic disruption, although there is good evidence of an important role for the peripheral nervous system in the healing of fractures and skin injuries. Tissues such as ligament, with a low resting blood supply, are dependent on substantial increases in blood flow and vascular volume during the initial stages of repair. We hypothesized that this initial healing response would be strongly promoted by neurogenic inflammation. Since the saphenous nerve (a major sensory branch of the femoral nerve) supplies the medial half of the knee joint, we elected to use femoral nerve transection as a model to determine the role of sensory and autonomic innervation in the initial outcome of repair of the injured medial collateral ligament. Twelve adult, female NZW rabbits underwent right medial collateral ligament transection. Of these, six rabbits underwent right femoral nerve transection to disrupt the somatic sensory and autonomic nerve supply to the knee joint and six were kept neurologically intact (controls). At six weeks post-injury, the animals were assessed by laser Doppler perfusion imaging (LDI) to determine the local blood flow, at both the injury site and at the uninjured contralateral ligament. The animals were then killed, the knee joints were removed and the biomechanical characteristics of the healing bone-median collateral ligament (MCL)-bone complexes assessed. In a separate cohort of 16 rabbits, vascular volumes of the injured ligaments were measured by infusion of a carmine red/gelatin solution. At six weeks post-injury, in vivo measurement of perfusion with LDI revealed that normally innervated ligaments had an almost three-fold higher average blood flow. Carmine red/gelatin infusion revealed a 50% higher density of blood vessels as compared to denervated ligaments. The force required for ultimate failure was found to be 50% higher in normally innnervated MCL's as compared to denervated MCL's: 153.14 +/- 20.71 N versus 101.29 +/- 17.88 N (p < 0.05). Static creep was increased by 66% in denervated MCL's: 2.83 +/- 0.45% versus 1.70 +/- 0.12% (p < 0.05). Total creep was increased by 45% in denervated MCL's: 5.29 +/- 0.62% compared to 3.64 +/- 0.31% in innervated MCL's (p < 0.05). We conclude that intact innervation makes a critical contribution to the early healing responses of the MCL of adult rabbits.     

Plasticity of peptidergic innervation in healing rabbit medial collateral ligament

Background

Denervation substantially impairs healing of the medial collateral ligament (MCL). Because normal ligaments are sparsely innervated, we hypothesized that neuropeptide-containing neurons would sprout or proliferate after ligament transection, followed by later regression with healing, in a manner analogous to blood vessels.

Methods

We transected the right MCL in 9 mature female New Zealand white rabbits and killed 3 rabbits at 2, 6 or 14 weeks. Alternate sets of 12-mm serial sections of healing MCL scars were examined by fluorescent immunohistochemistry for substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and pan-neuronal marker PGP9.5.

Results

Normal MCLs had few peptidergic fibres located in the epiligament in a perivascular pattern. At 2 weeks, PGP9.5-, SP-and CGRP-positive fibres had increased in the epiligament adjacent to the injury. By 6 weeks, there were increases in CGRP-and PGP9.5-positive fibres in epiligament and scar, with similar but less marked increases in SP-positive fibres. At 14 weeks, there was notable regression of immunostained peptidergic nerve fibres in the scar.

Conclusion

This experiment shows evidence for a remarkable plasticity of ligament innervation after injury, supporting the idea that neuronal factors play a fundamental role in wound healing.     

Cellular senescence occurring in the rabbit medial collateral ligament during healing

Medial collateral ligament (MCL) healing proceeds in a temporally ordered fashion after injury. Despite the critical roles of fibroblasts during ligament repair, the phenotypic features of these healing fibroblasts have not been well characterized. Here, we show that healing MCL fibroblasts obtained from rabbits at 3‐week postinjury exhibited higher rates of senescent phenotypes and produced higher levels of TGF‐β1, collagens, α‐SMA, and matrix metalloproteinases (MMPs), than the corresponding fibroblasts from sham‐operated MCLs. Mechanical stretch further enhanced the cellular senescence and the expression of TGF‐β1, collagens, α‐SMA, and MMPs in both sham and healing MCL fibroblasts. In addition to MCL fibroblasts at 3‐week postinjury, the increased cellular senescence was also detected in healing MCL fibroblasts obtained at 4‐ and 6‐week postinjury. Most importantly, the association between the cellular senescence and ligament healing was confirmed in tissue sections by the senescence‐associated β‐galactosidase (SA‐β‐gal) staining. Using a recombinant TGF‐β1 and a neutralizing antibody, we found that those phenotypic changes, such as cellular senescence and the expression of collagens and MMPs, in MCL fibroblasts under mechanical loading conditions were regulated through TGF‐β1. Taken together, our results propose that cellular senescence and turnover of extracellular matrixes regulated by TGF‐β1 in MCL fibroblasts are critical for ligament healing. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31:81–90, 2012     

Integrin display increases in the wounded rabbit medial collateral ligament but not the wounded anterior cruciate ligament

The differential capacities of the anterior cruciate and medial collateral ligaments to heal may be related to differences in cellular function. This study tested the hypothesis that differential expression of integrins occurs in these ligaments after injury. The integrins are a family of cell surface receptors that mediate adhesion, migration, and other cellular functions critical to the healing of a wound. A similar complement and amount of the β₁ subfamily of integrins are known to be present on the unperturbed anterior cruciate and medial collateral ligaments in humans and rabbits. A partial laceration was surgically created in these two ligaments in 12 anesthetized New Zealand White rabbits. Immunohistochemistry was performed on sections from the ligaments at 1, 3, 7, and 10 days after injury, using monoclonal antibodies directed against the integrin subunits β₁, α₅, α₆, and α_v. Between 3 and 7 days, the wounded medial collateral ligament demonstrated a striking increase in staining for the β₁, α₅, and α_v subunits on the fibroblasts, within the repair site, and on capillary endothelium. Increased staining was most marked for the β₁ subunit and less marked for the α₅ and α_v subunits. The α₆ subunit stained exclusively vascular structures within the healing medial collateral ligament. In marked contrast, the anterior cruciate ligament, which does not mount an effective repair response, demonstrated no comparable alteration of integrin expression from baseline levels. This study demonstrates that increased expression of integrins occurs coincident with wound healing in the medial collateral ligament, whereas this expression remains at baseline levels in the nonhealing wounded anterior cruciate ligament. This observation suggests that a failure to alter expression of integrins subsequent to injury may play a role in the defective healing of the anterior cruciate ligament.     

Intraoperative graft tensioning alters viscoelastic but not failure behaviours of rabbit medial collateral ligament autografts

The effects of three different degrees of intraoperative graft tensioning on measures of ex vivo laxity, viscoelastic behaviour, and structural and material failure of isolated healing medial collateral ligament autografts were investigated in a rabbit model. The grafts were orthotopically replaced at one of three different loads (too tight, anatomic, or too loose) and were mechanically evaluated after 0, 12, 24, and 48 weeks of healing. Laxity of the ligament was influenced by intraoperative graft tensioning at time zero. However, after 12 weeks of healing, values for laxity were indistinguishable among the experimental groups. Cyclic load relaxation, a measure of viscoelastic behaviour, was significantly influenced by intraoperative graft tensioning, and this effect persisted even after 48 weeks of healing. Grafts placed under excessive tension relaxed one-third less than grafts placed under abnormally low in situ tension. The relevance of these differences remains to be determined. Intraoperative tensioning had no significant influence on characteristics of structural or material failure of the graft during the first year of healing. These results suggest that, in this model, control of graft tension at the time of placement and fixation does not improve the failure characteristics of the medial collateral ligament. The structural strength of the grafts collectively improved to nearly normal values after 48 weeks; however, material recovery was less complete. Failure loads averaged 89% of control values, whereas failure stress averaged only 52% after 48 weeks of healing.     

The biomechanical response to doses of TGF-beta 2 in the healing rabbit medial collateral ligament.

Ligament injuries result in significant disability in over 100,000 patients each year. Despite current methods of treatment, 13% of patients with medial collateral ligament (MCL) injury develop early signs of arthritis, suggesting an incomplete return of knee stability. The principal hypothesis of this work was that the addition of TGF-beta 2 to the healing MCL would accelerate the development of scar strength and stiffness. Forty-four rabbits were divided evenly into four groups, with each group receiving either 0.1, 1 or 5 microg of TGF-beta 2 and the fourth group receiving 1 microg TGF-beta 2 and 1 microg of PDGF. Each rabbit underwent bilateral transection of the MCL, with one side having treatment with one of four doses of growth factor and the other side left untreated. All animals were sacrificed at 6 weeks and the structural properties of maximum load at failure, stiffness, and energy absorbed at failure measured. All treatment groups demonstrated an increase in scar mass, but no group had a significant increase in scar load at failure at 6 weeks. The addition of 0.1 microg TGF-beta 2 led to a significant increase in scar stiffness. The addition of PDGF had no significant effect on any of the parameters studied. This study suggests the mechanical stiffness, but not the load at failure, of ligament scar can be significantly altered by the administration of TGF-beta 2.     

Physiological and mechanical adaptations of rabbit medial collateral ligament after anterior cruciate ligament transection

Progressive physiological and mechanical changes in the medial collateral ligament of the adult rabbit were investigated for as long as 48 weeks after disruption of the anterior cruciate ligament. Eighty-one New Zealand White rabbits were separated into experimental, sham-operated control, and normal control groups. The experimental group underwent unilateral transection of the right anterior cruciate ligament, sham-operated animals served as controls for comparison, and normal animals were evaluated as age-matched, undisturbed (no surgery) controls. Blood flow to the medial collateral ligament (as a physiological measure) and mechanical function (structural and material properties) were assessed at 6, 14, and 48 weeks. The results indicated that loss of the anterior cruciate ligament leads to early mechanical deterioration of the medial collateral ligament with a corresponding loss of physiological homeostasis. Six to 14 weeks after the transection, values for cross-sectional area of the medial collateral ligaments rapidly increased to 1.5 times control values. The ligament became twice as large as the control ligament by 48 weeks. Concomitantly, medial collateral ligament stress at failure of the medial collateral ligament complex decreased rapidly 6-14 weeks after the transection and eventually fell to one-half that of controls by 48 weeks. In terms of low-load behaviour, laxity and load relaxation were significantly greater than that of controls 6 weeks after transection and were further increased by 14 weeks. By 48 weeks, laxity values had recovered somewhat and load-relaxation measures had recovered to near control values. At both 6 and 14 weeks, a statistically significant elevation in blood flow was demonstrated compared with controls. By 48 weeks, however, blood flow was no different from that of the sham-operated control. Thus, early after transection of the anterior cruciate ligament, both low-load and high-load mechanical properties of the medial collateral ligament deteriorated and the rate of blood flow was temporarily elevated. By 48 weeks, blood flow declined to near control values, with a corresponding recovery in viscoelastic behaviour. These findings suggest that, after transection of the anterior cruciate ligament, viscoelastic behaviour of the medial collateral ligament may be related to changes in blood flow and that restoration of normal flow patterns and vascular responses may be linked to tne recovery of some low-load mechanical properties in the anterior cruciate ligament-deficient medial collateral ligament.     

Natural history of healing in the repaired medial collateral ligament

The purpose of this study was to assess morphologically the healing of repaired medial collateral ligaments (MCLs) in a rabbit model. Healing ligaments were examined grossly and histologically at various intervals, from 3 days to 2 ½ years after injury, and compared with the appearances of normal age-, sex-, and activity-matched controls. Results show that all ligaments healed by bridging scar formation rather than true ligament regeneration. Increases in cellularity and temporary matrix disorganization along the entire length of the ligaments during healing suggest a combination of diffuse mechanical damage from their failure in tension and regional inflammatory injury (in excess of surgical exposure alone) from the processes of degradation and replacement. Substance that was not injured physically in this model demonstrated complete recovery, while that replaced by scar did not. Healing processes were similar to those of other highly specialized soft tissues (e.g., tendons), with short phases of hemorrhage and inflammation, an intermediate phase of proliferation, and a prolonged phase of remodeling. Failure of repairs to maintain anatomical apposition of torn ends may have contributed to the delay of these healing processes by increasing scar mass. Incomplete scar remodeling at 2 ½ years, however, suggests much slower MCL healing than previously reported and probably, therefore, a longer period for potential treatment influence.     

肝细胞生长因子对大鼠内侧副韧带损伤后愈合的影响

[目的]观察肝细胞生长因子对大鼠内侧副韧带(medial collateral ligament,MCL)损伤愈合后组织学及生物力学特性恢复的作用。[方法]成年雄性SD大鼠46只,随机分为实验组和对照组,每组23只。制备右膝关节MCL断裂模型,实验组每只大鼠在伤口局部注入5μg肝细胞生长因子,然后以5-0可吸收线褥式缝合;对照组注入等量生理盐水后缝合伤口。至术后第4周,无损伤情况下将实验组及对照组愈合处韧带取下,进行组织学检查、电镜检查及生物力学特性检查。[结果]HE染色见实验组胶原纤维排列较整齐,而对照组胶原纤维排列紊乱。电镜观察见实验组胶原纤维直径较对照组明显增粗,差异有统计学意义(P<0.05)。实验组愈合的MCL极限负荷和刚度均大于对照组,差异有显著意义(P<0.01)。[结论]肝细胞生长因子可以在组织学及生物力学特性方面促进内侧副韧带损伤愈合。本实验可以为内侧副韧带损伤后优质愈合提供一种新方法及理论依据。     

Biochemical heterogeneity within the maturing rabbit medial collateral ligament

The purpose in this investigation was to determine the biochemical composition of the normal rabbit medial collateral ligament (MCL) along its length during growth and maturation. Water content and hexosamine concentration as an index of glycosaminoglycan content and collagen concentration were quantified and results compared statistically for anatomically identified MCL segments at various ages. These data demonstrate differences in all parameters at different locations along the ligament and at different ages. Biochemical differences were noted between midsubstance and periinsertional areas. There were subtle differences between the two insertion sites of this ligament at all ages. These results indicate that the rabbit MCL is not homogeneous biochemically along its length and that its matrix composition changes with growth and maturation.     

The healing medial collateral ligament following a combined anterior cruciate and medial collateral ligament injury--a biomechanical study in a goat model.

The ideal treatment of a combined anterior cruciate ligament (ACL) and medial collateral ligament (MCL) injury to the knee is still debated. In particular, the question of whether reconstruction of the ACL can provide the knee with sufficient multidirectional stability to allow for effective MCL healing needs to be better elucidated. Therefore, the first objective of this study was to quantify the changes in the function of goat knees between time-zero and 6 weeks following a combined ACL/MCL injury treated with ACL reconstruction. Using a robotic/universal force-moment sensor testing system, the kinematics of the knee and in situ forces in the ACL/ACL graft as well as in the sham-operated and healing MCL were evaluated in response to (1) a 67 N anterior-posterior (A-P) tibial load and (2) a 5 Nm varus-valgus (V-V) moment. The second objective was to evaluate the structural properties of the healing femur-MCL-tibia complex (FMTC) and the mechanical properties of the healing MCL at 6 weeks under uniaxial tension.In response to the 67 N A-P tibial load, the A-P translations for the experimental knee increased by as much as 4.5 times from time-zero to 6 weeks (p<0.05). Correspondingly, the in situ forces in the ACL graft decreased by as much as 45% (p<0.05). There was no measurable changes of the in situ force in the healing MCL. In response to a 5 Nm V-V moment, V-V rotations were twice as much as controls, but similar for both time periods. From time-zero to 6 weeks, the in situ forces in the ACL graft dropped by over 71% (p<0.05), while the in situ force in the healing MCL was as much as 35+/-19 N.In terms of the structural properties of the healing FMTC, the stiffness and ultimate load values at 6 weeks reached 53% and 29% of sham-operated contralateral controls, respectively (p<0.05). For the mechanical properties of the healing MCL substance, the values for tangent modulus and tensile strength were only 13% and 10% of sham-operated controls, respectively (p<0.05). These results suggest that the ACL graft stabilized the knee initially, but became loose over time. As a result, the healing MCL may have been required to take on excessive loads and was unable to heal sufficiently as compared to an isolated MCL injury.     

钒酸盐促进大鼠内侧副韧带损伤后组织学及生物力学特性恢复的研究

[目的]观察钒酸盐对大鼠内侧副韧带(medial collateral ligament,MCL)损伤愈合后组织学及生物力学特性的影响。[方法]选择40只成年雄性SD大鼠,随机分2组进行实验。制备右膝关节MCL断裂模型。在MCL断裂模型制备前1周至术后6周,实验组大鼠每日给予钒酸盐25mg灌胃1次,对照组给予等量生理盐水,至术后第6周,无损伤情况下将实验组及对照组愈合处韧带取下,进行Ⅰ型胶原免疫组织化学染色及生物力学特性检查。[结果]钒酸盐组愈合处韧带Ⅰ型胶原表达有明显增加,与对照组比较,差异有显著性意义(P0.05)。钒酸盐组愈合的MCL极载负荷和刚度均大于对照组,差异有显著意义(P0.01)。[结论]钒酸盐可以有效的改善愈合后韧带的组织学及生物力学特性。因此,本实验可以为将来临床治疗韧带损伤提供一种新的途径及理论依据。     

Medial collateral knee ligament healing: Combined medial collateral and anterior cruciate ligament injuries studied in rabbits

We examined the histological appearance and biochemical properties of the healing medial collateral ligament (MCL) of a rabbit knee after combined MCL and anterior cruciate ligament (ACL) injury treated with ACL reconstruction and with or without MCL repair. By so doing, we hoped to understand better our previous biomechanical observations (Ohno et al. 1995) and possibly learn where to focus future investigation into improving the quality of the healing MCL.

Ligaments were examined at 6 and 12 weeks of healing. We found healing of all ligaments with hypercellularity and fibroblast elongation along the axis of loading, as expected. Unexpected, however, was the finding of multiple osteophytes in both the repaired and nonrepaired specimens at the medial borders of the joint and at the MCL insertions. These were felt to affect possibly the biomechanics of the MCL by causing stress risers at the point where they undermine the ligament. Biochemically, we demonstrated a correlation between collagen content and hydroxypyridinium crosslinks and modulus of elasticity. While this implies that the modulus is dependent on collagen content and hydroxypyridinium crosslink density, modulus is also probably dependent on other factors such as collagen organization, type and internal structure. Overall, the detailed characterization and correlation between the histological, biochemical, and biomechanical properties of the healing MCL in the severe knee injury model provide insight into the functional behavior of the healing MCL.     

Soft-tissue “flaws” are associated with the material properties of the healing rabbit medial collateral ligament

This study evaluated microscopic flaws in the healing rabbit medial collateral ligament and their significance in terms of the material properties of this ligament during healing. A gap injury was created in the midsubstance of the medial collateral ligament in the right hindlimb of 15 skeletally mature (12 months old) New Zealand White rabbits. At postoperative intervals of 3, 6, or 14 weeks, histomorphometric analysis of the flaws was carried out in subgroups of animals. The medial collateral ligaments from four of the left hindlimbs (randomly selected) were used as uninjured contralateral controls. In one histologic section of each area of scar tissue and the analogous area in the controls, specified tissue flaws (blood vessels, fat cells, hypercellular areas, loose matrix, disorganized matrix, or a combination of these) were measured by four independent and blinded observers. The results showed that the mean total area of the flaws, as a percentage of the total section, and the mean area of the largest flaw decreased with healing time in each healing group but did not achieve control values by 14 weeks. Because it was not possible to test the healing medial collateral ligaments mechanically prior to measurement of the flaws (due to the destructive nature of failure testing), the data on the flaws were compared with the material strength and stiffness of a separate series of similarly injured and mechanically tested medial collateral ligaments (data published previously). A maximum likelihood statistical analysis showed a very strong functional association between the mean area of the largest flaw and the stress at failure (p < 0.004) and between the mean flaw area as a percentage of the total section area and the elastic modulus (p < 0.001). This study therefore demonstrates that it is possible to quantify material flaws in scar tissue in rabbit medial collateral ligaments, that these flaws become smaller with healing time as the scar remodels, and that flaws are functionally associated with the material properties of the ligament in this model (larger flaws with less tensile strength and more flaws with less stiffness).     

Exogenous transforming growth factor beta 1 alone does not improve early healing of medial collateral ligament in rabbits.

OBJECTIVE: To determine whether transforming growth factor beta 1 (TGF-beta1) improves early ligament healing. DESIGN: Experimental, controlled study of medial collateral ligaments (MCLs) in rabbits' knees. SETTING: Research laboratory. SUBJECTS: Sixteen skeletally mature, New Zealand White female rabbits. INTERVENTIONS: Ten rabbits had a standardized gap injury made in the MCL of both knees. Three weeks later, a second operation was performed to inject 7 microg of TGF-beta1 in a carrier solution into the right knee MCL, while the left knee MCL was injected with carrier alone. The rabbits were killed 3 weeks after the injection of TGF-beta1 (6 weeks after the original injury). Six of the rabbits (12 knees) had no operation on the MCL and served as external normal controls. OUTCOME MEASURES: Biomechanical measures of the femur-MCL-tibia complex. Histologic evaluation of MCL cell and matrix organization. Transmission electron microscopy measures of MCL fibril diameters. RESULTS: There were no statistically significant differences in the biomechanical measures, fibril diameter distributions and histologic evaluation of the injured MCLs treated with TGF-beta1 or carrier alone. Both groups of injured MCLs were significantly different from normal MCLs. CONCLUSIONS: The results indicate that the dosage and route of delivery of TGF-beta1 did not lead to overt improvement in the healing of the injured MCL. Whether different doses or delivery methods, alone or in combination with TGF-beta1, or other growth factors would lead to improvement remains to be determined.     

Myofibroblasts in the healing lapine medial collateral ligament: Possible mechanisms of contraction

The specific objective of this study was to determine the chronology of the appearance of the myofibroblast in the healing ligament. The overall goal of our work is to elucidate the cellular mechanism of contraction in this tissue. The myofibroblast has been found to be responsible for wound contraction in many tissues and to be the cause of the contracture in several pathological conditions. This cell type contains the actin isoform previously thought to be unique to smooth muscle cells and displays certain characteristic features at the ultrastructural level. In 26 New Zealand White male rabbits, the right medial collateral ligament was transected, whereas the left medial collateral ligament received a sham operation. The central third of the ligament (ligament scar tissue) was evaluated at 2, 3, 6, 8, 10, and 12 weeks postoperatively by immunohistochemical techniques, transmission electron microscopy, and Western blot analyses. Three other rabbits served as anatomic controls. During the early reparative phase (2 and 3 weeks after transection), there was an increase in the number of cells containing α-smooth muscle actin as well as augmentation of the α-smooth muscle actin content within each cell—a finding attributed to smooth muscle cells and pericytes associated with neovascularity. No myofibroblasts were detected at this stage, immediately postoperatively, or in the sham-operation controls. Ligaments in the remodeling phase of healing (6, 8, 10, and 12 weeks) exhibited α-smooth muscle actin in fibroblasts (myofibroblasts) as well as in vascular pericytes and smooth muscle cells. During this stage of healing, transmission electron microscopy demonstrated an increase in the number of cells displaying myofibroblastic features. It was estimated that at 12 weeks of healing 10% of the cells at the site of injury were myofibroblasts. This is the first definitive finding of myofibroblasts in the injury site of the healing ligament, to our knowledge. The appearance of myofibroblasts in the 6–12 week healing period, the interval during which the ligament has been shown to contract in studies by other investigators, is a rationale for a hypothesis that a cellular contractile apparatus comprising α-smooth muscle actin (i.e., the myofibroblast) may contribute to the recovery of original ligament length (and normal in situ strain).     

Origin of the medial ulnar collateral ligament.

The anatomic features of the origin of the anterior medial collateral ligament of the elbow were studied in 10 cadaver elbows to determine the percentage of the medial epicondyle that can be removed without violating the ligament, and whether or not this ligament attaches to the condyle as well as to the epicondyle. In all specimens the anterior medial collateral ligament originated exclusively from the anteroinferior surface of medial epicondyle and had no attachment to the condyle. Only 20% of the width of the medial epicondyle in the coronal plane can be removed without violating a portion of the origin of the anterior medial collateral ligament, an essential stabilizer of the elbow. Excision of the entire epicondyle for ulnar neuropathy would completely detach this ligament from its origin and might therefore potentiate instability. Since the ligament originates on the anteroinferior surface of the epicondyle, more bone can be removed with less violation of the anterior medial collateral ligament origin if the plane of the osteotomy lies between the sagittal and coronal planes.