John G. Lane

Follow-up of Osteochondral Plug Transfers in a Goat Model A 6-Month Study

Background Osteochondral transfer procedures are increasingly used to resurface full-thickness articular cartilage defects. There has not been long-term assessment/description of autogenous donor and recipient sites. Hypothesis The healing process occurs at the donor/host cartilage and bone interfaces. Study Design Histologic, biochemical, and biomechanical changes were assessed 6 months after an osteochondral transfer in a goat model. Methods Eight adult goats were studied. In the 6 osteochondral transfer goats, 2 autogenous plugs were transferred from the femoral trochlea to defects in the weightbearing portion of the medial femoral condyle. The goats were allowed free range for 6 months. Randomly assigned plugs were assessed. Results Knees of the sacrificed animals had preservation of the joint space with mild chondromalacic changes in both transfer and contralateral control groups. Histologically, no evidence of cartilage (host/donor) healing was seen. Subchondral bone of the plug was contiguous with the surrounding recipient bone. Cellular viability in the autogenous osteochondral plug was seen, and 35SO4 uptake of the articular cartilage was not statistically different from the contralateral control condyle. The indentation stiffness of the transfer plug (mosaicplasty) and the contralateral donor site were similar—much stiffer than normal cartilage including surrounding condylar cartilage. Large structural stiffness of transferred cores and donor sites appeared to be related to their thinner cartilage layer. Conclusions At 6-month follow-up, a cleft between host and transferred articular regions remained, with no integration between the two. Clinical Relevance Autogenous transplantation of osteochondral plugs is possible with integration of subchondral bone and preservation of chondral viability.

Arthroscopic staple capsulorrhaphy: A long-term follow-up

Fifty-four shoulders with recurrent anterior shoulder instability were evaluated following arthroscopic staple capsulorrhaphy. Average follow-up for those with only the index surgery was 39 months. Eighteen patients (33%) experienced at least one episode of postoperative instability. Ten underwent an open reconstructive procedure. Routine radiographs at time of follow-up demonstrated loose staples in 15% of asymptomatic patients. Range of motion was preserved following surgery. There was no loss of forward elevation. An average of 5 degrees of external rotation and one spinal segment in internal rotation were lost following surgery. Forty-three percent of overhead athletes were able to return to their preinjury level of activity. Caution should be taken when considering arthroscopic staple capsulorrhaphy as recurrence rates are higher than those following open reconstruction. However, range of motion and functional level are well-maintained. When capsulorrhaphy is performed, consideration should be given to routine staple removal following adequate capsular healing.

A morphologic, biochemical, and biomechanical assessment of short-term effects of osteochondral autograft plug transfer in an animal model.

PURPOSE The objective of this study was to assess the short-term changes that occur after an osteochondral autograft plug transfer from the femoral trochlea to the medial femoral condyle in a goat model. TYPE OF STUDY Articular cartilage repair animal study. METHODS Six adult male goats were used in this study. Two 4.5-mm osteochondral plugs were transferred from the superolateral femoral trochlea to 2 recipient sites in the central portion of the medial femoral condyle for a survival period of 12 weeks. Postmortem, the global effects of the procedure were assessed by gross morphologic inspection and by analyzing the synovial DNA for inflammatory response. The recipient sites were also evaluated histologically and biomechanically. Metabolic activity was determined by (35)SO(4) uptake, and viability was assessed using a live/dead stain and by confocal laser microscopy. RESULTS There was no evidence of significant gross morphologic or histologic changes in the operative knee as a result of the osteochondral donor or recipient sites. The patella, tibial plateau, and medial meniscus did not show any increased degenerative changes as a result of articulating against the donor or recipient sites of the osteochondral autografts. Analysis of synovial DNA revealed no inflammatory response. Biomechanically, 6- to 7-fold greater stiffness was noted in the cartilage of the transferred plugs compared with the control medial femoral condyle. Furthermore, on histologic examination, the healing subchondral bone interface at the recipient site had increased density. Glycosaminoglycan synthesis as determined by (35)SO(4) uptake was upregulated in the transplanted cartilage plug relative to the contralateral control, showing a repair response at the site of implantation. And finally, confocal microscopy showed 95% viability of the transferred plugs in the medial femoral condyle region. CONCLUSIONS Our findings demonstrate the ability to successfully transfer an osteochondral autograft plug with maintenance of chondrocyte cellular viability. The transferred cartilage is stiffer than the control medial femoral condyle cartilage, and there is concern regarding the increased trabecular mass in the healing subchondral plate, but these do not result in increased degenerative changes of the opposing articular surfaces in the short term.

Can osteochondral grafting be augmented with microfracture in an extended-size lesion of articular cartilage?

Background: Both microfracture and osteochondral autografting procedures have been useful in treating osteochondral lesions. Hypothesis: Combining microfracture and osteochondral autografting procedures can extend the size of lesions that can be treated with either technique. Study Design: Descriptive laboratory study. Methods: Eight adult goats underwent osteochondral autograft transfer of a 4.5-mm femoral trochlea plug into an 8-mm full-thickness chondral defect. Microfracture was performed in the gap region surrounding the autograft. The animals were allowed normal activity until the end of the experiment at 6 months. At harvest, the knees were assessed grossly, and then evaluation was performed by histology, histomorphometry, biochemistry, and biomechanics. Results: The osteochondral plugs healed well, with integration of the bone and preservation of the chondral cap. The chondral gap between the host site articular cartilage and the transferred plug had decreased from 3 mm at implant to less than 0.1 mm. Histologic analysis demonstrated regions of variable cartilage repair, with integration of the cartilage layer at some sites but incomplete healing at others. Histomorphometry demonstrated filling of the chondral gap to 75% to 85% of the normal volume. Biochemical analysis revealed greater than 90% type II collagen at most sites, with some areas containing 80% type II collagen. Biomechanical indentation testing indicated that the repaired area had variable thickness and stiffness, with a trend of increased stiffness in the bulk graft and decreased softness at the proximal microfracture interface site. Conclusion: The performance of a combined microfracture and osteochondral autograft transfer procedure to resurface a large chondral defect appears promising. Clinical Relevance: This combined technique shows promise for treatment of large chondral defects with a single operative procedure with autogenous tissue that is safe and potentially would have a shorter period of rehabilitation, similar to that of osteochondral transfers and microfracture, in a cost-effective setting.

Matrix Assessment of the Articular Cartilage Surface After Chondroplasty With the Holmium:YAG Laser

The goal of this study was to evaluate, histologically and biochemically, repair of the articular cartilage in a rabbit joint after the use of the holmium:yttrium-alumi num-garnet laser in a cartilage chondroplasty model. In 30 New Zealand White rabbits, chondroplasty was per formed with the laser at an intensity of 0.8 J at a rate of 10 Hz. The animals were sacrificed 12 weeks after surgery. Histologically, the safranin O staining index of proteoglycan correlated well with the biochemical re sults, illustrating a decrease of proteoglycan in the repaired articular cartilage after laser articular cartilage chondroplasty. The damaged articular cartilage sur face after the laser application was extensive. The damaged area observed was gradually distributed along the radius from the central point of the laser beam application. Biochemically, the amount of glycos aminoglycan in the repaired tissue (8 ± 2 mg of hex osamine per gram of dry cartilage) was statistically less when compared with that in the sham-treated tissue (40 ± 5 mg). The amount of sulfate incorporated into proteoglycans was 8 to 10 times less in the chondro plasty model compared with the control, suggesting that cell viability was greatly reduced in the treated tissues or expression of proteoglycans was greatly reduced. In the subchondral area, histologic evaluation showed the lack of osteocytes in lacunae of the bone tissue after use of laser energy. The architecture of the subchondral bone in the chondroplasty area was dam aged, with damage also seen in the membranes of the blood vessels.

Effect of Supraspinatus Tendon Injury on Supraspinatus and Infraspinatus Muscle Passive Tension and Associated Biochemistry

BACKGROUND Injury to the supraspinatus and infraspinatus tendons and the associated atrophic changes to the muscle remain a common clinical problem. Specifically, increased muscle stiffness has been implicated in failure of the repair and poor functional outcomes. We present a comparison of the passive mechanical properties and associated biochemical studies from patients with and without torn supraspinatus tendons. METHODS Muscle biopsy samples (n = 40) were obtained from twenty patients undergoing arthroscopic shoulder surgery. Passive mechanical tests of both individual fibers and fiber bundles as well as analysis of titin molecular weight and collagen content were performed. RESULTS At the fiber-bundle level, a significant increase in passive modulus was observed between intact supraspinatus samples (mean [and standard error], 237.41 ± 59.78 kPa) and torn supraspinatus samples (515.74 ± 65.48 kPa) (p < 0.05), a finding that was not observed at the single fiber level. Within the torn samples, elastic moduli in the supraspinatus were greater than in the infraspinatus at both the single fiber and the fiber-bundle level. There was a significant positive correlation between bundle elastic modulus and collagen content (r(2) = 0.465) in the supraspinatus muscle as well as a significant positive correlation between tear size and bundle elastic modulus (r(2) = 0.702) in the torn supraspinatus samples. CONCLUSIONS Supraspinatus muscle passive tension increases in a tendon tear size-dependent manner after tendon injury. The increase in muscle stiffness appears to originate outside the muscle cell, in the extracellular matrix. CLINICAL RELEVANCE Muscle stiffness after rotator cuff tendon injury is more severe with large tears. This finding supports the concept of early intervention, when tendon tears are smaller, and interventions targeting the extracellular matrix.

Muscle progenitor cell regenerative capacity in the torn rotator cuff

Chronic rotator cuff (RC) tears affect a large portion of the population and result in substantial upper extremity impairment, shoulder weakness, pain, and limited range of motion. Regardless of surgical or conservative treatment, persistent atrophic muscle changes limit functional restoration and may contribute to surgical failure. We hypothesized that deficits in the skeletal muscle progenitor (SMP) cell pool could contribute to poor muscle recovery following tendon repair. Biopsies were obtained from patients undergoing arthroscopic RC surgery. The SMP population was quantified, isolated, and assayed in culture for its ability to proliferate and fuse in vitro and in vivo. The SMP population was larger in muscles from cuffs with partial tears compared with no tears or full thickness tears. However, SMPs from muscles in the partial tear group also exhibited reduced proliferative ability. Cells from all cuff states were able to fuse robustly in culture and engraft when injected into injured mouse muscle, suggesting that when given the correct signals, SMPs are capable of contributing to muscle hypertrophy and regeneration regardless of tear severity. The fact that this does not appear to happen in vivo helps focus future therapeutic targets for promoting muscle recovery following rotator cuff repairs and may help improve clinical outcomes.

Muscle Gene Expression Patterns in Human Rotator Cuff Pathology

BACKGROUND Rotator cuff pathology is a common source of shoulder pain with variable etiology and pathoanatomical characteristics. Pathological processes of fatty infiltration, muscle atrophy, and fibrosis have all been invoked as causes for poor outcomes after rotator cuff tear repair. The aims of this study were to measure the expression of key genes associated with adipogenesis, myogenesis, and fibrosis in human rotator cuff muscle after injury and to compare the expression among groups of patients with varied severities of rotator cuff pathology. METHODS Biopsies of the supraspinatus muscle were obtained arthroscopically from twenty-seven patients in the following operative groups: bursitis (n = 10), tendinopathy (n = 7), full-thickness rotator cuff tear (n = 8), and massive rotator cuff tear (n = 2). Quantitative polymerase chain reaction (qPCR) was performed to characterize gene expression pathways involved in myogenesis, adipogenesis, and fibrosis. RESULTS Patients with a massive tear demonstrated downregulation of the fibrogenic, adipogenic, and myogenic genes, indicating that the muscle was not in a state of active change and may have difficulty responding to stimuli. Patients with a full-thickness tear showed upregulation of fibrotic and adipogenic genes; at the tissue level, these correspond to the pathologies most detrimental to outcomes of surgical repair. Patients with bursitis or tendinopathy still expressed myogenic genes, indicating that the muscle may be attempting to accommodate the mechanical deficiencies induced by the tendon tear. CONCLUSIONS Gene expression in human rotator cuff muscles varied according to tendon injury severity. Patients with bursitis and tendinopathy appeared to be expressing pro-myogenic genes, whereas patients with a full-thickness tear were expressing genes associated with fatty atrophy and fibrosis. In contrast, patients with a massive tear appeared to have downregulation of all gene programs except inhibition of myogenesis. CLINICAL RELEVANCE These data highlight the difficulty in treating massive tears and suggest that the timing of treatment may be important for muscle recovery. Specifically, earlier interventions to address tendon injury may allow muscles to respond more appropriately to mechanical stimuli.

Matrix Assessment of the Articular Cartilage Surface after Chondroplasty with the Holmium: Yttrium-Aluminum-Garnet Laser A Long-Term Study

A long-term in vivo study was performed to assess biochemical changes after laser repair of articular cartilage. Forty New Zealand White rabbits were sacrificed 26 weeks after undergoing an articular cartilage chondroplasty with use of a holmium:yttrium-aluminum-garnet laser at 0.8 joules per pulse and a rate of 10 Hz. Glycosaminoglycan content in the repaired tissue decreased significantly with both perpendicular (19.59 ± 5.6 μg hexosamin/mg of dry tissue) and tangential delivery (14.78 ± 4.5 μg/mg) compared with the sham-treated tissue (39.6 ± 5.0 μg/mg). Cellular viability was also significantly decreased. Sulfate incorporation was decreased to 203 ± 142 cpm/mg of dry cartilage in the tangential mode and 461 ± 209 cpm/mg in the tangential mode, compared with the sham at 1845 cpm/mg. Uptake of [3H]thymidine decreased to 463 ± 473 cpm/mg of dry tissue and 455 ± 170 cpm/mg in the tangential and perpendicular modes, respectively, compared with 2465 cpm/mg in the sham tissue. There were no significant differences between the tangential and perpendicular delivery modes in any assessments performed. The short-term chondrocyte destruction previously noted in a 12-week study after laser treatment was not reversed during a longer-term 26-week study, and cellular viability was not recovered, suggesting that the loss of chondrocyte function may be permanent.

The role of the peripheral and central nervous systems in rotator cuff disease

Rotator cuff (RC) disease is an extremely common condition associated with shoulder pain, reduced functional capacities, and impaired quality of life. It primarily involves alterations in tendon health and mechanical properties that can ultimately lead to tendon failure. RC tendon tears induce progressive muscle changes that have a negative impact on surgical reparability of the RC tendons and clinical outcomes. At the same time, a significant base of clinical data suggests a relatively weak relationship between RC integrity and clinical presentation, emphasizing the multifactorial aspects of RC disease. This review aims to summarize the potential contribution of peripheral, spinal, and supraspinal neural factors that may (1) exacerbate structural and functional muscle changes induced by tendon tear, (2) compromise the reversal of these changes during surgery and rehabilitation, (3) contribute to pain generation and persistence of pain, (4) impair shoulder function through reduced proprioception, kinematics, and muscle recruitment, and (5) help explain interindividual differences and response to treatment. Given the current clinical and scientific interest in peripheral nerve injury in the context of RC disease and surgery, we carefully reviewed this body of literature with a particular emphasis on suprascapular neuropathy that has generated a large number of studies in the past decade. Within this process, we highlight the gaps in current knowledge and suggest research avenues for scientists and clinicians.