Aim: Osteoarthritis can be a progressive disabling disease, which results from the pathological imbalance of degradative and reparative processes. The synovium, bone, and cartilage are each well established sites involved in the pathophysiological mechanisms that lead to progressive joint degeneration. However, the role of meniscus is not known enough. We studied the distribution of cartilage oligomeric matrix protein (COMP) in man menisci and its changes in osteoarthritis

Patients and Methods: We studied 30 internal menisci from patients with knee osteoarthritis that underwent a total knee arthroplasty and meniscal tissue get from partial arthroscopic meniscectomy in 5 young patients that suffered internal meniscus tear within three months after the damage.

Meniscal samples were processed for histology, immunohistochemistry and in situ hybridization, for assessment of cell density, cells actively dividing as well as apoptotic cells, distribution of COMP and estimate the proteoglycan content.

Results: Osteoarthritic meniscus demonstrated areas depleted of cells and significant decrease in COMP immunostaining. Cell clusters were found around meniscal tears. We did not find cells activity dividing in the osteoarthritic group, but there were dividing cells in meniscectomy group. Proteoglycan staining was decreased in meniscus from osteoarthritis group.

Conclusions: Osteoarthritis leads to decrease cell population in menisci, loose of COMP as well as altered matrix organization. The role of meniscus in osteoarthritis of the knee is no clear but our results demonstrate changes in COMP and cells in osteoarthritis menisci. These changes reveal an altered scaffold and changes in the meniscus function. Perhaps these alterations have influence on development of knee osteoarthritis.

Meniscus injury is one of the causes of secondary osteoarthritis (OA). Cartilage oligomeric matrix protein (COMP) is a major component of the extracellular matrix of the musculoskeletal system. This study was undertaken to evaluate the changes occurring in meniscus from the knees of anterior cruciate ligament (ACL) transected rabbits during the early stages of OA development, especially regarding COMP changes.

Ten skeletally mature white New Zealand male rabbits underwent ACL transaction of the right knee joint. Left knee joints were used as controls. Animals were sacrificed at 4 and 12 weeks post-surgery. Meniscal tissues were processed for histology and immunohistochemistry.

The number of cells and positive cells were counted per high-power field (HPF). Anti-COMP antiserum was obtained according to Hauser et al. with minor modifications. Monoclonal Ki67 antibody was used to find out cells undergoing active division. TUNEL reaction was used for the study of apoptosis. Alcian blue staining was used to study glycosaminoglycans.

At 4 weeks post-ACL section 2/5 of the medial menisci presented with incomplete vertical posterior tears, while all lateral menisci were no altered. At 12 weeks post-ACL section 5/5 of the medial menisci and 2/5 of lateral menisci presented tears.

At 4 weeks postsurgery menisci showed: a weak increase of cells with a significant increase of cells undergoing active division; an increase in the number of apoptotic cells; glycosaminoglycans staining was increased and COMP staining was weakly increased. At 12 weeks postsurgery cells per HPF reverted to normal number; the number of cells undergoing active division decrease below normal; whereas the number of apoptotic cells was still elevated; glycosaminoglycans staining was more elevated than at 4 weeks postsurgery and COMP staining of extracellular matrix remain elevated.

Areas of large and abundant cell clusters were seen post-ACL around menisci tears.

We concluded that after ACL transaction, extracellular matrix changes and altered cell distribution occur early in the meniscus. Cellular division as well as apoptosis occur early too. Elevated concentrations of COMP after ACL transection might indicate meniscus changes early in osteoarthritis process.

Introduction and Objectives: Acetabular bone defects in hip replacement therapy present difficulties in terms of achieving stable, long-lasting fixation of the implant. Various surgical techniques exist to correct this problem. In this study we analysed the clinical and radiographic progression of a series of patients treated with fragmented grafts using the X-Change acetabular revision method.

Materials and Methods: From November 1988 to February 1998, 24 patients were treated, with an average age of 64.5 (±7) at the time of surgery. Patients were evaluated clinically preoperatively and were evaluated using the Harris scale at the end of the follow-up period. Defects were classified according to Paprosky’s classification of acetabular bone defects. Radiographic studies were used to evaluate upward and medial migration of the acetabular component and to look for signs of loosening. Follow-up time was a minimum of 12 months, with an average of 56.2 months.

Results: Average score on the Harris scale went from 49.7 points (±12.9) preoperatively to 88.2 points (±14.1) on follow-up. There was no graft incorporation in 5 patients (20%). There were 3 infections, 2 prosthetic dislocations, and one case of pulmonary thromboembolism. Upward migration of the cup (from the upper obturator line) was 0.48 cm (±0.72) postoperatively and 0.48 cm (±0.84) at follow-up. Medial migration (measured from Kohler’s line) was −0.16 cm (±0.50) postoperatively and −0.09 cm (±0.56) on follow-up. Cup angle (measured at the anteroposterior plate of the pelvis) changed from 48.9° (±5°) to 56° (±7°) at the conclusion of the follow-up period.

Discussion and Conclusions: This reconstructive technique provides stable, long-lasting fixation of the implant with complication rates similar to those described in the literature. We consider it a useful technique in the management of this type of defect, particularly in young patients who need to recover acetabular bone stock.