Background: The successful treatment of chondral and osteochondral defects of the weight-bearing surfaces is a challenge for orthopaedic surgeons. Autologous osteochondral transplantation is one method that can be used to create hyaline or hyaline-like repair in the defect area. This paper describes the results after ten years of clinical experience with autologous osteochondral mosaicplasty.

Methods: Clinical scores, imaging techniques, arthroscopy, histological examination of biopsy samples, and cartilage stiffness measurements were used to evaluate the clinical outcomes and quality of the transplanted cartilage in 831 patients undergoing mosaicplasty.

Results: According to these investigations, good-to-excellent results were achieved in 92% of the patients treated with femoral condylar implantations, 87% of those treated with tibial resurfacing, 79% of those treated with patellar and/or trochlear mosaicplasties, and 94% of those treated with talar procedures. Long-term donor-site disturbances, assessed with use of the Bandi score, showed that patients had 3% morbidity after mosaicplasty. Sixty-nine of eighty-three patients who were followed arthroscopically showed congruent gliding surfaces, histological evidence of the survival of the transplanted hyaline cartilage, and fibrocartilage filling of the donor sites. Complications of the surgery included four deep infections and thirty-six painful postoperative hemarthroses.

Conclusions: On the basis of these promising results and those of other similar studies, autologous osteochondral mosaicplasty appears to be an alternative for the treatment of small and medium-sized focal chondral and osteochondral defects of the weight-bearing surfaces of the knee and other weight-bearing synovial joints.

Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints: ten years of experimental and clinical experience.

Joint pain and loss of mobility are among the most common causes of impairment in middle-aged and older people36,134. In many instances, the degeneration of articular cartilage and alterations in other joint tissues that result from the loss of structure and function of articular cartilage cause the pain and the loss of motion28,46,47,85,118,150. This occurs most frequently in the clinical syndrome of idiopathic or primary osteoarthrosis, but it may also result from joint injury or from developmental, metabolic, and inflammatory disorders that destroy the articular surface, causing secondary osteoarthrosis28,46,118. An understanding of the degeneration of articular cartilage, osteoarthrosis, and the potential for restoring an articular surface depends to a large extent on an appreciation of the biological behavior and the responsiveness of articular cartilage to injury and disease. Of considerable importance is the observation, first reported centuries ago and confirmed by multiple investigators over the last fifty years, that adult articular cartilage does not have the capacity to repair structural damage resulting from injury or disease29,32,71. This observation has contributed to the view that adult articular cartilage is an inert bearing surface, like high-density polyethylene or metal, and that degeneration of the articular surface with age is the result of mechanical wear with inevitable, irreversible loss of structure and mechanical performance resulting from joint use62. The implication of this view is that, other than limiting joint use or loading, little or nothing can be done to prevent the degeneration of articular cartilage, and the most appropriate treatment for advanced degeneration of cartilage leading to the clinical syndrome of osteoarthrosis is replacement of the articular surface. Alternatively, if articular cartilage is …

http://jbjs.org/content/jbjsam/79/4/612.full.pdf

Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Articular Cartilage. Part II: Degeneration and Osteoarthrosis, Repair, Regeneration, and Transplantation*†

The acute and repetitive impact and torsional joint loading that occurs during participation in sports can damage articular surfaces causing pain, joint dysfunction, and effusions. In some instances, this articular surface damage leads to progressive joint degeneration. Three classes of chondral and osteochondral injuries can be identified based on the type of tissue damage and the repair response: (1) damage to the joint surface that does not cause visible mechanical disruption of the articular surface, but does cause chondral damage and may cause subchondral bone injury; (2) mechanical disruption of the articular surface limited to articular cartilage; and (3) mechanical disruption of articular cartilage and subchondral bone. In most instances, joints can repair damage that does not disrupt the articular surface if they are protected from additional injury. Mechanical disruption of articular cartilage stimulates chondrocyte synthetic activity, but it rarely results in repair of the injury. Disruption of subchondral bone stimulates chondral and bony repair, but it rarely restores an articular surface that duplicates the biologic and mechanical properties of normal articular cartilage. In selected patients, surgeons have used operative treatments including penetrating subchondral bone, soft tissue grafts, and cell transplants and osteochondral autografts and allografts to restore articular surfaces after chondral injuries. Experimental studies indicate that use of artificial matrices and growth factors also may promote formation of a new joint surface. However, an operative treatment of an articular surface injury that will benefit patients must not just provide a new joint surface, it must produce better long-term joint function than would be expected if the injury was left untreated or treated by irrigation and debridement alone. Therefore, before selecting a treatment for a patient with an articular cartilage injury, the surgeon should define the type of injury and understand its likely natural history.

Articular cartilage injuries.

Background: Osteochondritis dissecans of the knee is a challenging clinical problem. We previously reported on the early successful results of autologous chondrocyte transplantation for the treatment of focal cartilage defects. The purpose of the present study was to assess the intermediate to long-term results of this technique in a large group of patients with osteochondritis dissecans. Methods: Fifty-eight patients with radiographically documented osteochondritis dissecans of the knee underwent treatment with autologous chondrocyte transplantation between 1987 and 2000 and were assessed clinically with use of standard rating scales. Twenty-two patients consented to arthroscopic second-look evaluation of graft integrity. Results: The mean age of the patients at the time of autologous chondrocyte transplantation was 26.4 years (range, fourteen to fifty-two years). Seven patients were less than eighteen years old. Thirty-five patients (60%) had juvenile-onset disease, and forty-eight patients (83%) had had a mean of 2.1 prior operations. The defect was located on the medial femoral condyle in thirty-nine patients and on the lateral femoral condyle in nineteen. The mean lesion size was 5.7 cm 2 (range, 1.5 to 12.0 cm 2 ), and the mean defect depth was 7.8 mm (range, 4 to 15 mm). After a mean duration of follow-up of 5.6 years, 91% of the patients had a good or excellent overall rating on the basis of a clinician evaluation and 93% had improvement on a patient self-assessment questionnaire. The Tegner-Wallgren, Lysholm, and Brittberg-Peterson VAS scores were all improved. The macroscopic quality of graft integrity averaged 11.2 on a 12-point scale, with only one graft having a score of 90% of patients. We recommend the wider use of autologous chondrocyte transplantation for this condition.

Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: results at two to ten years.

Articular cartilage can tolerate a tremendous amount of intensive and repetitive physical stress. However, it manifests a striking inability to heal even the most minor injury. Both the remarkable functional characteristics and the healing limitations reflect the intricacies of its structure and biology. Cartilage is composed of chondrocytes embedded within an extracellular matrix of collagens, proteoglycans, and noncollagenous proteins. Together, these substances maintain the proper amount of water within the matrix, which confers its unique mechanical properties. The structure and composition of articular cartilage varies three-dimensionally, according to its distance from the surface and in relation to the distance from the cells. The stringent structural and biological requirements imply that any tissue capable of successful repair or replacement of damaged articular cartilage should be similarly constituted. The response of cartilage to injury differs from that of other tissues because of its avascularity, the immobility of chondrocytes, and the limited ability of mature chondrocytes to proliferate and alter their synthetic patterns. Therapeutic efforts have focused on bringing in new cells capable of chondrogenesis, and facilitating access to the vascular system. This review presents the basic science background and clinical experience with many of these methods and information on synthetic implants and biological adhesives. Although there are many exciting avenues of study that warrant enthusiasm, many questions remain. These issues need to be addressed by careful basic science investigations and both short- and long-term clinical trials using controlled, prospective, randomized study design.

Articular Cartilage Repair

Osteochondritis dissecans in two adults with a large osteochondral defect on the weight-bearing surface was treated by transplantation of an autogeneic osteochondral fragment. The graft was transplanted from the normal portion of the medial femoral condyle, which in extension was in contact with nei

The transplantation of an autogeneic osteochondral fragment for osteochondritis dissecans of the knee.

The rotational alignment tヲfthe lovver limbs of 24 patients who developed r巴currentdislocation of the patella were measured by means of computed axial tomography. The femoral anteversion and the external rotation of the knee joint of these patients respectively showed 31.9土15.2° and 9.2土6.8° on the average. These figures were significantly larger than those of the control. The average external tibial torsion was 23.l土8.8°,showing no significant difference from that of the control. The external rotation of the knee joint of the patients with generalized joint laxity were significantly greater than that of the patients without g巴neralizedjoint laxity. Such rotational malalignment as observed in these patients can be regarded as a cause of recurr巴ntdislocation of the patella. Introduction Among what hav巴beenreported as possible causes of recurrent dislocation of the patella are trochlea dysplasia, patella dysplasia, vastus medialis obliques dysplasia, increased Q-angle, high riding patella, joint laxity and rotational malalignment such as femoral anteversion or external tibial torsiona,4,s,s,9>. However, the objective analysis of rotational alignment has not been reported in recurrent dilocation of the patella. We report here the measurements of the rotational alignment of the lower limbs of the patients with recurrent dislocation of the patella by computed axial tomography (CAT). Patients and Methods Twenty-five patients, 20 women and 4 men with recurrent dislocation of the patella, participated in the study. Their median age was 21 years, range 13 to 34 y巴ars. The median ag巴at the fin;t dislocation was 14.3 years, range 7 to 20 years. The joint involved consisted of 15 right patellae and 13 left. The rotational alignment of the 48 lower limbs of the 24 patients was ex『 amined by CAT scan of the proximal femur, knee joint and ankle joint. When the CAT scan

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The Rotational Alignment of the Lower Limbs in Recurrent Dislocation of the Patella

Measurement of the intracellular free calcium ion concentration using an inverted epi-illumination cytofluorometer

We carried out DNA cytofluorometry with propidium iodide stain on the 17 cases of soft tissue tumors including giant cell tumor of the tendon sheath, pigmented villonodular synovitis, 2 hemangiomas, 3 lipomas, 5 schwannomas, 3 neurofibromas, liposarcoma and synovial sarcoma. The benign tumors were characterized by regular polyploidization with very few S-phase cells, indicating slow tumor growth. Most of the malignant soft tissue tumors were associated with remarkable polyploidization with an increase in S-phase cells. However, some malignant tumors did not show polyploidization. We concluded, therefore, that an increase in S-phase cells is an important, cytofluorometric criterion for malignancy of soft tissue tumors.

DNA cytofluorometry of soft tissue tumors

https://www.jstage.jst.go.jp/article/jbmm1983/1/1/1_1_1/_pdf

Fumiharu Yamashita

Papers

The transplantation of an autogeneic osteochondral fragment for osteochondritis dissecans of the knee.

The Rotational Alignment of the Lower Limbs in Recurrent Dislocation of the Patella

Measurement of the intracellular free calcium ion concentration using an inverted epi-illumination cytofluorometer

DNA cytofluorometry of soft tissue tumors

An Attempt to apply Feulgen-DNA Cytofluorometry to the Analysis of the Rat Chondrocytes