The findings suggest an active role of VEGF in the pathogenesis of OA and render support to a possible role for subchondral bone sclerosis in the pathogenesis of cartilage degradation.
Osteogenesis around implants is affected by the physical and chemical characteristics of the biomaterials used. The osteoprogenitor cells must migrate to the implant site and synthesize and secrete a mineralizable extracellular matrix. Because this is neo-bone formation, the mechanism by which the cells calcify their matrix involves extracellular organelles called matrix vesicles in a process termed "primary mineralization". Two different methods for assessing the effects of implant materials on primary mineralization are presented in this report. In the first approach, different implant materials used in dentistry and orthopedic surgery were placed in rat tibial bones after marrow ablation. Two groups of implants were used, bone-bonding and non-bonding materials. We examined the effects of the materials on calcification morphometrically by quantitating changes in matrix vesicle morphology and distribution in endosteal tissue around implants as compared with normal endosteal bone healing. In addition, matrix vesicles were isolated from the endosteal tissue around the implant as well as from the contralateral limb and were examined biochemically. The results demonstrated that bone-bonding materials induced a greater increase in matrix vesicle enzyme activity than did non-bonding materials. However, all materials caused changes in matrix vesicles that were different from those seen in normal endosteal bone formation following injury. The effects of implant materials on biochemical markers of mineralization, including specific activities of matrix vesicle alkaline phosphatase and phospholipase A2 and phosphatidylserine content, demonstrated a high correlation with the morphometric observations with regard to enhancement and/or delay of primary mineralization. In the other approach, we used a radioisotopic method to evaluate the effects of implant materials on primary mineralization. This analysis revealed that implants alter bone healing, as shown by the differential uptake of 99mTc and 32P in different bone compartments. Decreased 32P uptake by the organic phase in the presence of bone-bonding implants suggests that cleavage of 99mTcMD32P into its technetium and methylene diphosphonate moieties was inhibited by the presence of the implants. In summary, these approaches to evaluating the effects of materials on primary mineralization demonstrate that the marrow ablation model can easily distinguish between bone-bonding and non-bonding materials. The use of this model can be valuable in the development of new materials.
The interface of alkali-poor glass ceramic implanted in femora of male Sprague-Dawley rats shows soft tissue, chondroid, osteoid, and bone in connection with the implant. The ultrastructure of the interface with soft tissue mainly exhibits a corrosion process, during which the dissolution of the crystalline phase of the glass ceramic precedes the dissolution of the glassy phase. Macrophages are involved in this process phagocytosing debris of the glassy phase and removing as well as dissolving the remainders of the glass ceramic. Under circumstances not yet fully understood, the corrosion stops, and ground substance like material is deposited, which can be, at least partially, mineralized. After the disappearance of macrophages, chondroblasts, and/or osteoblasts lay down collagen fibrils and ground substance in which matrix vesicles are discernible, representing initial foci of mineralization. Areas with bone connection display collagen fibers and deposits of apatite crystals in close relationship to the bulk glass ceramic as well as small particles mainly derived from the glassy phase of the implant, providing the micromorphological substrate for the shearing and tensile strength of the interface between glass ceramic and bone.
The present paper reports alterations in osteogenesis recorded in mandibular condyles 3-18 days after the removal of marrow tissue from tibial bones. Computerized histomorphometric evaluation of undecalcified condyles revealed a considerable increase in the thickness of condylar cartilage, in particular, the zone of provisional calcification. Measurements of the subcartilaginous trabecular bone suggested an increase in the number of osteoblasts and in their activity. The systemic enhancement of osteogenesis may be initiated by circulating factors released at the affected limb during regeneration of the marrow.
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