PubMed · 728045
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P F Matzen, U Pfüller. 1978. [Trace elements in human articular cartilage].. https://pubmed.ncbi.nlm.nih.gov/728045/
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Osteoarthritis (OA), one of the most common age-related chronic disorders of articular cartilage, joints, and bone tissue, represents a major public health problem. Genetic studies have identified multiple gene variations associated with an increased risk of OA. These findings suggest that there is a large genetic component to OA and that the disorder belongs in the multigenetic, multifactorial class of genetic diseases. Studies of chondrodysplasias and associated hereditary OA have provided a better understanding of the role of structural genes in the maintenance and repair of articular cartilage, in the regulation of chondrocyte proliferation and gene expression, and in the pathogenesis of OA.
Although characterised by having a synovial membrane lining the nonarticulating surfaces within the joint capsule, in some ways the temporomandibular joint (TMJ) is an atypical joint. This paper highlights the differences between the TMJ and other movable joints with a description of the structure, innervation blood supply and musculature. Also included are details of how the TMJ moves--the effectors of movement and the various reflexes controlling movement of the joint.
Immunohistochemical studies have confirmed the innervation of bone with neuropeptidergic neurons containing vasoactive intestinal polypeptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP). In this study, we report effects of VIP on connective tissue cell metabolism. VIP stimulated PGE2 production in human articular chondrocytes, human osteoblast-like cells and human synovial cells, however, stromelysin production was unaffected. VIP also stimulated cAMP production in human osteoblast-like cells, but not in human articular chondrocytes or synovial cells. These findings are suggestive of a role of VIP in connective tissue cell metabolism which may contribute to the inflammatory processes of arthritis.