Search PubMed⌕ Search

Biomedical subjects

T D Cooke

Publications and source records attributed to T D Cooke.

At least 73 records · Page 4Linked to original sources
PubMed1986

Clinical features of osteoarthritis in the elderly.

Osteoarthritis (OA), the commonest form of arthritis, is an important cause of chronic morbidity. Assessment of patients with OA can be improved by the recognition of several patterns with which this disorder can present. When these patterns are delineated by a careful history, physical examination, appropriate radiographs and laboratory tests, it often leads to a more precise diagnosis and ultimately better management of these patients. The standard classification of primary and secondary OA, while useful, should be expanded to include clinically relevant patterns of disease.

Adult↗
PubMed1986

Immune pathology in polyarticular osteoarthritis.

Although osteoarthritis (OA) generally is considered a disorder of mechanical origin, the common occurrence of chronic mononuclear cell infiltrates in the synovium in conjunction with immunofluorescent evidence for immune-reactant products in cartilage of surgical case specimens (knees, hips, and peripheral joints) has suggested the local involvement of immune processes in the arthritis. Further, the findings of polyarthropathy in the majority of these cases have indicated the propensity for a systemic disorder. Wide variations were noted in both synovial and cartilage immune changes, quite different to those found in rheumatoid arthritis, along with the frequent asymptomatology of the many joints involved. These features, with and without other causative factors, suggest that immune reactions of local and/or systemic origin occur at times in a population at risk for joint degradation.

Cartilage, Articular↗
PubMed1985

Descriptive anatomy of fibrocartilaginous menisci in the finger joints of the hand.

Observations were made from the dissection of 156 digital joints (thumbs excluded). In all joints fibrocollagenous menisci projected into the articular cavity from a ring-like structure based on the joint capsule. These meniscal structures separated the articulating cartilage surfaces at the margins of the joint. Histological examination confirmed a fibrocartilaginous nature of the tissue which demonstrated positive staining for proteoglycans and collagen fibers. Although generally similar in form, these meniscal structures varied in extent when compared between joint groups. The greatest amount and articular contribution was noted in metacarpophalangeal joints with least being found distally.

Aged↗
PubMed1985

Universal bone cutting device for precision knee replacement arthroplasty and osteotomy.

Since malplacement contributes most to loosening of total knee replacements (TKR), a jig was devised, aligned to and mounted on the tibia, with a 3 degrees of freedom sliding saw. A central distractor, attached to the jig, positions and aligns the knee at 0 degrees or 90 degrees. The femur is then rigidly linked to the jig for bone cutting. Resurfacing designs (Cloutier and Townley) have been regularly implanted, aligned +/- 1 degree. This precision should minimize loosening and improve function.

Aged↗
PubMed1985

Nicolas Andry Award, 1984. Deleterious interactions of immune complexes in cartilage of experimental immune arthritis. I. The erosion of pannus-free hyaline cartilage.

Immune complexes were detected by plain and immunoelectron microscopy amongst electron-dense material that rapidly formed and extended over and into the cartilaginous surfaces of immune arthritic rabbits' knees. The sinuous extension of electron-dense material into the surface matrix was associated with fragmentation and detachment, resulting in erosions. The findings implicate the formation of immune complexes in the destructive process of the matrix. Since the eroded pannus-free matrix of rheumatoid cartilage surfaces contains extensive concentrations of immune complexes, the data of this immune arthritis model suggest a causative relation between immune complexes and matrix loss in rheumatoid arthritis.

Animals↗
PubMed1985

Pathogenetic mechanisms in polyarticular osteoarthritis.

This communication has attempted to review causal processes in polyarticular osteoarthritis (poly-OA). Since mechanical features are an almost constant feature of OA joint deterioration, their interplay, both in static and dynamic form, has been stressed. Age-related polyarticular cartilage softening is expounded as an example of degeneration and atrophy--a process not to be confused with OA which is considered as an age-accelerated disorder. I have stressed the influence of genetic factors, best exemplified as a single gene aberration in the occurrence of Heberden's nodes, while a polygenetic interplay may be involved in other forms of hand GOA. These features may predispose an individual to polyarthropathy. The mechanisms by which such genetic factors promote such changes are unknown but attention is drawn to the lack of symptoms in osteoarthritic joints of many if not most poly-OA cases. This occurrence could represent a relative lack of normal proprioceptive feedback or an unusual tolerance to pain. Genetically determined influences marked by the occurrence of hand OA predispose mechanically deranged joints in that individual to deteriorate more rapidly. Mechanically abnormal joints do not inevitably deteriorate, but, in combination with other local and/or systemic factors (genetic, metabolic, hormonal or immune) may undergo accelerated degeneration to which process each additional factor may contribute. Thus in genetically predisposed poly-OA hand cases, local deformity combined with crystal deposition and laxity may provoke dramatic destruction and subluxation. Since mechanical features attend almost all OA joint disease, attention is drawn to a poorly recognized malformation of the knee denoted as dysplasia. Such deformities, well recognized at the hip and shoulder, could occur at other sites in which OA is commonly seen (i.e. DIP joints). Immune-complex deposition probably occurs from time to time in GOA joints. Such events may be associated with local inflammation and aggravate the degradation of cartilage. The available data indicate distinctive differences in the nature and form of such immunopathology to RA in which disease immune-complex deposition in cartilage may play an integral role in tissue destruction and chronic inflammation.

Aged↗
PubMed1984

Pathogenesis of chronic inflammation in experimental ferritin-induced arthritis. V. Electron microscopic localization of specific antibodies in the synovial membrane.

Antibody synthesis by the arthritic synovium of rabbits with antigen-induced arthritis has been demonstrated, but knowledge of the details of the specific localization of antibody in the membrane is limited. Specific antibody in the synovium of ferritin-induced arthritis was detected by electron microscopic observation of bound ferritin. The specific antibodies were localized in the cisternae of the endoplasmic reticulum and perinuclear spaces within plasma cells. In the extracellular matrix, specific antibody was found distributed as a network within collagen bundles and in the basement membrane of the subsynovial small blood vessels.

Animals↗
PubMed1984

Destruction of rabbit knee hyaline cartilage associated with surface antigen-antibody interaction during the Arthus reaction of antigen-induced arthritis.

Ultrastructural changes occurring in rabbit hyaline cartilage were studied during the early stages of antigen-induced arthritis. After one hour, small deposits of electron-dense material (EDM) were noted at depths up to about 3 micron from the surface. During subsequent stages, the number of EDM deposits did not increase, but by 12 hours they had grown to large aggregates. At the surface, extensive deposition and growth eventually resulted in exfoliation of surface layers of cartilage, exposing a fissured matrix. From previous evidence, EDM has been equated with immune complexes (antigen and homologous antibody). The mechanism of cartilage destruction is therefore closely linked to reactions of antigen and antibody within the hyaline cartilage. Mechanical and/or biochemic processes may be involved, but cells do not appear to participate in the destructive process, at least not in regions remote from pannus.

Animals↗
PubMed1983

An experimental polyarthritis associated with systemic antigen excess in immune rabbits.

UNLABELLED: Rabbits were immunized with bovine serum albumin and later challenged intraperitoneally with the same antigen. Polyarthritis, characterized by synovial lining layer hyperplasia and leukocyte infiltration, was conditional on animals having excess free serum antigen in the presence of circulating immune complexes (IC). Nonimmune controls did not develop polyarthritis following antigen challenge. Data are presented that strongly suggest that synovitis was triggered by deposition of IC in the synovia. During the chronic phase of polyarthritis the synovium was clear of antigen but there was marked retention within joint fibrocartilage, suggesting that antigen, immobilized locally, may maintain the chronic synovitis. CLINICAL RELEVANCE: There are several animal models in which experimental arthritis has been induced by antigenic challenge. The resemblance of the lesions to those of human rheumatoid arthritis has provided the rationale for studying the immune events associated with the onset of acute and maintenance of chronic phases of experimental arthritis.

Animals↗
PubMed1983

Immune regulation of collagenase secretion in rheumatoid and osteoarthritic synovial cell cultures.

Primary cultures of synovial cells were obtained by proteolytic dispersion of synovial tissue from patients with rheumatoid arthritis (n = 19), psoriatic arthritis (n = 2), osteoarthritis (n = 13) and other joint problems (n = 3). The levels of endogenously secreted collagenase were variable from patient to patient but did not differ significantly between rheumatoid arthritis and osteoarthritis. The endogenous collagenase secretion was likely a consequence of mononuclear cell factor (MCF) release from monocytes/macrophages which have been shown to be present among the heterogeneous primary rheumatoid synovial cell population (Dayer et al., 1976). As also demonstrated by these investigators, medium containing MCF can be generated from peripheral blood mononuclear cells in a T lymphocyte-dependent process by the addition of phytohemagglutinin (PHA). The addition of such medium stimulated collagenase secretion from all our synovial cell cultures regardless of the endogenous level. Protein synthesis but not synovial cell proliferation was required for MCF stimulation of collagenase secretion. The direct addition of PHA to primary synovial cell cultures stimulated collagenase secretion in some but not all cases indicating the presence of T lymphocytes in these positively-responding cultures. In some of these primary synovial cell cultures in which the addition of PHA stimulated collagenase secretion, secretion was also stimulated by the addition of collagen peptides, native collagen, proteoglycan or purified protein derivative of tuberculin. We propose that, in these instances, MCF release is mediated by antigen-sensitized lymphocytes. Antigen-responsive cultures were not restricted to the rheumatoid population. Our data are compatible with the idea that infiltrated lymphocytes in inflamed synovial tissue become sensitized to cartilage and joint capsule components released during tissue degradation and contribute to matrix destruction by mediating MCF release with consequent stimulation of collagenase synthesis and secretion from synovial cells.

Antigens↗
PubMed1983

Immune complex mediated destruction of cartilage in antigen-induced arthritis of rabbits.

Antigen-induced arthritis of rabbits is used as a model to study pannus-free destruction of cartilage in rheumatoid arthritis (RA) by transmission and scanning electron microscopy, incorporating plain and immune labeling techniques. During the acute "arthus" phase of the RA, immune complexes form and persist in these tissues. We observed the progressive formation of electron dense material rich in immune complexes within a millimicron of the hyaline cartilage surfaces that preceded erosion and loss of surface tissue. Polymorphonuclear neutrophils congregated at the cartilage margins to engulf immune complexes at and within the cartilage surfaces. The changes occurred in regions of hyaline and fibrocartilage free of pannus. Immune complex formation appeared to be a central feature of the cartilage destructive changes, and may be central to mechanisms of tissue loss and similar to those observed in RA.

Animals↗
PubMed1983

The specific in vitro antibody-mediated retention of bovine serum albumin by porcine hyaline articular cartilage.

Porcine hyaline articular cartilage (HAC) has been used to investigate the interaction of bovine serum albumin (BSA) and anti-BSA with articular collagenous tissues in vitro. There was a marked retention of 125I-labelled BSA by plugs of HAC (a) exposed to rabbit anti-BSA for 1-2 h at 37 degrees C prior to a similar incubation with the antigen, or (b) exposed to the antigen and then to antibody. The specifically retained radiolabelled BSA was localized in or at the articular surface of the plugs. In the absence of specific antibody a relatively small amount of the antigen was retained. Exposure of HAC to multiple cycles of antibody and antigen treatment resulted in an increased retention of the 125I-BSA. There was a concomitant increase in the retention of the anti-BSA and the capacity of the treated plugs to fix complement. The forces that maintained the labelled antigen in the tissue were not readily reversed by excess unlabelled BSA. Pre-formed, soluble BSA/anti-BSA complexes did not appear to penetrate the tissue unless the HAC was first exposed to anti-BSA. The results suggest that the antibody-mediated, surface oriented retention of 125I-BSA results from the formation of immune complexes in the tissue.

Animals↗