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At least 1,423 records · Page 79Linked to original sources
PubMed1986

Transection of the canine anterior cruciate ligament: a concise review of experience with this model of degenerative joint disease.

Transection of the anterior cruciate ligament in dogs is probably the most widely used model for degenerative articular disease. Two techniques, the percutaneous stab and arthrotomy, are currently employed. Reported results of the degree of cartilage damage and the time of onset of lesions vary considerably in the literature. Several papers described overt fibrillation as early as 6 weeks post-operatively while others found only mild changes up to nearly 4 years. Critical analysis of the model revealed that parameters such as the breed of dog, its age, weight, amount of exercise and technique of surgery may influence the onset and severity of lesions. Further research is essential to define the relative importance of each.

Age Factors↗
PubMed1985

The torn meniscus, the torn anterior cruciate ligament, and their relationship to degenerative joint disease.

A retrospective review of 350 knees was carried out to determine the effect, if any, of a torn meniscus and a torn anterior cruciate ligament on the articular surfaces of the knee. There were no professional or college athletes in this group, although a few were enthusiastic sandlot-type players. The time interval between injury and surgery was known, as was the state of the articular surfaces, which were graded from 1 to 4. As the time interval between injury and surgery increased, so did the incidence of lesions of the articular surfaces, although in most cases these lesions were quite minor. On the basis of this and other studies, it was concluded that the torn meniscus does not pose a significant threat to the integrity of the articular cartilage; this was also true in those patients in whom the anterior cruciate ligament was torn.

Cartilage, Articular↗
PubMed1996

Oral tolerance: mechanisms and possible role in inflammatory joint diseases.

Decreased systemic immune responsiveness to a specific antigen following exposure to that antigen by the enteric route is termed 'oral tolerance.' Oral tolerance is revealed when attempts are made to parenterally immunize the host to the same antigen that was previously administered orally or intragastrically. A similar phenomenon is also seen following antigen exposure via the nasal mucosa and a related phenomenon is seen following antigen exposure in the upper respiratory tract. There has been a marked renewal of interest in the mechanisms that underlie oral tolerance because of its potential role for preventing and treating autoimmune and inflammatory diseases and IgE-mediated allergic disorders. The specific factors that determine whether or not the host develops mucosal tolerance to an antigen administered by the mucosal route are also of substantial importance for those involved in mucosal vaccine development. Furthermore, putative abnormalities in the ability of the host to develop mucosal tolerance may play a pathogenetic role in certain autoimmune and allergic diseases and disorders. Several well-defined immunological mechanisms mediate oral tolerance. These include the induction, following mucosal antigen exposure, of regulatory populations of T-cells that can down-regulate specific immune responses (e.g. DTH) via the production of specific cytokines (e.g. TGF-beta 1, IL-10 and IL-4). In addition, clonal anergy, clonal deletion and antibody-mediated suppression can be shown to play a role in the induction and maintenance of mucosal tolerance in several experimental systems. In animal studies, the onset of collagen-induced, adjuvant-induced, antigen-induced and pristane-induced arthritis has been delayed and the severity of ongoing disease diminished following feeding collagen type II. Mucosal tolerance has been clearly demonstrated in humans and clinical studies have been undertaken to treat rheumatoid arthritis using a similar approach. Results of initial clinical studies in rheumatoid arthritis indicated a modest improvement and further studies are ongoing in this and other autoimmune diseases (e.g. multiple sclerosis, autoimmune uveitis and insulin-dependent diabetes). This approach, if successful, could offer a new and novel therapeutic modality for preventing autoimmune and allergic disorders, and modulating ongoing disease.

Administration, Oral↗
PubMed2001

Surface expression of CC- and CXC-chemokine receptors on leucocyte subsets in inflammatory joint diseases.

Chemokine receptors play a crucial role in the recruitment of leucocyte subsets into inflamed tissue. Using FACS analysis we have studied the surface expression of different CC- and CXC-chemokine receptors on synovial fluid (SF) and peripheral blood leucocytes from 20 patients with various forms of arthritis. In the SF the majority T cells stained positive for CCR5 (93%) and CCR2 (57%), compared to the peripheral blood (36% and 25%). In addition, most of the T cells expressed CXCR4 in both compartments, with a somewhat higher percentage in the SF (90%) versus peripheral blood (83%). To date little information is available on chemokine receptor expression on monocytes in arthritis. We report a marked increase of CCR5(+) monocytes in the SF (87%) compared to the peripheral blood (22%). In contrast, the frequency of CXCR1(+), CXCR2(+), CXCR4(+) and CCR1(+) monocytes was considerably lower in the SF than in the peripheral blood. Moreover, we report the expression CXCR4 on neutrophils in the SF. Approximately 60% of neutrophils stained positive for CXCR4 in the SF, while in the peripheral blood the number of CXCR4(+) neutrophils was low (24%). Surface expression of CXCR1 and CXCR2 was significantly reduced on SF neutrophils (53% and 68%) compared to the peripheral blood. Chemokine receptors are differentially expressed on leucocyte subsets in arthritis. The identification of their pattern of expression might help to identify suitable targets for therapeutic intervention.

Alleles↗