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[Posttraumatic, degenerative inflammable joint diseases. VIII. The tuberculous joint inflammation].
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Radiological pathology and diagnosis of degenerative joint disease in the stifle joint of the dog.
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Degenerative joint disease of the hip joint in Hereford bullocks.
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Degenerative joint disease.
Management of degenerative joint disease depends on the nature of the process and distribution of the joint disease. Simple modalities such as rest or exercise may be appropriate. Analgesics have a role to play, as do anti-inflammatory drugs and intraarticular corticosteroid injections.
Synovial fluid cytokines and eicosanoids as markers of joint disease in horses.
OBJECTIVE: To evaluate the value of various synovial fluid cytokines and eicosanoids to diagnose joint disease or categories of joint disease. STUDY DESIGN: Prospective acquisition of clinicopathologic data. ANIMALS OR SAMPLE POPULATION: Client-owned or donated horses: 50 joints with no evidence of disease; 28 joints with acute disease; 32 joints with chronic disease; 9 joints with cartilage damage and no other signs of joint disease. METHODS: Concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), prostaglandin E(2) (PGE(2)), thromboxane B(2) (TXB(2)), prostaglandin F1-alpha (PGF(1)-alpha), and leukotriene B(4) (LTB(4)), were measured in equine synovial fluid by immunoassay and categorized according to duration and degree of joint disease. Any test value for a given category that was different from normal was further analyzed for sensitivity (S), specificity (Sp), and operating point (most valid test cutoff value). Likelihood ratios and predictive values were calculated at the operating point. Mediator concentrations were correlated to synovial fluid white blood cell count. Tests were reported as poor, fair, good, or excellent based on predictive values of <.25,.25-.5,.5-.75, or >.75, respectively. RESULTS: TNF synovial fluid concentration as a predictor of joint disease was good, and the value of TNF (maximum S and Sp) indicating joint disease was >36 pg/mL. IL-1beta as a predictor of joint disease was good, and the value of IL-1beta indicating joint disease was >4.5 pg/mL. IL-6 concentration was an excellent predictor of joint disease. Any IL-6 in synovial fluid indicated joint disease and correlated highly with synovial fluid white blood cell count (P <.0001). PGE(2) was a good-excellent predictor of disease (positive predictive value [PPV] = 0.75), and the concentration indicating joint disease was >22.5 pg/mL. The diagnostic PGF(1)-alpha concentration indicating severe chronic joint disease was identified to be >16.5 pg/mL with very high sensitivity (S = 1) and specificity (Sp =.89). PGF(1)-alpha concentrations > 9.5 pg/mL had a good PPV (.69) and NPV (.6) for any joint disease. TBX(2) concentrations below 31.5 pg/mL (S =.57; Sp =.61) were a very good predictor of joint disease (PPV =.72). LTB(4) concentration appeared to be greater in severe acute joint disease than normal joints; this was not significant (P =.15) and correlated highly with synovial fluid white blood cell count (P =.0001). CONCLUSIONS: The ability of a single value from a joint in an adult horse predicting the presence of joint disease was often good (.5-.75), and was excellent (> or =.75) for IL-6 and PGE(2). TNF-alpha and IL-1beta were no more effective than white blood cell count in screening for joint disease. IL-6 was the most sensitive and specific for joint disease and could be an excellent screening test for the presence of joint disease when lameness is difficult to identify or is intermittent. PGE(2) would be a functional screening test for the presence of any joint disease and offers a differentiating feature because values were not influenced by white blood cell count. PGF(1)-alpha values > 16.5 pg/mL identified chronic severe joint disease and may be clinically useful when there are minimal radiographic changes but substantial articular cartilage degradation.
On the structural and physiological basis of the influence of exercise, movement and immobilization in inflammatory joint diseases.
In inflammatory joint diseases the protein concentration often is high in the synovial fluid and, in rheumatoid arthritis at least, probably also in the extra-articular connective tissue. This alters the Starling equilibrium. Peculiarities of the circulation of blood and lymph in articular units and basic physiological principles might explain not only why this readily manifests as joint effusions, but also the influence of exercise, movement, immobilization and posture on the activity of non-bacterial synovitides.
Differences in nitric oxide production by superficial and deep human articular chondrocytes: implications for proteoglycan turnover in inflammatory joint diseases.
During inflammatory joint diseases, chondrocytes are exposed to cytokines such as IL-1 that induce the synthesis of nitric oxide (NO). Chondrocytes from different zones of the articular cartilage are known to have different metabolic properties. In the present study, we have demonstrated that chondrocytes recovered from the superficial zone of normal, human, articular cartilage synthesize approximately 2 to 3 times as much NO in response to IL-1 as chondrocytes recovered from the deep zone of the same cartilage. Production of NO by normal cartilage in response to IL-1 was also found to decrease with age. Addition of the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMA, 1 mM) blocked NO production by cells of both zones. L-NMA completely reversed the suppression of proteoglycan synthesis imposed by IL-1 in deep chondrocytes, but produced only partial reversal in superficial cells. As noted previously, IL-1 failed to elicit a strong catabolic response in cultures of human cartilage. In the presence of L-NMA, however, IL-1 reduced the metabolic t(1/2) of proteoglycans by approximately 50% in both the superficial and deep zones. This suggests that NO has, directly or indirectly, an anticatabolic effect in human cartilage. These data confirm the metabolic heterogeneity of human chondrocytes, and suggest that NO may be involved to different degrees as an endogenous modulator of the turnover of the cartilaginous matrix in different zones of articular cartilage.
Prosthetic replacement of the condylar head for temporomandibular joint disease.
Temporomandibular joint replacement was performed in 8 adults who had intraarticular ankylosis, 6 who had end-stage osteoarthritis, and 12 who had rheumatoid arthritis. Three methods of replacement were used; an ulnar head prosthesis (8 patients), an interpositional implant (11 patients), and a Proplast-coated metallic prosthesis (7 patients). The mean age of the 26 patients (19 women and 7 men) at surgery was 38 years (range 17 to 58 years), and the mean follow-up was 36 months (range 3 to 84 months). Relief of pain was experienced by 23 patients, and maintenance or improvement of incisal opening was experienced by 21. Prosthetic replacement of the condylar head for end-stage disease is highly successful in the patients for whom it is indicated.
The role of arthroscopy in ankle and subtalar degenerative joint disease.
Treatment options for degenerative joint disease of the ankle and subtalar joints are limited. When conservative management fails, the only effective procedure is arthrodesis. With the advent of the small arthroscope and the development of better instrumentation and distraction techniques, small joint arthroscopy has gained popularity as an important diagnostic and therapeutic tool in the treatment of ankle and subtalar disorders. Although the benefits of arthroscopic ankle arthrodesis are well established, and arthroscopic subtalar arthrodesis has been described recently, the role of arthroscopic debridement for degenerative joint disease of the ankle and subtalar joints remains controversial. Traditionally, operative arthroscopy for ankle arthritis has not met with great success; however, recent studies have shown that it can provide an interim alternative to arthrodesis in early arthritis with preserved range of motion. Lesions associated with arthritis, such as impinging osteophytes and loose bodies, can be treated effectively with arthroscopy.
[International decade of bone and joint diseases (The Bone and Joint Decade 2000-2010) -- a multidisciplinary action].
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Plasma and synovial fluid endothelin-1 and nitric oxide concentrations in horses with and without joint disease.
OBJECTIVE: To compare plasma and synovial fluid endothelin-1 (ET-1) and nitric oxide (NO) concentrations in clinically normal horses and horses with joint disease. ANIMALS: 36 horses with joint disease, and 15 horses without joint disease. PROCEDURE: Horses with joint disease were assigned to 1 of the 3 groups (ie, synovitis, degenerative joint disease [DJD], or joint sepsis groups) on the basis of findings on clinical and radiographic examination and synovial fluid analysis. Endothelin-1 and NO concentrations were measured in plasma from blood samples, collected from the jugular vein and ipsilateral cephalic or saphenous vein of the limb with an affected or unaffected joint, as well as in synovial fluid samples obtained via arthrocentesis from the involved joint. RESULTS: Plasma ET-1 concentrations between affected and unaffected groups were not significantly different. Median concentration and concentration range of ET-1 in synovial fluid obtained from the joint sepsis group (35.830 pg/mL, 7926 to 86.614 pg/mL; n = 7) were significantly greater than values from the synovitis (17.531 pg/mL, 0.01 to 46.908 pg/mL; 18), DJD (22.858 pg/mL, 0.01 to 49.990 pg/mL; 10), and unaffected (10.547 pg/mL, 0.01 to 35.927 pg/mL; 10) groups. Plasma and synovial fluid NO concentrations between affected and unaffected groups were not significantly different. CONCLUSIONS AND CLINICAL RELEVANCE: Endothelin-1 is locally synthesized in the joints of horses with various types of joint disease. Synovial fluid concentrations of ET-1 varied among horses with joint disease, with concentrations significantly higher in the synovial fluid of horses with joint sepsis. These results indicate that ET-1 may play a role in the pathophysiologic mechanism of joint disease in horses.
Assay of synovial fluid parameters: hyaluronan concentration as a potential marker for joint diseases.
Synovial fluids from the knees of patients with degenerative joint disease (n = 29), osteoarthritis (n = 16), diabetic arthropathy (n = 12), gout (n = 7) and acute inflammatory joint disease (n = 7) were investigated by high-performance size-exclusion chromatography combined with multiangle laser light scattering detection and differential refractometry. These data were compared with the viscosities of the same samples measured by rotation viscometry with one low shear rate, as well as with C reactive protein. The median value of the weight-average molecular weight of hyaluronan in synovial fluids, which differed less than the viscosity of these groups, varied between 1.09 x 10(6) g/mol (range 0.849-1.63 x 10(6) g/mol) (acute-inflammatory joint disease) and 1.91 x 10(6) g/mol (range 1.06-3.48 x 10(6) g/mol) (degenerative joint disease). The correlation between viscosity and hyaluronan concentration was much better than between viscosity and weight-average molecular weight. Changes in C reactive protein concentration were correlated with the disease activity. The concentration of hyaluronan was significantly higher in the cases of degenerative joint disease and diabetic arthropathy. These results suggest that synovial fluid concentration of hyaluronan is appropriate as a prognostic value in the evaluation of different kinds of joint diseases.
The pattern of involvement of appendicular degenerative joint disease.
Patterns of degenerative joint disease are investigated in the shoulder, elbow, hip, and knee joints of the macerated remains of approximately 800 individuals from 20th century American and two prehistoric populations. Age is an important contributory factor in all joints, but its effects are seen most directly in the shoulder and hip. Patterns of right-left involvement also indicate the elbow is the most susceptible area to local factors. Multiple joint involvement is seen more often in females from contemporary populations but more often in males from archeological groups. No significant association is found between degenerative involvement and osteometric measurements, and cause of death is probably only incidentally associated with degenerative disease.
Systemic therapies for joint disease in horses.
Systemic therapies for joint disease may be prescribed when a single joint is involved or when multiple sites are affected. The precise therapeutic regimen recommended depends on the duration,cause, and site(s) of injury and is often an adjunct to intra-articular or supportive therapies. If the clinical signs of joint disease are acute and moderate in severity, nonsteroidal anti-inflammatory drugs are often administered to alleviate pain and inflammation. When aiming for more of a generalized maintenance or chondro-protective regimen, an alternative medication, such as hyaluronan,polysulfated glycosaminoglycan, or a nutraceutical will commonly be prescribed.
Degenerative joint disease with osteochondrosis of the proximal interphalangeal joint in young horses.
Degenerative joint disease of the proximal interphalangeal joint was diagnosed in 9 joint of 6 horses. All of the horses were 3 years old or younger and the affected joints were in the hindlimbs. Radiographic evidence of osteochondrosis involving the distal end of the proximal phalanx was apparent in 5 joints. Lameness and local soft tissue swelling were prominent in all cases. In 1 horse euthanatized tissues because of lameness, histologic examination of joint tissues revealed osteochondrosis as well as severe osteoarthritis. Surgical arthrodesis of the affected joint was performed on 2 horses, one of which became sound.
[Incidence of circulatory diseases in inflammatory and degenerative joint diseases].
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Degenerative joint disease: cartilage or vascular disease?
The aetiology of degenerative joint disease is multifactorial, but one main cause is overloading (mechanical stress). While until recently it was well accepted that this represented primarily a disorder of cartilage with reactive subchondral changes, there is now some evidence that it might be primarily a subchondral problem with secondary changes in the articular cartilage. Early subchondral changes include redistribution of blood supply with marrow hypertension, oedema and probably micro-necrosis. These findings are very similar to those in avascular necrosis of bone and raise the question of a vascular aetiology. While these first reports need further proof, it seems clear that the articular cartilage and subchondral regions are one functional unit, in which the subchondral region is more stress sensitive. Recently described channels connecting these two regions strengthen this opinion. These new concepts are exciting and may make a major impact in the near future on the management of and research into degenerative joint disease.