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BACKGROUND: Glucosamine and chondroitin sulfate are used to treat osteoarthritis. The multicenter, double-blind, placebo- and celecoxib-controlled Glucosamine/chondroitin Arthritis Intervention Trial (GAIT) evaluated their efficacy and safety as a treatment for knee pain from osteoarthritis. METHODS: We randomly assigned 1583 patients with symptomatic knee osteoarthritis to receive 1500 mg of glucosamine daily, 1200 mg of chondroitin sulfate daily, both glucosamine and chondroitin sulfate, 200 mg of celecoxib daily, or placebo for 24 weeks. Up to 4000 mg of acetaminophen daily was allowed as rescue analgesia. Assignment was stratified according to the severity of knee pain (mild [N=1229] vs. moderate to severe [N=354]). The primary outcome measure was a 20 percent decrease in knee pain from baseline to week 24. RESULTS: The mean age of the patients was 59 years, and 64 percent were women. Overall, glucosamine and chondroitin sulfate were not significantly better than placebo in reducing knee pain by 20 percent. As compared with the rate of response to placebo (60.1 percent), the rate of response to glucosamine was 3.9 percentage points higher (P=0.30), the rate of response to chondroitin sulfate was 5.3 percentage points higher (P=0.17), and the rate of response to combined treatment was 6.5 percentage points higher (P=0.09). The rate of response in the celecoxib control group was 10.0 percentage points higher than that in the placebo control group (P=0.008). For patients with moderate-to-severe pain at baseline, the rate of response was significantly higher with combined therapy than with placebo (79.2 percent vs. 54.3 percent, P=0.002). Adverse events were mild, infrequent, and evenly distributed among the groups. CONCLUSIONS: Glucosamine and chondroitin sulfate alone or in combination did not reduce pain effectively in the overall group of patients with osteoarthritis of the knee. Exploratory analyses suggest that the combination of glucosamine and chondroitin sulfate may be effective in the subgroup of patients with moderate-to-severe knee pain.

A 49 year old black man with scoliosis presented with bilateral shoulder swelling eventually shown to be due to neuropathic arthropathy related to underlying syringomyelia. The synovial fluid was highly inflammatory, but cultures from synovial fluid and synovial tissue were all sterile. Profuse fat droplets were noted and considered as a possible cause of the inflammation. This is an unusual presentation of neuropathic arthropathy in a patient who was also harbouring an adenocarcinoma that was undetected until later. [ABSTRACT FROM PUBLISHER]

Injection of autologous blood into rabbit joints induces an inflammatory reaction with Maltese cross-like birefringent spherulites. Similar microspherules seen in human joint fluids may be formed by lipids derived from breakdown of erythrocytes and other cells. [ABSTRACT FROM PUBLISHER]

We describe three women with unexplained acute monoarthritis and birefringent lipid spherules or lipid liquid crystals in their synovial fluid. Synovial fluid aspirated within 24 hours of onset showed leucocyte counts ranging from 10 X 10(9) to 46 X 10(9)/1 with 91-95% polymorphonuclear cells. Numerous positively birefringent 2-6 micron microspherules were seen inside and outside polymorphonuclear cells. These were dissolved in alcohol-ether but were not digested by uricase. Other non-birefringent globules of similar size that stained with Sudan black B were also seen. Transmission electron microscopy identified osmiophilic homogeneous or multilamellated material in phagocytic vacuoles. Serum lipids, lipase, and repeated joint radiographs were normal. Arthritis subsided completely after treatment with colchicine in one patient and nonsteroidal anti-inflammatory agents in two. Thus birefringent microspherules can be found in association with acute, otherwise unexplained, arthritis. It seems possible that certain lipid liquid crystals may induce synovial inflammation similar to inflammation seen in other crystal induced arthritides. [ABSTRACT FROM PUBLISHER]

Polyarthritic episodes in seven patients during the course of chronic sarcoidosis involved the knees and less frequently other joints. Synovial effusions were non-inflammatory or mildly inflammatory. Needle synovial biopsies 10 days to seven weeks after the onset of joint symptoms have revealed varying patterns, including mild lining cell proliferation, occasional vascular congestion, diffuse infiltrates with lymphocytes and histiocytes, but no granulomas. These studies show distinctly less inflammation than in rheumatoid arthritis. Granulomas need not be identifiable in synovium in all chronic sarcoidosis with arthritis. [ABSTRACT FROM PUBLISHER]

Although the aetiology of the spondylarthritic diseases, ankylosing spondylitis and Reiter's syndrome, is obscure, a clue to the pathogenesis might be an animal model, adjuvant arthritis. Rats with this disease develop a spectrum of pathology with marked similarity to the spondylarthritides. Since peptidoglycan, a major cell wall component of most bacteria is causally implicated in adjuvant arthritis, we sought evidence that peptidoglycan exposure accompanies both Reiter's syndrome and ankylosing spondylitis. Antibodies to the D-Ala-D-Ala moiety of peptidoglycan were measured by a sensitive and specific ELISA. Antibodies were elevated significantly in patients with ankylosing spondylitis or Reiter's syndrome, but not in patients with rheumatoid arthritis or degenerative joint disease in comparison with normal controls. The findings should be considered preliminary, since only a minority of patients had increased antibody titres. However, the findings are compatible with the hypothesis that peptidoglycan is causally related to spondylarthritis. Antibodies to other moieties in the peptidoglycan molecule might be a more sensitive test for significant exposure. [ABSTRACT FROM PUBLISHER]

Silicon-containing particles were identified by transmission electron microscopy (TEM) in thin sections of two synovial fluids, which also contained calcium pyrophosphate dihydrate (CPPD) crystals, aspirated during acute attacks of pseudogout. Such particles, which are interpreted as probably being artefacts from glassware, were electron dense and similar in appearance to some CPPD or hydroxyapatite crystals. [ABSTRACT FROM PUBLISHER]

Transmission electron microscopic studies of synthetic and natural monosodium urate crystals dried on formvar coated grids showed identical internal structures in all crystals. At higher magnification the crystals' surface showed angular or wavy irregularities, and more rarely some crystals appeared to have other tiny crystals on the surface. Protein-like surface coating was not observed except in crystals from one asymptomatic patient in whom synovial fluid was loaded with monosodium urate crystals, but no inflammatory cells were present. Heated synthetic monosodium urate crystals retained the ultrastructural characteristics in their interior but they lost their needle or rod-like shape. Transmission electron microscopic study of monosodium urate crystals dried on formvar coated grids provides a quick method of investigating crystal ultrastructure. [ABSTRACT FROM AUTHOR]

A 33-year-old white female of English descent with beta thalassaemia trait developed painful recurring bilateral knee effusion at age 15 years. Trauma was denied. Synovial analyses revealed noninflammatory effusions with normal complement, no inclusions, and no crystals. Knee x-rays normal at ages 18 and 26, showed mild osteoarthritic changes at age 33. Laboratory tests for other known causes of arthritis were repeatedly normal or negative. Bone densitometry was below normal. Light microscopy of the synovial membrane showed no significant abnormalities and no iron deposition. Electron microscopic findings included multilamination of vascular basement membranes and large amounts of thin fibrils surrounding many connective tissue cells. Treatment with salicylates did not prevent recurrence of effusions, and quadriceps strengthening and joint rest were moderately successful in relieving pain. Intra-articular corticosteroids on 2 occasions were not helpful. Whether her knee arthritis is purely secondary to the para-articular bone thinning from the chronic marrow expansion remains to be determined. [ABSTRACT FROM AUTHOR]

Hydroxyapatite crystals were incubated with human polymorphonuclear leucocytes and samples examined by light and electron microscopy after 3, 8, 30, and 120 minutes' incubation. Phagocytosis of crystals occurred at 3 minutes and increased with incubation. Degranulation of neutrophils, loss of cytoplasmic density, and cell necrosis were greatest in cells mixed with apatite and increased with time. Avid in vitro phagocytosis of hydroxyapatite crystals lends further support to the potential of these crystals as causes of human arthritis. [ABSTRACT FROM PUBLISHER]

Two patients with sickle cell disease presented with joint pain and early x-ray evidence of articular cartilage loss. Both later developed increasingly destructive arthritis with chronic synovitis identified in synovial biopsies. One patient developed demonstrable aseptic necrosis. Destructive arthropathy is much less common than the frequent transient effusions in sickle cell disease. [ABSTRACT FROM AUTHOR]