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PubMedDate not supplied

Degenerative joint disease in poultry--differences in composition and morphology of articular cartilage are associated with strain susceptibility.

The morphology and basic biochemical composition of articular cartilage from two strains of fowl were examined. Broiler breeder fowl are considered susceptible to degenerative joint disease (DJD); histological examination of one-year-old broiler breeders showed in some samples, articular cartilage thinning, fibrillation and chondrocyte cluster formation, features considered typical of DJD. Examination of similar samples from laying strain fowl showed only minor age-related changes such as some slight cartilage thinning and very mild fibrillation. The articular cartilage from the broiler breeder birds was significantly more hydrated with a higher uronic acid content than that of the laying strain birds. In addition, unloaded articular surfaces such as the proximal humerus had significantly higher amounts of uronic acid than the loaded cartilage surfaces of the proximal tarsometatarsus and the distal tibiotarsus; this suggested that the joint loading may have a role in any biochemical differences found between joints and between strains of fowl. These findings concur with other reports in mammals that showed increased hydration and uronic acid in association with early DJD and in models of osteoarthritis (OA). Thus, despite some differences between avian and mammalian articular cartilage, studies on avian DJD may give insights into mammalian disease.

Animals↗
PubMed1993

Generation of substance P carbamate in neutral aqueous solution. Relevance to inflammatory joint diseases.

High-field proton (1H) nuclear magnetic resonance (NMR) spectroscopy has been employed to evaluate the formation of substance P carbamate in aqueous solution. Equilibration of substance P with physiologically relevant concentrations of bicarbonate (2.50 x 10(-2) mol.dm-3) at pH 7.00 generated a new multiplet signal centred at 4.13 ppm in its NMR spectrum, characteristic of the alpha-proton of peptide carbamate species. High-field 1H NMR spectroscopy also demonstrated that the model dipeptide, Arg-Gly, formed a carbamate in neutral aqueous solutions containing 2.50 x 10(-2) mol.dm-3 HCO3-. The physiological significance of these results is discussed in view of the central roles of vasoactive neuropeptides in human joint diseases and the hypercapnic environment of the inflamed rheumatoid joint.

Arthritis, Rheumatoid↗
PubMed2003

Inter-examiner reliability of the diagnosis of cervical pillar hyperplasia (CPH) and the correlation between CPH and spinal degenerative joint disease (DJD).

BACKGROUND: Cervical pillar hyperplasia (CPH) is a recently described phenomenon of unknown aetiology. Its clinical importance is poorly understood at the present time; therefore, the objective of this study was to determine (1) the inter-examiner reliability of detecting CPH and (2) if there is a clinically important correlation (r > 0.4) between the number of cervical spine levels showing signs of degenerative joint disease (DJD) and CPH. METHODS: The sample consisted of 320 radiographs of human male and female subjects who ranged from 40 to 79 years of age. The inter-examiner reliability of assessing the presence/absence of pillar hyperplasia was evaluated on 50 neutral lateral radiographs by two examiners using line drawings and it was quantified using the kappa coefficient of concordance. To determine the presence/absence of hyperplastic pillars as well as the presence/absence of DJD at each intervertebral disc and zygapophysial joint, 320 AP open mouth, AP lower cervical and neutral lateral radiographs were then examined. The unpaired t-test at the 5% level of significance was performed to test for a statistically significant difference between the number of levels affected by DJD in patients with and without hyperplasia. The Spearman's rho at the 5% level of significance was performed to quantify the correlation between DJD and age. RESULTS: The inter-examiner reliability of detecting cervical pillar hyperplasia was moderate with a kappa coefficient of 0.51. The unpaired t-test indicated that there was no statistically significant difference (p > 0.05) between the presence/absence of cervical pillar hyperplasia and the number of levels affected by DJD in an age-matched population, regardless of whether all elements were considered together, or the discs and facets were analyzed separately. A Spearman correlation rank of 0.67 (p < 0.05) suggested a moderately strong correlation between the number of elements (i.e. discs/facets) affected, and the age of the individual. CONCLUSION: Cervical pillar hyperplasia is a reasonable concept that requires further research. Its evaluation is easy to learn and acceptably reliable. Previous research has suggested that CPH may affect the cervical lordosis, and therefore, alter biomechanics which may result in premature DJD. This current study, however, indicates that, globally, CPH does not appear to be related to the development of DJD.

Adult↗
PubMed1984

The tissue architecture of synovial membranes in inflammatory and non-inflammatory joint diseases. II. The localization of mononuclear cells as detected by monoclonal antibodies directed against T-lymphocyte subsets and natural killer cells.

Tissue specimens of synovial membranes from patients with rheumatoid arthritis (RA) and non-inflammatory joint diseases were analyzed with a panel of monoclonal antibodies directed towards T-lymphocyte subsets and natural killer (NK) cells. In the RA group, mononuclear cell infiltrations in the synovium presented a distinguished pattern as compared to the non-RA group. Inflammatory synovial membranes displayed an increased level of cells recognized by the monoclonal antibodies OKT4 and OKT8, especially attributable to the broadened layer of synoviocytes and to the fibrous synovial tissue. No significant difference in the RA patients was observed with regard to the percentage of OKT4 and OKT8 positive cells in different investigated compartments of the synovium, e.g., diffuse inflamed synovial tissue, fibrous synovial tissue, and perivascular infiltrations. OKT4 and OKT8 positive staining was additionally observed on spindle-shaped cells present in the fibrous and diffuse inflamed synovium. OKT10 binding cells were located in the deeper layers of synoviocytes, in the inflamed synovial tissue, and in one case in perivascular areas, whereas HNK 1 positive cells were scattered in the fibrous synovial and perivascular cells, as well as in lymphocyte clusters of synovium in RA patients.

Antibodies, Monoclonal↗
PubMed1986

Gastrointestinal peptides in serum and synovial fluid from patients with inflammatory joint disease.

The concentrations of immunoreactive vasoactive intestinal polypeptide (ir-VIP), immunoreactive pancreatic polypeptide (ir-PP), ir-somatostatin, and ir-secretin were measured in serum and synovial fluid from patients suffering from various inflammatory joint diseases. One group of patients were not taking any medication, while another group received anti-inflammatory treatment at the time of sampling. High levels of ir-VIP in the synovial fluid were observed in the untreated group of patients, and the concentration of ir-VIP in the synovial fluid was significantly higher than in parallel serum samples. On the other hand, no significant differences in the concentrations of the other peptides were observed either between serum and synovial fluid or between the two groups of patients. It is suggested that VIP is released locally at the inflammatory site and that VIP may be of significance in inflammatory disorders.

Adult↗
PubMed1992

Investigation of joint disease.

The role of nuclear medicine in the diagnosis and management of the major arthropathies is critically reviewed, with particular reference to osteoarthritis, rheumatoid and similar forms of arthritis, ankylosing spondylitis, non-specific back pain, gout, the neuropathic joint, avascular necrosis, infection and the consequences of prosthetic joint insertion. Attention is drawn both to practical applications and deficiencies in current techniques and knowledge.

Adult↗
PubMed1988

Deep heat in the treatment of inflammatory joint disease.

There is now a growing body of clinical evidence suggesting a therapeutic approach to cancer and prostatic hypertrophy by using hyperthermia. It is proposed that such a hyperthermic modality can produce thermal synovectomy in inflammatory arthritis. Heating the joint cavity up to 42 deg C can inhibit the enzymatic effect of collagenase, oxygenase, and other enzymes playing a role in the inflammatory process. If this hypothesis is correct, therapeutic intervention using hyperthermia may offer hope for the treatment of isolated inflammatory joint diseases.

Arthritis↗
PubMed2003

X-linked spondyloepiphyseal dysplasia tarda: molecular cause of a heritable disorder associated with early degenerative joint disease.

Spondyloepiphyseal dysplasia tarda (SEDT) is a genetically heterogeneous disorder often associated with the early onset of osteoarthrosis. The X-linked recessive form (SEDL) affects men and is characterized by reduced height, arm span exceeding total height, and barrel chest deformity. The radiographic phenotype comprises a hump-shaped deformity of vertebral bodies and mild epiphyseal dysplasia of the femoral head associated with early signs of hip arthrosis. The disorder is caused by mutations in the SEDL (or sedlin) gene on Xp22.12-p22.31. In 4 male patients from a German family, we identified a new nonsense mutation in SEDL exon 4 (C74A). The carrier status for the mutation could be confirmed in 2 women of the family, both of whom show no obvious signs of bone and joint diseases. SEDT should be kept in mind as a differential diagnosis in men with early "primary" bilateral osteoarthrosis.

Adult↗
PubMed2006

Supplements and injections for joint disease.

Dietary supplements and single joint treatments are gaining increasing popularity, with evidence of efficacy in randomized controlled trials compared with placebo, and minimal side-effects compared with some more traditional therapies. This article clarifies some of the newer approaches and the science behind them.

Adrenal Cortex Hormones↗
PubMedDate not supplied

[Recommendations for the diagnosis and treatment of latent and active tuberculosis in patients with inflammatory joint diseases treated with tumour necrosis factor alpha inhibitors].

The Portuguese Society of Rheumatology (SPR) and the Portuguese Society of Pulmonology (SPP) have developed guidelines for the diagnosis and treatment of latent tuberculosis infection (LTBI) and active tuberculosis (AT) in patients with inflammatory joint diseases (IJD), namely rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, treated with tumour necrosis factor alpha (TNF-alpha) antagonists. Due to the high risk of tuberculosis (TB) in patients with IJD, LTBI and AT screening should be performed as soon as possible, ideally at the moment of IJD diagnosis. Even if TB screening was performed at the beginning of the disease, the evaluation should be repeated before starting anti-TNF-alpha therapy. When TB (LTBI orAT) treatment is indicated, it should be performed before the beginning of anti-TNF-alpha therapy. If the IJD activity requires urgent anti-TNF-alpha therapy, these drugs can be started after two months of antituberculosis therapy in AT cases, or after one month in LTBI cases. Chest X-ray is mandatory for all patients. If abnormal, e.g. Gohn complex, the patient should be treated as LTBI; residual lesions require the exclusion of AT and patients with history of untreated or incomplete TB treatment should be treated as LTBI. In cases of suspected active lesions, AT diagnosis should be confirmed and adequate therapy initiated. Tuberculin skin test (TST), with two units of RT23, should be performed in all patients. If induration is less than 5 mm, the test should be repeated after 1 to 2 weeks, on the opposite forearm, and should be considered negative if the result is again inferior to 5 mm. Positive TST implicates LTBI treatment. IfTST is performed in immunosupressed IJD patients, LTBI treatment should be offered to the patient before starting anti-TNFalpha therapy, even in the presence of a negative test.

Arthritis↗
PubMed1983

Etodolac, aspirin, and placebo in patients with degenerative joint disease: a twelve-week study.

Thirty patients from a private practice were enrolled in an investigation designed to compare the efficacy and safety of a new nonsteroidal anti-inflammatory drug, etodolac, with those of aspirin and placebo in ameliorating pain, inflammation, and functional deficits associated with degenerative joint disease. The 12-week, double-blind, parallel-group study was divided into drug-titration and maintenance periods and was preceded by a washout period of up to two weeks. There were ten patients in each of the three treatment groups. The mean daily maintenance dosages of etodolac and aspirin were 384 mg and 4,322 mg, respectively. Etodolac was significantly (less than or equal to 0.05) more effective than placebo according to 11 of 15 clinical indexes of efficacy: three assessments of the range of motion of the knee joint, and one each of pain while standing, pain while walking, pain while climbing stairs, the average of pains while bearing weight, pain at night, joint tenderness, patient's self-evaluation, and the time required to walk 50 feet. Aspirin was significantly more effective than placebo in only three assessments: two of the range of motion of the knee joint and one of pain while standing. One patient taking etodolac, three patients taking aspirin, and six patients taking placebo withdrew from the trial because of insufficient therapeutic response. There were four withdrawals due to adverse effects, two in the aspirin group and two in the placebo group. Adverse effects (tinnitus and hearing loss) leading to withdrawal of one of the two aspirin patients were probably due to drug administration. No significant side effects were reported by patients in the etodolac group.

Acetates↗
PubMed1975

Tryptophan metabolism in the joint diseases.

Tryptophan metabolites through kynurenine pathway and 5-hydroxytryptophan pathway in the synovial fluid, blood and urine of patients with rheumatoid arthritis and those with osteoarthritis were investigated in order to know the specificity of the tryptophan metabolism, especially the role of serotonin in the joint diseases. A metabolic map of tryptophan in the synovial fluid was also made. It was found that tryptophan in rheumatoid arthritis was metabolized mainly to anthranilic acid through kynurenine in the kynurenine pathway, whereas in osteoarthritis the pathway of kynurenic acid and nicotinic acid was characteristic. Otherwise in 5-hydroxytryptophan pathway there were no significant differences in the levels of 5-hydroxytryptamine and 5-hydroxyindole acetic acid in the synovial fluid between rheumatoid arthritis and osteoarthritis but the activity of monoamine oxidase in the synovial fluid was higher in osteoarthritis than in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMedDate not supplied

[Guidelines for the diagnosis and treatment of latent tuberculosis infection and active tuberculosis in patients with inflammatory joint diseases proposed for treatment with tumour necrosis factor alpha antagonist drugs].

The Portuguese Society of Rheumatology (SPR) and the Portuguese Society of Pulmonology (SPP) have developed guidelines for the diagnosis and treatment of latent tuberculosis infection (LTBI) and active tuberculosis (AT) in patients with inflammatory joint diseases (IJD), namely rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, treated with tumour necrosis factor alpha (TNF-a) antagonists. Due to the high risk of tuberculosis (TB) in patients with IJD, LTBI and AT screening should be performed as soon as possible, ideally at the moment of IJD diagnosis. Even if TB screening was performed at the beginning of the disease, the evaluation should be repeated before starting anti-TNF-a therapy. When TB (LTBI or AT) treatment is indicated, it should be performed before the beginning of anti-TNF-a therapy. If the IJD activity requires urgent anti-TNF-a therapy, these drugs can be started after two months of antituberculosis therapy in AT cases, or after one month in LTBI cases. Chest X-ray is mandatory for all patients. If abnormal, e.g. Gohn complex, the patient should be treated as LTBI; residual lesions require the exclusion of AT and patients with history of untreated or incomplete TB treatment should be treated as LTBI. In cases of suspected active lesions, AT diagnosis should be confirmed and adequate therapy initiated. Tuberculin skin test (TST), with two units of RT23, should be performed in all patients. If induration is less than 5 mm, the test should be repeated after 1 to 2 weeks, on the opposite forearm, and should be considered negative if the result is again inferior to 5 mm. Positive TST implicates LTBI treatment. If TST is performed in immunosuppressed IJD patients, LTBI treatment should be offered to the patient before starting anti-TNF-a therapy, even in the presence of a negative test.

Arthritis↗
PubMed1989

Thrombospondin and fibronectin are synthesized by neutrophils in human inflammatory joint disease and in a rabbit model of in vivo neutrophil activation.

Using 35S-methionine metabolic labeling, we studied de novo synthesis and secretion of proteins by activated polymorphonuclear neutrophils (PMN) from two different sources. PMN isolated from inflammatory synovial fluid of patients with inflammatory joint disease were first analyzed. The protein synthetic activity of these cells was compared with that of nonactivated PMN isolated from the peripheral blood of the same patient. Similar studies were conducted on glycogen-activated PMN from the peritoneal cavity of rabbits and results were compared with nonactivated peripheral blood PMN isolated from the same rabbit. Cells were labeled for a period of 16 to 20 h and supernatants were analyzed by one and two dimensional gel electrophoresis. In both models, the activated PMN showed a marked increase in the synthesis and secretion of thrombospondin as identified by immunoisolation with antibodies to this protein. The production of thrombospondin by activated cells paralleled a similar increase in production of another extracellular matrix and cell adhesion protein, fibronectin. The proportion of thrombospondin synthesis and secretion relative to total protein was approximately 1% in both human- and rabbit-activated PMN. For fibronectin, this proportion was in the 0.02% range. Although fibronectin mRNA accumulation in activated PMN could be demonstrated by Northern blots, we were not able to obtain similar results for thrombospondin mRNA. This could be caused by the rapid turnover of this transcript because it is known to contain an adenine uridine-rich 3' untranslated sequence. We conclude that activated PMN are capable of producing thrombospondin. Furthermore, glycogen-activated rabbit peritoneal fluid PMN represent a valuable and relevant source of activated PMN for studying the protein synthetic events of these cells in the context of inflammation.

Animals↗