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At least 505 records · Page 28Linked to original sources
PubMed2001

Defective gp130-mediated signal transducer and activator of transcription (STAT) signaling results in degenerative joint disease, gastrointestinal ulceration, and failure of uterine implantation.

The receptor subunit gp130 transduces multiple cell type-specific activities of the leukemia inhibitory factor (LIF)/interleukin (IL)-6 family of cytokines through the signal transducer and activator of transcription (STAT) and src homology 2 domain-bearing protein tyrosine phosphatase (SHP)-2/ras/Erk pathways. To define STAT-dependent physiological responses, we generated mice with a COOH-terminal gp130(DeltaSTAT) "knock-in" mutation which deleted all STAT-binding sites. gp130(DeltaSTAT) mice phenocopyed mice deficient for IL-6 (impaired humoral and mucosal immune and hepatic acute phase responses) and LIF (failure of blastocyst implantation). However, unlike mice with null mutations in any of the components in the gp130 signaling pathway, gp130(DeltaSTAT) mice also displayed gastrointestinal ulceration and a severe joint disease with features of chronic synovitis, cartilaginous metaplasia, and degradation of the articular cartilage. Mitogenic hyperresponsiveness of synovial cells to the LIF/IL-6 family of cyto-kines was caused by sustained gp130-mediated SHP-2/ras/Erk activation due to impaired STAT-mediated induction of suppressor of cytokine signaling (SOCS) proteins which normally limits gp130 signaling. Therefore, the joint pathology in gp130(DeltaSTAT) mice is likely to arise from the disturbance of the otherwise balanced activation of the SHP-2/ras/Erk and STAT signaling cascades emanating from gp130.

Animals↗
PubMedDate not supplied

Effects of body mass and genotype on avian degenerative joint disease pathology and articular cartilage proteoglycan distribution.

OBJECTIVE: The objective of this study was to investigate the role of body mass and genotype in the development of avian degenerative joint disease (DJD). METHODS: Layer strain and broiler strain fowl, fed either ad libitum or on a restricted diet, were kept under identical conditions for up to a year. At various time points cartilage samples were taken from the distal tibiotarsus (DTT), proximal tarsometatarsus, antitrochanter and proximal humerus. All samples were assessed for gross morphology and histopathology, and in some samples the cartilage proteoglycan distribution was investigated by Safranin O staining. RESULTS: Layer strain fowl did not develop DJD. Heavy ad libitum fed broiler strain fowl developed DJD earlier and more severely than lighter, feed restricted, broiler strain fowl. The articular surface of the DTT was worst affected by DJD. Safranin O staining of DTT samples (age 180 days) from the ad libitum fed broilers revealed variable proteoglycan distribution in the articular cartilage. Some areas were intensely stained throughout all zones, whereas other areas showed no staining in any zone. Age matched, non-diseased DTT samples from feed restricted broilers showed a more consistent staining pattern with little staining in the surface zone and more in the middle and deep zones. CONCLUSIONS: These data indicate that avian DJD is body mass mediated in broiler strain fowl, and that proteoglycan distribution is altered in diseased cartilage.

Animals↗
PubMed2006

Determination of characteristics of degenerative joint disease using optical coherence tomography and polarization sensitive optical coherence tomography.

BACKGROUND AND OBJECTIVES: Previous studies have demonstrated that optical coherence tomography (OCT) could be used to delineate alterations in the microstructure of cartilage, and have suggested that changes in the polarization state of light as detected by OCT could provide information on the birefringence properties of articular cartilage as influenced by disease. In this study we have used both OCT and polarization sensitive optical coherence tomography (PS-OCT) technologies to evaluate normal and abnormal bovine articular cartilage according to established structural, organizational, and birefringent characteristics of degenerative joint disease (DJD) in order to determine if this technology can be used to differentiate various stages of DJD as a minimally invasive imaging tool. MATERIALS AND METHODS: Fresh bovine femoral-tibial joints were obtained from an abattoir, and 45 cartilage specimens were harvested from 8 tibial plateaus. Whole ex vivo specimens of normal and degenerative articular cartilage were imaged by both OCT and PS-OCT, then fixed and processed for histological evaluation. OCT/PS-OCT images and corresponding histology sections of each specimen were scored according to a modified Mankin structural grading scale and compared. RESULTS: OCT and PS-OCT imaging allowed structural evaluation of intact articular cartilage along a 6 mm surface length to a depth of 2 mm with a transverse resolution of 12 microm and an axial resolution of 10 microm. The OCT and PS-OCT images demonstrated characteristic alterations in the structure of articular cartilage with a high correlation to histological evaluation (kappa = 0.776). The OCT images were able to demonstrate early to advanced structural changes of articular cartilage while the optical phase retardation images obtained by PS-OCT imaging were able to discriminate areas where disorganization of the cartilage matrix was present, however, these characteristics are much different than those reported where OCT images alone were used to characterize tissue birefringence. No evidence of differences in OCT or PS-OCT images were detected between specimens of similar structural characteristics where proteoglycan was judged present or absent by safranin-O Fast Green staining. CONCLUSIONS: The combined use of OCT and PS-OCT technologies to obtain images from a single system is able to demonstrate and discriminate between characteristics of very early stages of surface irregularities not previously reported for OCT imaging, to deep clefts and collagen matrix disorganization for tissue at depths of up to 2 mm with good correlation to histology. PS-OCT and accumulated optical phase retardation images of articular cartilage as constructed from alterations in Stokes vector parameters appear to give a valuable but different assessment of alterations in tissue birefringence and organization than have been reported for OCT images obtained with the use of polarized or non-polarized light sources. This is the first time that alterations in the polarization state of light reflected from within the tissue have been demonstrated to be consistent with changes observed in the orientation and organization of the collagen matrix in advanced stages of DJD. The degree of phase transformation of light reflected from within the tissue as determined by PS-OCT imaging does not appear to be altered by the presence or absence of proteoglycan.

Animals↗
PubMedDate not supplied

Pathogenesis of degenerative joint disease produced by in vivo freezing of rabbit articular cartilage.

In vivo freezing of rabbit lateral femoral arterial cartilage with a cryoprobe produces an osteoarthritic-like condition in 12 months. Previous studies have established that the chondrocytes are killed by the freezing process. A loss of stainable mucopolysaccharide occurs. The collagen content of the lesional tissue does not change. The present study investigates the extracellular lysosomal enzyme content, collagen type (I or II), and histologic changes which produce chondrocyte cell clusters in the frozen tissue in response to freezing or articular cartilage. The results indicate that after the initial 30 days there is no significant rise in the extracellular lysosomal enzyme content of the experimental tissue compared with controls. Type II, or cartilage, collagen remains the major constituent of the lesional tissue. Histologic examination at six- to 12-month intervals suggests that chondrocyte clones are produced by invasion by the underlying viable subchondral bone. These results provide insight into the pathogenesis of degenerative joint disease and the rationale of treatment by the use of inhibitors of vascular invasion of articular cartilage.

Animals↗
PubMed1996

Inflammatory joint disease: the role of cytokines, cyclooxygenases and reactive oxygen species.

Cytokines are known to have a key role in the onset and development of inflammatory joint disease, including rheumatoid arthritis and osteoarthritis. The effects of some cytokines on the cells and tissues involved in inflammation of the joint are well catalogued, but recent discoveries of new cytokines, and interest in intracellular signalling molecules, have thrown new light on the way in which cytokines mediate the cellular responses that lead to inflammation. Here, recent work on the roles of cytokines, cyclooxygenases, nitric oxide and other reactive oxygen species, in the cellular pathways that lead from cytokine receptor to inflammation, are discussed.

Arthritis↗
PubMed2006

Inclination of the patellar ligament in relation to flexion angle in stifle joints of dogs without degenerative joint disease.

OBJECTIVE: To measure the angles between the patellar ligament and the tibial plateau and between the patellar ligament and the common tangent at the tibiofemoral contact point (TFCP) throughout the full range of motion of the stifle joint in dogs and determine the flexion angles at which the patellar ligament is perpendicular to the tibial plateau or to the common tangent. SAMPLE POPULATION: 16 hind limbs from cadavers of 9 adult dogs without radiographically detectable degenerative joint disease. PROCEDURES: Mediolateral radiographic views of the stifle joints from full extension through full flexion were obtained (10 degrees increments). Angles between the tibial and femoral long axes (beta), between the patellar ligament and the tibial plateau gamma), and between the patellar ligament and the common tangent at TFCP (alpha) were measured. Data were analyzed via simple linear regression. RESULTS: In canine stifle joints, angles gamma and alpha decreased linearly with increasing flexion (angle beta). The patellar ligament was perpendicular to the tibial plateau and perpendicular to the common tangent at the TFCP at 90 degrees and 110 degrees of flexion, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: By use of the conventionally defined tibial plateau, data suggest that at approximately 90 degrees of flexion in stifle joints of dogs, shear force in the sagittal plane exerted on the proximal portion of the tibia shifts the loading from the cranial to the caudal cruciate ligament. Analyses involving the common tangent at the TFCP (a more anatomically representative reference point) identified this crossover point at approximately 110 degrees of joint flexion.

Animals↗
PubMed1999

Secondary amyloidosis has decreased in patients with inflammatory joint disease in Finland.

We studied whether the high incidence of secondary amyloidosis (SA) is a consistent finding in patients with inflammatory joint disease. A total of 4508 biopsies of patients with rheumatoid arthritis, psoriatic arthritis or ankylosing spondylitis were studied at the Rheumatism Foundation Hospital during 1987-1997. The results show that the annual number of findings of SA was reduced from 68 to less than 10. We suggest that a change in medication towards more frequent use of cytostatic agents is the reason for the reduction in incidence of SA.

Amyloidosis↗
PubMed2005

Chondroprotective drugs in degenerative joint diseases.

Catabolic cytokine and anabolic growth factor pathways control destruction and repair in osteoarthritis (OA). A unidirectional TNF-alpha/IL-1-driven cytokine cascade disturbs the homeostasis of the extracellular matrix of articular cartilage in OA. Although chondrocytes in OA cartilage overexpress anabolic insulin-like growth factor (IGF) and its specific receptor (IGFRI) autocrine TNF-alpha released by apoptotic articular cartilage cells sets off an auto/paracrine IL-1-driven cascade that overrules the growth factor activities that sustain repair in degenerative joint disease. Chondroprotection with reappearance of a joint space that had disappeared has been documented unmistakably in peripheral joints of patients suffering from spondyloarthropathy when treated with TNF-alpha-blocking agents that repressed the unidirectional TNF-alpha/IL-1-driven cytokine cascade. A series of connective tissue structure-modifying agents (CTSMAs) that directly affect IL-1 synthesis and release in vitro and down-modulate downstream IL-1 features, e.g. collagenase, proteoglycanase and matrix metalloproteinase activities, the expression of inducible nitric oxide synthase, the increased release of nitric oxide, and the secretion of prostaglandin E(2), IL-6 and IL-8, have been shown to possess disease-modifying OA drug (DMOAD) activities in experimental models of OA and in human subjects with finger joint and knee OA. Examples are corticosteroids, some sulphated polysaccharides, chemically modified tetracyclines, diacetylrhein/rhein, glucosamine and avocado/soybean unsaponifiables.

Antirheumatic Agents↗
PubMed1985

Aging in the musculoskeletal system of rhesus monkeys: II. Degenerative joint disease.

In order to discuss the rate and onset of adult aging in rhesus monkeys, 55 adult animals from the Wisconsin Regional Primate Research Center and the University of Wisconsin Psychology Primate Laboratory were examined. Degenerative joint disease (DJD) at the hip and spine was scored, and loss of passive joint mobility at the hip was measured. Development of DJD at both the hip and spine was significantly and positively correlated with age. Spinal changes, especially at the thoraco/lumbar intervertebral symphyses, appeared to develop somewhat more rapidly than hip degeneration. In some individuals, DJD was observed soon after the completion of growth, but pronounced changes seldom occurred before the middle of the second decade of life. Similarly, age-dependent losses of passive joint mobility appeared to begin early in ontogeny and to become increasingly pronounced in the aging adult. Although interspecific comparisons are difficult due to intraspecies and intraindividual variation, the timing of musculoskeletal aging in the rhesus spine and hip differs from that observed in humans in a way that parallels previously documented species differences in patterns of musculoskeletal growth. These observations and data on age-related change in other systems, suggest that rates and durations of many ontogenetic processes in rhesus monkeys are approximately three times as fast and one-third as long as those of the corresponding human processes. Importantly, differences in the timing of reproduction do not appear to follow the same scaling factor observed in other systems. Although reproduction may, therefore, be under separate control, the consistent pattern observed in other aspects of somatic growth and aging supports the hypothesis (Cutler, 1976; Sacher, 1978) that evolutionary changes in ontogeny have resulted from selection acting upon a few genes with widespread regulatory effects.

Aging↗
PubMed1996

High doses of interleukin-12 inhibit the development of joint disease in DBA/1 mice immunized with type II collagen in complete Freund's adjuvant.

Collagen-induced arthritis (CIA) is an (autoimmune) joint disease readily elicited in DBA/1 mice by immunization with type II collagen (CII) emulsified with complete Freund's adjuvant. It is a destructive arthritis involving about 50% of the limbs and occurs with an incidence of 70% to 100%. In this study we evaluated the effect of mouse recombinant interleukin-12 (mrIL-12) on CIA. Administration of mrIL-12 at high doses (1 micrograms/mouse, daily) for 2 or 3 weeks delayed the onset and reduced the incidence of CIA. Furthermore, the severity of CIA was much milder and in most cases restricted to single digits of the paws. Short-term administration of high doses of IL-12 exerted some, but less pronounced, disease-suppressing effect. In contrast, 10-fold lower doses of IL-12 given during the first 3 weeks, or high doses of IL-12 administered therapeutically proved to be ineffective. Only those regimens of IL-12 treatment that ameliorated CIA were associated with a down-regulation of the CII-specific antibody response. A strong inhibition of CII-specific IgG1 antibodies (10- to 20-fold) and a moderately (2- to 6-fold) suppressed IgG2b response was observed, whereas the level of CII-specific IgG2a antibodies remained high. Taken together, the results indicate that some initial events in the induction of CIA in DBA/1 mice injected with CII emulsified with CFA are suppressed by treatment with high doses of IL-12.

Animals↗
PubMed1992

Pathology of osteonecrosis of the femoral head. A review of experience at the Hospital for Joint Diseases, New York.

Pathological examination of the resected femoral heads from approximately 2000 total hip replacement operations carried out at the Hospital for Joint Diseases from 1984 to 1989 identified the presence of osteonecrosis in 345 patients (377 femoral heads). In 232 patients the osteonecrosis, referred to as "idiopathic," had occurred in the absence of a subcapital fracture. The present paper describes the pathology of the necrotic lesions in these 232 patients. The use of undecalcified sections and microradiography provides evidence of bone marrow calcification which, at the margin of the lesion, is sufficient to influence the radiographic features of the lesion significantly. Although a subchondral fracture is an almost constant feature of osteonecrosis when it occurs in a femoral head with a normal articular cartilage, no such fracture was found in cases in which osteonecrosis had occurred in an osteoarthritic joint.

Adult↗