safranine-t and Temporomandibular-Joint-Disorders

safranine-t has been researched along with Temporomandibular-Joint-Disorders* in 4 studies

Other Studies

4 other study(ies) available for safranine-t and Temporomandibular-Joint-Disorders

ArticleYear
Histomorphometry in antigen-induced arthritis of the rabbit temporomandibular joint.
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 2015, Volume: 44, Issue:1

    Juvenile idiopathic arthritis (JIA) of the temporomandibular joint (TMJ) can cause severe growth disturbances of the craniomandibular system. Antigen-induced arthritis (AIA) of the rabbit TMJ is simulating the inflammatory process of the TMJ in JIA. The aim of this study was to investigate the effect of a systemic administration of the tumor necrosis factor-alpha (TNF-α) antagonist etanercept on AIA in rabbits by means of three different histological staining methods.. After sensitization, a bilateral arthritis of the TMJ was induced and maintained by repeated intra-articular administrations of ovalbumin in 12 New Zealand white rabbits aged 10 weeks. From the 13th week of age, 6 of the 12 rabbits received weekly subcutaneous injections of etanercept, and the other 6 animals remained without therapy. Another 6 animals served as controls, receiving no treatment or intra-articular injections at all. After euthanasia at the age of 22 weeks, all TMJs were retrieved en bloc. Sagittal sections were cut and stained with hematoxylin-eosin (H-E), Safranin-O for the evaluation of the Mankin score, and tartrate-resistant acid phosphatase (TRAP).. In the arthritis group, a chronic inflammation with degeneration of the articular cartilage was visible. In the etanercept group, the signs of cartilage degeneration were significantly reduced but present. In contrast, the joints in the control group were inconspicuous. A strong correlation between the Mankin score and TRAP-positive cells could be found.. Antigen-induced arthritis causes severe damage in the TMJ of young rabbits. An improvement seems to be achievable by a systemic administration of etanercept.

    Topics: Acid Phosphatase; Animals; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Experimental; Arthritis, Juvenile; Biomarkers; Cartilage, Articular; Coloring Agents; Disease Models, Animal; Etanercept; Female; Freund's Adjuvant; Injections, Intra-Articular; Injections, Subcutaneous; Isoenzymes; Mandibular Condyle; Osteoclasts; Ovalbumin; Phenazines; Rabbits; Random Allocation; Tartrate-Resistant Acid Phosphatase; Temporomandibular Joint Disorders; Time Factors

2015
Effect of different doses of transforming growth factor-β₁ on cartilage and subchondral bone in osteoarthritic temporomandibular joints.
    The British journal of oral & maxillofacial surgery, 2013, Volume: 51, Issue:3

    Transforming growth factor-beta (TGF-β) plays an important part in the repair of cartilage in osteoarthritis. It has been hypothesised that intra-articular injection of TGF-β₁ promotes repair of cartilage and protects the subchondral bone from damage in osteoarthritic temporomandibular joints (TMJs). We made bilateral partial perforations of the disc to induce osteoarthritic joints in 36 rabbits. TGF-β₁ 20, 40, or 80 ng were injected into the right joint, and vehicle alone was injected into the left joint. Four additional animals were used as normal controls. Microcomputed tomography was used to quantify the three-dimensional microarchitecture of subchondral bone, followed by assessment of the proteoglycan content. All joints treated with TGF-β₁ were covered by a layer of well-organised fibrocartilage, and had increased proteoglycan content and normal microarchitectural properties, whereas the joint treated by vehicle alone had typical osteoarthritis-related degradation of cartilage and sclerosis of subchondral bone. These results suggested that TGF-β₁ is an effective way of treating osteoarthritis of the TMJ.

    Topics: Animals; Bone Density; Calcification, Physiologic; Cartilage, Articular; Chondrocytes; Coloring Agents; Disease Models, Animal; Fibrocartilage; Image Processing, Computer-Assisted; Imaging, Three-Dimensional; Injections, Intra-Articular; Male; Mandibular Condyle; Osteoarthritis; Phenazines; Proteoglycans; Rabbits; Random Allocation; Sclerosis; Temporomandibular Joint Disc; Temporomandibular Joint Disorders; Transforming Growth Factor beta1; X-Ray Microtomography

2013
Expression of chondromodulin-1 in the temporomandibular joint condylar cartilage and disc.
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology, 2010, Volume: 39, Issue:4

    The temporomandibular joint (TMJ) cartilage consists of condylar cartilage and disc and undergoes continuous remodeling throughout post-natal life. To maintain the integrity of the TMJ cartilage, anti-angiogenic factors play an important role during the remodeling process. In this study, we investigated the expression of the anti-angiogenic factor, chondromodulin-1 (ChM-1), in TMJ cartilage and evaluate its potential role in TMJ remodeling.. Eight TMJ specimens were collected from six 4-month-old Japanese white rabbits. Safranin-O staining was performed to determine proteoglycan content. ChM-1 expression in TMJ condylar cartilage and disc was determined by immunohistochemistry. Three human perforated disc tissue samples were collected for investigation of ChM-1 and vascular endothelial growth factor (VEGF) distribution in perforated TMJ disc.. Safranin-O stained weakly in TMJ compared with tibial articular and epiphyseal cartilage. In TMJ, ChM-1 was expressed in the proliferative and hypertrophic zone of condylar cartilage and chondrocyte-like cells in the disc. No expression of ChM-1 was observed in osteoblasts and subchondral bone. ChM-1 and VEGF were both similarly expressed in perforated disc tissues.. ChM-1 may play a role in the regulation of TMJ remodeling by preventing blood vessel invasion of the cartilage, thereby maintaining condylar cartilage and disc integrity.

    Topics: Angiogenesis Inhibitors; Animals; Bone Remodeling; Cartilage, Articular; Cell Proliferation; Chondrocytes; Coloring Agents; Epiphyses; Female; Humans; Hypertrophy; Intercellular Signaling Peptides and Proteins; Mandibular Condyle; Membrane Proteins; Osteoblasts; Phenazines; Proteoglycans; Rabbits; Rats; Rats, Inbred Lew; Temporomandibular Joint; Temporomandibular Joint Disc; Temporomandibular Joint Disorders; Tibia; Vascular Endothelial Growth Factor A

2010
Development and histologic characterizations of an animal model of antigen-induced arthritis of the juvenile rabbit temporomandibular joint.
    Journal of dental research, 1995, Volume: 74, Issue:12

    Children with juvenile rheumatoid arthritis or juvenile chronic arthritis often exhibit temporomandibular joint (TMJ) involvement accompanied by pain, dysfunction, and growth abnormalities. Despite the severe functional and developmental consequences of this disease, its pathogenesis remains poorly understood, but important insights may be provided by a suitable animal model of this disease. The purpose of this study was to develop and histologically characterize a juvenile animal model of antigen-induced arthritis of the TMJ. Arthritis was induced with an intra-articular administration of ovalbumin in previously sensitized 10-week-old male New Zealand white rabbits. Sham-treated and untreated rabbits were used as controls. The TMJs were retrieved en bloc at 5, 10, 15, 35, and 55 days post-challenge for histology and matrix histochemistry. Antigen-treated joints demonstrated severe arthritis, including mononuclear cell infiltration, synovial lining and villous hyperplasia, and pannus formation, as early as 5 days after challenge; the arthritis was maintained up to 55 days post-challenge. A decrease in the area of the TMJ disc that stained positively for glycosaminoglycans was observed throughout the experimental period. Loss of collagen staining was primarily localized to sites at the junction of the synovium with bone and fibrocartilage. The histopathologic features of this model of antigen-induced arthritis of the juvenile rabbit TMJ are similar to those observed previously in adult animal models of experimental arthritis and in human rheumatoid arthritis. This animal model will be useful for understanding the pathogenesis of juvenile rheumatoid arthritis of the TMJ, and for exploring the mechanisms for aberrant craniofacial growth.

    Topics: Analysis of Variance; Animals; Arthritis, Experimental; Arthritis, Juvenile; Cartilage, Articular; Collagen; Coloring Agents; Disease Models, Animal; Extracellular Matrix Proteins; Glycosaminoglycans; Histocytochemistry; Male; Ovalbumin; Phenazines; Rabbits; Synovial Membrane; Synovitis; Temporomandibular Joint Disorders

1995