Expression of matrix metalloproteinases and aggrecanase in the synovial fluids of patients with symptomatic temporomandibular disorders

Yoshida, Kan; Takatsuka, Shigeyuki; Hatada, Eriko; Nakamura, Hiroyuki; Tanaka, Akira; Ueki, Koichiro; Nakagawa, Kiyomasa; Okada, Yasunori; Yamamoto, Etsuhide; Fukuda, Ryuuzi

doi:10.1016/j.tripleo.2005.07.013

Cited by 46 publications

(32 citation statements)

References 26 publications

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“…In a recent study, up to 72 % of newly diagnosed RA patients were found to have TMJ involvement24. This percentage is close to those found in studies of RA patients with longer disease duration21,25–27 or in pediatric patients with juvenile idiopathic arthritis28,29, a disease with RA-like features.…”

Section: Discussionsupporting

confidence: 69%

Osteoarthritis-like damage of cartilage in the temporomandibular joints in mice with autoimmune inflammatory arthritis

Ghassemi-Nejad

Kobezda

Rauch

et al. 2011

Osteoarthritis and Cartilage

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Summary Objective To study temporomandibular joint (TMJ) involvement in an autoimmune murine model of rheumatoid arthritis (RA), a disease characterized by inflammatory destruction of the synovial joints. Although TMJ dysfunction is frequently found in RA, TMJ involvement in RA remains unclear, and TMJ pathology has not been studied in systemic autoimmune animal models of RA. Methods Proteoglycan (PG) aggrecan-induced arthritis (PGIA) was generated in genetically susceptible BALB/c mice. TMJs and joint tissues/cartilage were harvested for histological and immunohistochemical analyses and RNA isolation for quantitative polymerase chain reaction. Serum cytokine levels were measured in mice with acute or chronic arthritis, and in non-arthritic control animals. Results Despite the development of destructive synovitis in the limbs, little or no synovial inflammation was found in the TMJs of mice with PGIA. However, the TMJs of arthritic mice showed evidence of aggrecanase- and matrix metalloproteinase-mediated loss of glycosaminoglycan-containing aggrecan, and in the most severe cases, structural damage of cartilage. Serum levels of pro-inflammatory cytokines, including interleukin (IL)-1β, were elevated in arthritic animals. Expression of the IL-1β gene was also high in the inflamed limbs, but essentially normal in the TMJs. Local expression of genes encoding matrix-degrading enzymes (aggrecanases and stromelysin) was upregulated to a similar degree in both the limbs and the TMJs. Conclusion We propose that constantly elevated levels of catabolic cytokines, such as IL-1β, in the circulation (released from inflamed joints) create a pro-inflammatory milieu within the TMJ, causing local upregulation of proteolytic enzymes and subsequent loss of aggrecan from cartilage.

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Section: Discussionsupporting

confidence: 69%

Osteoarthritis-like damage of cartilage in the temporomandibular joints in mice with autoimmune inflammatory arthritis

Ghassemi-Nejad

Kobezda

Rauch

et al. 2011

Osteoarthritis and Cartilage

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“…The elevation of MMP2 was also revealed in TMJ displacement disks (15). Overexpression of MMP1 or MMP2 in synovial fluid is considered as a biochemical marker for TMJ OA (16,17). Up-regulation of MMP1 and MMP2 was also found in other fibrocartilage tissue diseases, such as degenerated intervertebral disks (18,19).…”

Section: Discussionmentioning

confidence: 97%

IL‐1β‐regulating angiogenic factors expression in perforated temporomandibular disk cells via NF‐κB pathway

Cai

Meng

et al. 2016

J Oral Pathology Medicine

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“…Collagen type II resists forces, and proteoglycan as aggrecan provides compressibility and elasticity in the articulating surface (67). Two major families of enzymes are responsible for cartilage degradation: matrix metalloproteinases (MMPs) and aggrecanases (68). MMPs are zinc-dependent endopeptidases with a wide spectrum of substrate specificities and consist of at least 19 different members.…”

Section: Breakdown Of Extracellular Matrixmentioning

confidence: 99%

The many faces of the genetics contribution to temporomandibular joint disorder

Oakley

Vieira

2008

Orthod Craniofacial Res

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Expression of matrix metalloproteinases and aggrecanase in the synovial fluids of patients with symptomatic temporomandibular disorders

Cited by 46 publications

References 26 publications

Osteoarthritis-like damage of cartilage in the temporomandibular joints in mice with autoimmune inflammatory arthritis

Osteoarthritis-like damage of cartilage in the temporomandibular joints in mice with autoimmune inflammatory arthritis

IL‐1β‐regulating angiogenic factors expression in perforated temporomandibular disk cells via NF‐κB pathway

The many faces of the genetics contribution to temporomandibular joint disorder

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