osteoprotegerin and Temporomandibular-Joint-Disorders

The aim of this study was to review the cytokine profiles in the synovial fluid (SF) of patients with temporomandibular joint disorders (TMJD). Databases were searched from 1965 till September 2015 using different combinations of the following key words: "Temporomandibular joint"; "Cytokine"; "disorder"; and "synovial fluid" and "inflammation". Titles and abstracts of studies identified using the above-described protocol were screened and checked for agreement. Full-texts of articles judged by title and abstract to be relevant were read and independently evaluated. Hand-searching of the reference lists of potentially relevant original and review articles was also performed. The pattern of the present systematic review was customized to mainly summarize the relevant data. Fifteen studies were included. In 12 studies, cytokine profile of patients with TMJD was assessed using enzyme linked immunosorbent assay; and in 2 studies, histological analysis was performed to assess the cytokine profile of patients with TMJD. Patients with TMJD presented raised levels of interleukin (IL)-6 in 8 studies, IL-1beta (1β) in 5 studies and tumor necrosis factor-alpha (TNF-α) in 5 studies. Two studies showed no significant difference in TNF-α levels in patients with and without TMJD; and IL-1β levels were comparable in patients with and without TMJD in 2 studies. Raised levels of IL-6, TNF-α, IL-1β, IL-8, and IFN-γ in the SF have been associated with inflammation in patients with TMJD. Cytokines IL-10, osteoclastogenesis inhibitory factor/osteoprotegerin (OCIF/OPG), and VEGF found in the SF of TMJs could have an anti-inflammatory effect.

Topics: Cytokines; Humans; Inflammation Mediators; Interleukin-10; Osteoarthritis; Osteoprotegerin; Synovial Fluid; Temporomandibular Joint Disorders; Vascular Endothelial Growth Factor A

The aim of this study was to evaluate the association between genetic polymorphisms and the comorbid presence of chronic systemic arthralgia in patients with articular temporomandibular disorders (TMD). Subjects were evaluated for the presence of TMD and asked about the presence of chronic joint pain. Four groups were included in the study: articular TMD and systemic arthralgia (n=85), no articular TMD and systemic arthralgia (n=82), articular TMD and no systemic arthralgia (n=21), no articular TMD and no systemic arthralgia (control, n=72). A total of 14 single nucleotide polymorphisms in the OPG, RANK, and RANKL genes were investigated. In the statistical analysis, a P-value of <0.05 was considered significant. For the OPG gene, an association was observed between the group with chronic arthralgia and joint TMD and the control group (P=0.04). There was also a tendency towards an association of the haplotype CGCCAA with an increased risk of developing chronic joint pain, even in the absence of TMD (P=0.06). For the RANK gene, the AGTGC haplotype was associated with the lowest risk of presenting chronic joint pain in individuals without TMD (P=0.03). This study supports the hypothesis that changes in the OPG and RANK genes influence the presence of chronic joint pain in individuals with and without TMD.

Topics: Adolescent; Adult; Aged; Arthralgia; Chronic Disease; Comorbidity; Cross-Sectional Studies; Female; Genotype; Haplotypes; Humans; Linkage Disequilibrium; Male; Middle Aged; Osteoprotegerin; Polymorphism, Single Nucleotide; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Temporomandibular Joint Disorders

This study aimed to investigate genetic variations in the osteoprotegerin-encoding gene (TNFRSF11B) in patients with temporomandibular joint ankylosis (TMJA).. The sample comprised 17 patients diagnosed with TMJA, of both sexes with ages ranging from 6 to 57 years old. TNFRSF11B mutational analysis was performed using the Sanger sequencing method with DNA extracted from oral cells, and the functional impact prediction of the variants was assessed using bioinformatic analysis.. Sequencing analysis identified 15 (88.23%) patients that presented at least 1 genetic variant in TNFRSF11B. The mutation rs202090603 (p.E33K) was found in 6 individuals, and rs140782326 (p.V281M), rs11573942 (p.L295), and rs1375250340 (p.I389T) were identified in 1 subject each. According to the pathogenicity potential of mutations, 3 variants were considered of low impact (rs2073618, rs202090603, and rs2228568) and 3 as disease causing (rs140782326, rs11573942, and rs1375250340). The variant rs202090603 (p.E33K) was found in the first cysteine domain with differences in the loop positions of p.E33K mutated the 3D structure of osteoprotegerin.. Two polymorphisms (rs2073618 and rs2228568) and the mutations rs202090603 (p.E33K), rs140782326 (p.V281M), rs11573942 (p.L295), and rs1375250340 (p.I389T) in the TNFRSF11B gene may be associated with TMJA.

Topics: Adolescent; Adult; Ankylosis; Child; Female; Humans; Male; Middle Aged; Mutation; Osteoprotegerin; Temporomandibular Joint; Temporomandibular Joint Disorders; Young Adult

To evaluate the association between polymorphisms in genes that regulate bone metabolism, such as OPG, RANK, RANKL, and HIF1A, in patients with temporomandibular joint (TMJ) ankylosis.. The sample consisted of 181 individuals, the study included 17 individuals with TMJ ankylosis and 164 controls. DNA was extracted from buccal epithelial cells. The genotyping of genetic polymorphisms in OPG (rs2073618), RANK (rs3826620), RANKL (rs9594738), and HIF1A (rs2301113 and rs2057482) was performed by real-time PCR using TaqMan™ technology (Applied Biosystems). The data were subjected to statistical analysis with a level of significance of 0.05.. The OPG (rs2073618) polymorphism was associated with TMJ ankylosis, both in the additive model and in the dominant model (p < 0.05). In the additive model, when the individuals carried the CC genotype, they presented as 10.80 times more likely to develop the condition (p = 0.03). In the dominant model, individuals that carried at least one C allele were 5.76 times more likely to have TMJ ankylosis, than those with the G allele (p = 0.01).. The polymorphism rs2073618 of OPG is a possible marker that is associated with the risk of manifestation of TMJ ankylosis.

Topics: Ankylosis; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Osteoprotegerin; Patients; Polymorphism, Single Nucleotide; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Temporomandibular Joint; Temporomandibular Joint Disorders

Degenerative changes of condylar subchondral bone occur frequently in temporomandibular disorders. Although psychologic stresses and occlusal abnormalities have been implicated in temporomandibular disorder, it is not known if these risks represent synergistic comorbid factors that are involved in condylar subchondral bone degradation that is regulated by the sympathetic nervous system. In the present study, chronic immobilization stress (CIS), chemical sympathectomy, and unilateral anterior crossbite (UAC) were sequentially applied in a murine model. Norepinephrine contents in the subjects' serum and condylar subchondral bone were detected by ELISA; bone and cartilage remodeling parameters and related gene expression in the subchondral bone were examined. Subchondral bone loss and increased subchondral bone norepinephrine level were observed in the CIS and UAC groups. These groups exhibited decreased bone mineral density, volume fraction, and bone formation rate; decreased expressions of osterix, collagen I, and osteocalcin; but increased trabecular separation, osteoclast number and surface, and RANKL expression. Combined CIS + UAC produced more severe subchondral bone loss, higher bone norepinephrine level, and decreased chondrocyte density and cartilage thickness when compared to CIS or UAC alone. Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine level in all experimental subgroups when compared to the vehicle-treated counterparts. Norepinephrine also decreased mRNA expression of osterix, collagen I, and osteocalcin by mesenchymal stem cells at 7 and 14 d of stimulation and increased the expression of RANKL and RANKL/OPG ratio by mesenchymal stem cells at 2 h. In conclusion, CIS and UAC synergistically promote condylar subchondral bone loss and cartilage degradation; such processes are partially regulated by norepinephrine within subchondral bone.

Topics: Animals; Bone Density; Bone Resorption; Cartilage, Articular; Cell Count; Cell Culture Techniques; Chondrocytes; Collagen Type I; Disease Models, Animal; Female; Immobilization; Malocclusion; Mandibular Condyle; Mesenchymal Stem Cells; Mice; Mice, Inbred C57BL; Norepinephrine; Osteocalcin; Osteoclasts; Osteogenesis; Osteoprotegerin; RANK Ligand; Risk Factors; Stress, Psychological; Sympathectomy, Chemical; Temporomandibular Joint Disorders; Transcription Factors

Dietary loading has been reported to have an effect on temporomandibular joint (TMJ) remodeling via periodontal-muscular reflex. We therefore examined whether reducing dietary loading decreased TMJ degradation induced by the unilateral anterior crossbite prosthesis as we recently reported.. Forty 6-week-old female C57BL/6J mice were randomly divided into two experimental and two control groups. One experimental and one control group received small-size diet and the other two groups received large-size diet. Unilateral anterior crossbite prosthesis was created in the two experimental groups. The TMJ samples were collected 3 weeks after experimental operation. Histological changes in condylar cartilage and subchondral bone were assessed by Hematoxylin & Eosin, toluidine blue, Safranin O and tartrate-resistant acid phosphatase staining. Real-time polymerase chain reaction (PCR) and/or immunohistochemistry were performed to evaluate the expression levels of Collagen II, Aggrecan, a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5) and RANKL/RANK/OPG in TMJ condylar cartilage and/or subchondral bone.. Thinner and degraded cartilage, reduced cartilage cellular density, decreased expression levels of Collagen II and Aggrecan, loss of subchondral bone and enhanced osteoclast activity were observed in TMJs of both experimental groups. However, the cartilage degradation phenotype was less severe and cartilage ADAMTS-5 mRNA was lower while OPG/RANKL ratio in cartilage and subchondral bone was higher in the small-size than large-size diet experimental group. No differences of histomorphology and the tested molecules were found between the two control groups.. The current findings suggest that a lower level of functional loading by providing small-size diet could reduce TMJ degradation induced by the biomechanical stimulation from abnormal occlusion.

Topics: ADAM Proteins; ADAMTS5 Protein; Aggrecans; Animals; Body Weight; Cartilage, Articular; Collagen Type II; Dental Prosthesis; Diet; Disease Progression; Female; Malocclusion; Mandibular Condyle; Mastication; Mice; Mice, Inbred C57BL; Osteoarthritis; Osteoclasts; Osteoprotegerin; RANK Ligand; Temporomandibular Joint Disorders

The purposes of this research were to investigate the long-term responses of mandibular condylar cartilage to experimentally induced disordered occlusion and to evaluate changes in the expression of the SDF-1/CXCR4 axis.. Experimentally induced disordered occlusions were created in 8-week-old female Sprague-Dawley rats by orthodontic methods. After 24 weeks, remodeling of the mandibular condylar cartilage was assessed by hematoxylin and eosin staining. Protein and mRNA expression of SDF-1, CXCR4, MMP9, IL6, OPG, and RANKL were investigated by means of immunohistochemical staining and real-time polymerase chain reaction.. Obvious cartilage degenerative remodeling responses were observed; they appeared as uneven distributions of cellular disposition, loss of cartilage surface integrity, and cell-free areas. Regenerative responses presenting as thickening of the whole and the calcified cartilage layers in the experimental group were also observed. Compared with the age-matched controls, the protein and mRNA levels of SDF-1, CXCR4, MMP9, IL6, and OPG, but not RANKL, were increased in the experimental group (all, P <0.05). In addition, the mRNA level of RANKL/OPG showed a decreasing trend in the experimental group compared with the age-matched controls (P = 0.052).. This study demonstrated that long-term experimentally induced disordered occlusion leads to a combined response in degeneration and regeneration of mandibular cartilage, accompanied by active interaction of the SDF-1/CXCR4 axis and local upregulation of MMP9, IL6, and OPG.

Topics: Animals; Bone Remodeling; Cartilage, Articular; Chemokine CXCL12; Female; Interleukin-6; Malocclusion; Mandibular Condyle; Matrix Metalloproteinase 9; Osteoarthritis; Osteoprotegerin; RANK Ligand; Rats; Rats, Sprague-Dawley; Receptors, CXCR4; Regeneration; Temporomandibular Joint Disorders

The pathological changes of subchondral bone during osteoarthritis (OA) development in the temporomandibular joint (TMJ) are poorly understood. In the present study, we investigated the longitudinal alterations of subchondral bone using a rat TMJ-OA model developed in our laboratory. Changes in bone mass were examined by micro-CT, and changes in osteoblast and osteoclast activities were analyzed by real-time PCR, immunohistochemistry, and TRAP staining. Subchondral bone loss was detected from 8 weeks after dental occlusion alteration and reached the maximum at 12 weeks, followed by a repair phase until 32 weeks. Although bone mass increased at late stages, poor mechanical structure and lower bone mineral density (BMD) were found in these rats. The numbers of TRAP-positive cells were increased at 12 weeks, while the numbers of osteocalcin-expressing cells were increased at both 12 and 32 weeks. Levels of mRNA expression of TRAP and cathepsin K were increased at 12 weeks, while levels of ALP and osteocalcin were increased at both 12 and 32 weeks. These findings demonstrated that there is an active bone remodeling in subchondral bone in TMJs in response to alteration in occlusion, although new bone was formed with lower BMD and poor mechanical properties.

Topics: Animals; Bone Density; Bone Remodeling; Cathepsin K; Dental Occlusion, Traumatic; Dental Stress Analysis; Disease Models, Animal; Female; Mandibular Condyle; Osteoarthritis; Osteoblasts; Osteocalcin; Osteoclasts; Osteoprotegerin; Random Allocation; RANK Ligand; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Temporomandibular Joint; Temporomandibular Joint Disorders; X-Ray Microtomography

Temporomandibular joint osteoarthritis (TMJ OA) is a degenerative disease that affects both cartilage and subchondral bone. We used microarray to identify changes in gene expression levels in the TMJ during early stages of the disease, using an established TMJ OA genetic mouse model deficient in 2 extracellular matrix proteins, biglycan and fibromodulin (bgn(-/0)fmod(-/-)). Differential gene expression analysis was performed with RNA extracted from 3-week-old WT and bgn(-/0)fmod(-/-) TMJs with an intact cartilage/subchondral bone interface. In total, 22 genes were differentially expressed in bgn(-/0)fmod(-/-) TMJs, including 5 genes involved in osteoclast activity/differentiation. The number of TRAP-positive cells were three-fold higher in bgn(-/0)fmod(-/-) TMJs than in WT. Quantitative RT-PCR showed up-regulation of RANKL and OPG, with a 128% increase in RANKL/OPG ratio in bgn(-/0)fmod(-/-) TMJs. Histology and immunohistochemistry revealed tissue disorganization and reduced type I collagen in bgn(-/0)fmod(-/-) TMJ subchondral bone. Early changes in gene expression and tissue defects in young bgn(-/0)fmod(-/-) TMJ subchondral bone are likely attributed to increased osteoclast activity. Analysis of these data shows that biglycan and fibromodulin are critical for TMJ subchondral bone integrity and reveal a potential role for TMJ subchondral bone turnover during the initial early stages of TMJ OA disease in this model.

Topics: Animals; Arthritis, Experimental; Biglycan; Bone and Bones; Bone Remodeling; Cartilage, Articular; Disease Models, Animal; Extracellular Matrix Proteins; Fibromodulin; Gene Expression Profiling; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Oligonucleotide Array Sequence Analysis; Osteoarthritis; Osteoclasts; Osteoprotegerin; Proteoglycans; RANK Ligand; Reverse Transcriptase Polymerase Chain Reaction; Temporomandibular Joint Disorders

Several epidemiological studies have reported that temporomandibular disorder is more prevalent in women, which suggests the involvement of sex hormones, such as estrogen, in the pathogenesis of this disease. PCR amplification and Western blotting were employed to target the expression of estrogen receptors (ERs) in human fibroblast-like synovial and ATDC5 cells. The effect of estrogen was investigated through the expression of RANKL, osteoprotegerin (OPG), M-CSF/CSF-1 and c-fms. We showed expression of M-CSF/ CSF-1 and c-fms, with time-dependent increase in both after the addition of estrogen. Based on previous studies reporting that M-CSF/CSF-1 regulates the proliferation and differentiation of hemopoietic progenitor cells into mature macrophages, we put forward a new hypothesis based on the increased inflammation and tendency of females to suffer more from temporomandibular disorder (TMD) in the presence of external exacerbating factors. Detection of RANKL and OPG in ATDC5 and expression of both in HFLS was confirmed with complete disappearance of the RANKL band, and marked increase in the expression of OPG after 1 h from the addition of estrogen.

Topics: Aged; Animals; Blotting, Western; Bone Resorption; Cell Differentiation; Cell Line, Tumor; Cells, Cultured; Estrogens; Female; Fibroblasts; Gene Expression; Gonadal Steroid Hormones; Humans; Inflammation; Macrophage Colony-Stimulating Factor; Osteoprotegerin; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B; Receptor, Macrophage Colony-Stimulating Factor; Receptors, Estrogen; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Synovial Membrane; Temporomandibular Joint; Temporomandibular Joint Disorders

We investigated the effects of compressive mechanical stress on osteoclastogenesis of synovial cells to clarify the mechanism of osteoclast formation by those cells in temporomandibular joint (TMJ) disorders.. Synovial cells were isolated from rat knee joints and continuously compressed using a conventional method. The expression of receptor activator nuclear factor kappaB ligand (RANKL) mRNA and protein in synovial cells was analyzed by reverse transcriptase-polymerase chain reaction, immunoblotting, and immunofluorescence staining. Mouse bone marrow cells were cultured with synovial cells for 7 days to detect osteoclasts.. The expressions of RANKL mRNA and protein in synovial cells were increased with compressive force. When mouse bone marrow cells were cultured with continuously compressed synovial cells, tartrate-resistant acid phosphatase-positive multinucleated cells were formed. Osteoprotegerin completely inhibited osteoclast formation induced by culturing with compressed synovial cells.. Our results indicated that the expression of RANKL in compressed synovial cells enhanced osteoclast formation, whereas continuous compressive force may induce osteoclastic bone destruction in the TMJ.

Topics: Animals; Blotting, Western; Bone Marrow Cells; Cell Differentiation; Cells, Cultured; Coculture Techniques; Compressive Strength; Dental Stress Analysis; Male; Mice; Mice, Inbred Strains; Microscopy, Fluorescence; Osteoclasts; Osteoprotegerin; RANK Ligand; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; Stress, Mechanical; Synovial Membrane; Temporomandibular Joint Disorders

Although a recent study suggested the involvement of RANKL and osteoprotegerin (OPG) in the pathogenesis of bone-destructive disease, no study has focused on the RANKL:OPG ratio in the synovial fluid of patients with temporomandibular joint (TMJ) disorder. This communication reports on the concentrations of RANKL and OPG in synovial fluid from TMJ patients and healthy control individuals. In contrast to an unchanged concentration of RANKL, a strong decrease in the concentration of OPG was detected in the synovial fluid from patients with TMJ internal derangement. Treatment with the synovial fluid of osteoarthritis (OA) patients resulted in the high production of osteoclast-like cells from blood mononuclear cells in vitro, as well as in pit formation in dentin slices. The addition of anti-RANKL IgG or OPG attenuated OA-synovial fluid-induced osteoclast formation, suggesting that the increase in the RANKL:OPG ratio in the microenvironment of the joint has the potential to induce osteoclastogenesis in TMJ osteoarthritis.

Topics: Adult; Analysis of Variance; Case-Control Studies; Cell Differentiation; Cells, Cultured; Female; Humans; Immunoglobulin G; Joint Dislocations; Macrophage Colony-Stimulating Factor; Male; Monocytes; Osteoarthritis; Osteoclasts; Osteoprotegerin; RANK Ligand; Synovial Fluid; Temporomandibular Joint Disorders

Temporomandibular joint disorders (TMD) comprise a group of chronic painful conditions of mastication in the temporomandibular joint (TMJ). Although the association between TMD and internal derangement of the TMJ is well documented, the functional relevance is still unclear. Increased concentrations of inflammatory mediators have been identified in the synovial fluid of affected patients with TMD, suggesting an underlying degenerative or inflammatory process. The aim of this study was to generate a comprehensive cytokine expression profile in TMD.. 15 samples from patients with internal derangement of TMJ were analysed using a novel cytokine array that enables the analysis of 79 different cytokines simultaneously.. Cytokine levels were correlated with the presence of joint effusion (JE) determined by MRI. In the majority of synovial fluid samples, angiogenin (Ang), fibroblast growth factor (FGF)-9, insulin-like growth factor-binding protein (IGFBP)-3, interleukin (IL)-1alpha, IL-1beta, IL-8, inducible protein (IP)-10, macrophage inflammatory protein (MIP)-1beta, osteoprotegerin (OPG), transforming growth factor (TGF)-beta2, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, tumour necrosis factor (TNF)-beta and vascular endothelial growth factor (VEGF) were detectable. Furthermore, the expression levels of Ang, brain-derived neurotrophic factor (BDNF), FGF-4, FGF-9, IGFBP-2, IL-8, MIP-1beta, OPG, pulmonary and activation-regulated protein (PARC), TGF-beta2, TIMP-2 and VEGF were significantly associated with the presence of JE; among these, nine cytokines (Ang, BDNF, FGF-4, FGF-9, IGFBP-2, MIP-1beta, PARC, TGF-beta2 and TIMP-2) were hitherto not described in TMD.. This study confirmed previous reports of elevated cytokine levels in TMD. Additionally, we identified previously undescribed cytokines that were upregulated and correlated significantly with the presence of JE. We were able to identify novel cytokines that have hitherto not been described in TMD. Strategies targeting the identified cytokines may represent a novel therapy option in TMD.

Topics: Adult; Aged; Chemokine CCL4; Chemokine CXCL10; Chemokines, CXC; Cytokines; Female; Fibroblast Growth Factor 9; Humans; Insulin-Like Growth Factor Binding Protein 3; Interferon-gamma; Interleukin-1alpha; Interleukin-1beta; Interleukin-8; Macrophage Inflammatory Proteins; Male; Middle Aged; Osteoprotegerin; Ribonuclease, Pancreatic; Synovial Fluid; Temporomandibular Joint Disorders; Tissue Inhibitor of Metalloproteinase-1; Tissue Inhibitor of Metalloproteinase-2; Transforming Growth Factor beta2; Vascular Endothelial Growth Factor A

The aim of this study was to investigate the correlations among the expression of osteoprotegerin (OPG) in synovial tissue and the degree of synovitis, the degeneration of articular cartilage, and the adhesions in patients with internal derangement and osteoarthritis of the temporomandibular joint (TMJ). Study design The expression of OPG, which was detected immunohistochemically, and the degree of arthroscopy of 31 patients with internal derangement and osteoarthritis of the TMJ were assessed and the correlations between them were analyzed statistically.. OPG was expressed in the cytoplasm of the endothelial cells, synovial lining cells, and fibroblast cells. TMJs with osteoarthritis had a higher degree of articular cartilage degeneration than did TMJs with internal derangement. There was a correlation between the expression of OPG in the endothelial cells and the degree of the articular cartilage degeneration (P <.01).. The expression of OPG might be associated with the development of degenerative changes of articular cartilage.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Arthroscopy; Cartilage, Articular; Cytoplasm; Endothelium, Vascular; Female; Fibroblasts; Glycoproteins; Humans; Male; Middle Aged; Osteoarthritis; Osteoprotegerin; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor; Statistics, Nonparametric; Synovial Membrane; Synovitis; Temporomandibular Joint Disorders; Tissue Adhesions

The goal of this study was to measure the activities of osteoclastogenesis inhibitory factor/osteoprotegerin (OCIF/OPG), interleukin-1beta (IL-1beta), and tumour necrosis factor-alpha (TNF-alpha) in synovial fluid from 24 patients with internal derangement and 26 with osteoarthritis of the temporomandibular joint (TMJ). Five asymptomatic healthy volunteers were studied as control. Concentrations of OCIF/OPG, IL-1beta, and TNF-alpha were determined by enzyme-linked immunosorbent assay. The mean OCIF/OPG concentration in the patients with osteoarthritis (71 pg/ml) was significantly lower than those in the patients with internal derangement (160 pg/ml, P< 0.05) and the healthy volunteers (196 pg/ml, P< 0.01). In contrast, the IL-1beta and TNF-alpha concentrations were similar in all three groups. These results suggest that OCIF/OPG is associated with the pathogenesis of osteoarthritis of the TMJ. Perhaps, decreased OCIF/OPG concentrations promote osteoclastic activity and induce osteoarthritis of the TMJ.

Topics: Adolescent; Adult; Aged; Child; Female; Glycoproteins; Humans; Interleukin-1; Joint Dislocations; Male; Middle Aged; Osteoarthritis; Osteoprotegerin; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor; Synovial Fluid; Temporomandibular Joint Disorders; Tumor Necrosis Factor-alpha