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Deterioration of mechanical properties of discs in chronically inflamed TMJ.

ABSTRACT: Temporomandibular joint (TMJ) discs frequently undergo degenerative changes in arthritis. However, the biomechanical properties of pathogenic discs remain to be explored. In this study, we evaluated the effects of chronic inflammation on the biomechanical properties of TMJ discs in rats. Chronic inflammation of TMJs was induced by double intra-articular injections of complete Freund's adjuvant for 5 weeks, and biomechanical properties and ultrastructure of the discs were examined by mechanical testing, scanning electron microscopy, and transmission electron microscopy. The instantaneous compressive moduli of the anterior and posterior bands of discs in inflamed TMJs were decreased significantly compared with those in the control group. The instantaneous tensile moduli of the discs of inflamed TMJs also showed significant decreases in both the anterior-posterior and mesial-lateral directions. The relaxation moduli of the discs of inflamed TMJs showed nearly the same tendency as the instantaneous moduli. The surfaces of the discs of inflamed TMJs became rough and porous due to the loss of the superficial gel-like stratum, with many collagen fibers exposed and degradation of the sub-superficial collagen fibrils. Our results suggested that chronic inflammation of TMJ could lead to deterioration of mechanical properties and alteration of disc ultrastructure, which might contribute to TMJ disc displacement.

SUBMITTER: Wang XD

PROVIDER: S-EPMC4293775 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature

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Deterioration of mechanical properties of discs in chronically inflamed TMJ.

Wang X D XD Cui S J SJ Liu Y Y Luo Q Q Du R J RJ Kou X X XX Zhang J N JN Zhou Y H YH Gan Y H YH

Journal of dental research 20140929 11

Temporomandibular joint (TMJ) discs frequently undergo degenerative changes in arthritis. However, the biomechanical properties of pathogenic discs remain to be explored. In this study, we evaluated the effects of chronic inflammation on the biomechanical properties of TMJ discs in rats. Chronic inflammation of TMJs was induced by double intra-articular injections of complete Freund's adjuvant for 5 weeks, and biomechanical properties and ultrastructure of the discs were examined by mechanical t ...[more]

PMID: 25266714

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Project description:Heterotopic cartilage develops in certain pathologic conditions, including those affecting the human temporomandibular joint (TMJ), but the underlying molecular mechanisms remain obscure. This is in part due to the fact that a reliable animal model of such TMJ diseases is not available. Here, we show that aberrant chondrocyte differentiation and ectopic cartilage formation occur spontaneously in proteoglycan 4 (Prg4) mutant TMJ discs without further invasive procedure. By 2 mo of age, mutant disc cells displayed chondrocyte transdifferentiation, accompanied by strong expression of cartilage master gene Sox9 and matrix genes aggrecan and type II collagen. By 6 mo, heterotopic cartilage had formed in the discs and expressed cartilage hypertrophic markers Runx2 and ColX. The ectopic tissue grew in size over time and exhibited regional mineralization by 12 mo. Bone morphogenetic protein (BMP) signaling was activated with the ectopic chondrogenic cells and chondrocytes, as indicated by phosphorylated Smad 1/5/8 nuclear staining and by elevated expression of Bmp2, Bmpr1b, Bmpr2, and BMP signaling target genes. Likewise, we found that upon treatment with recombinant human BMP 2 in high-density micromass culture, mutant disc cells differentiated into chondrocytes and synthesized cartilage matrix more robustly than control cells. Importantly, a specific kinase inhibitor of BMP receptors drastically attenuated chondrogenesis in recombinant human BMP 2-treated mutant disc cultures. Unexpectedly, we found that Prg4 was expressed at joint-associated sites, including disc/muscle insertion and muscle/bone interface, and all these structures were abnormal in Prg4 mutants. Our data indicate that Prg4 is needed for TMJ disc integrity and function and that its absence leads to ectopic chondrogenesis and cartilage formation in conjunction with abnormal BMP signaling. Our findings imply that the BMP signaling pathway could be a potential therapeutic target for prevention or inhibition of ectopic cartilage formation in TMJ disease.

Project description:BackgroundTemporomandibular disorders (TMDs) have the highest prevalence in women of reproductive age. The role of estrogen in TMDs and especially in TMDs related pain is not fully elucidated. Voltage-gated sodium channel 1.7 (Nav1.7) plays a prominent role in pain perception and Nav1.7 in trigeminal ganglion (TG) is involved in the hyperalgesia of inflamed Temporomandibular joint (TMJ). Whether estrogen could upregulate trigeminal ganglionic Nav1.7 expression to enhance hyperalgesia of inflamed TMJ remains to be explored.MethodsEstrous cycle and plasma levels of 17?-estradiol in female rats were evaluated with vaginal smear and enzyme linked immunosorbent assay, respectively. Female rats were ovariectomized and treated with 17?-estradiol at 0 ?g, 20 ?g and 80 ?g, respectively, for 10 days. TMJ inflammation was induced using complete Freund's adjuvant. Head withdrawal thresholds and food intake were measured to evaluate the TMJ nociceptive responses. The expression of Nav1.7 in TG was examined using real-time PCR and western blot. The activity of Nav1.7 promoter was examined using luciferase reporter assay. The locations of estrogen receptors (ER? and ER?), the G protein coupled estrogen receptor (GPR30), and Nav1.7 in TG were examined using immunohistofluorescence.ResultsUpregulation of Nav1.7 in TG and decrease in head withdrawal threshold were observed with the highest plasma 17?-estradiol in the proestrus of female rats. Ovariectomized rats treated with 80 ?g 17?-estradiol showed upregulation of Nav1.7 in TG and decrease in head withdrawal threshold as compared with that of the control or ovariectomized rats treated with 0 ?g or 20 ?g. Moreover, 17?-estradiol dose-dependently potentiated TMJ inflammation-induced upregulation of Nav1.7 in TG and also enhanced TMJ inflammation-induced decrease of head withdrawal threshold in ovariectomized rats. In addition, the estrogen receptor antagonist, ICI 182,780, partially blocked the 17?-estradiol effect on Nav1.7 expression and head withdrawal threshold in ovariectomized rats. ER? and ER?, but not GPR30, were mostly co-localized with Nav1.7 in neurons in TG. In the nerve growth factor-induced and ER?-transfected PC12 cells, 17?-estradiol dose-dependently enhanced Nav1.7 promoter activity, whereas mutations of the estrogen response element at -1269/-1282 and -1214/-1227 in the promoter completely abolished its effect on the promoter activity.ConclusionEstradiol could upregulate trigeminal ganglionic Nav1.7 expression to contribute to hyperalgesia of inflamed TMJ.

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Deterioration of mechanical properties of discs in chronically inflamed TMJ.

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Deterioration of mechanical properties of discs in chronically inflamed TMJ.

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