Estrogen and progesterone receptors in temporomandibular joint discs of symptomatic and asymptomatic persons: A preliminary study

Abubaker, A. Omar; Raslan, Wassim F.; Sotereanos, George C.

doi:10.1016/s0278-2391(10)80448-3

Cited by 162 publications

(84 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although many epidemiological studies have reported a higher frequency of TMD in females than in males (Campbell et al, 1993; LeResche, 1997; Kapila and Xie, 1998), there has been controversy concerning the presence of ER␣ in the TMJ. Abubaker et al (1993) found ER␣ immunoreactivity in the articular disc of human TMJs; however, Campbell et al (1993) found no such immunoreactivity in the articular disc of a TMJ obtained from a TMD patient. Furthermore, some researchers have observed sexual dimorphism in ER expression in the baboon TMJ by autoradiography (Aufdemorte et al, 1986;Milam et al, 1987).…”

Section: Discussionmentioning

confidence: 93%

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Yamada¹,

Nozawa-Inoue²,

Kawano³

et al. 2003

Anat. Rec.

View full text Add to dashboard Cite

Numerous epidemiological studies have pointed out a higher frequency of temporomandibular disorder (TMD) in women than in men, which indicates the involvement of a sex hormone, such as estrogen, in the pathogenesis of TMD. Although estrogen is known to play pivotal roles in osteoarthrosis or rheumatoid arthritis in systemic joints, there have been few reports about the role of estrogen in the temporomandibular joint (TMJ). The effect of estrogen is generally mediated by the estrogen receptors (ERs) ER␣ (the predominant type) and ER␤. In this study we examined the expression of ER␣ protein and mRNA in the TMJ of adult male rats by immunocytochemistry and in situ hybridization histochemistry. Intense ER␣ immunoreactivity was localized in the synovial lining cells, stromal cells in the articular disc, and chondrocytes in the TMJ. These ER␣-immunopositive synovial lining cells are characteristic of cytoplasmic processes identified with confocal and immunoelectron microscopy, which indicates that they are synovial type B cells. In situ hybridization histochemistry confirmed intense signals for ER␣ in the synovial lining cells and the sublining fibroblasts at mRNA levels. The nuclei of chondrocytes showed an intense immunoreaction for ER␣ in the maturative and hypertrophic layers of the articular cartilage. In addition to the nuclear localization of ER␣, a weak immunoreaction appeared in the cytoplasm of some ER␣-positive cells. These findings support the hypothesis that TMJ tissue-at least in the male rat-has the potential to be an estrogen target tissue. Anat Rec Part A 274A: 934 -941, 2003.

show abstract

Section: Discussionmentioning

confidence: 93%

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Yamada¹,

Nozawa-Inoue²,

Kawano³

et al. 2003

Anat. Rec.

View full text Add to dashboard Cite

show abstract

“…TMD pain is significantly related to synovitis, internal derangement, and osteoarthritis, indicating that joint inflammation could be a major reason for TMD pain (Holmlund et al, 1989;Murakami et al, 1991;Israel et al, 1997;Kopp, 1998). Although sex-based differences in TMD pain perception may also be related to social and cultural factors, attention has long been paid to the possible roles that estrogens play in TMD (Abubaker et al, 1993;Okuda et al, 1996;LeResche et al, 1997LeResche et al, , 2003Cheng et al, 2000;Landi et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

17- -Estradiol Enhanced Allodynia of Inflammatory Temporomandibular Joint through Upregulation of Hippocampal TRPV1 in Ovariectomized Rats

Wu¹,

Bi²,

Kou³

et al. 2010

Journal of Neuroscience

105

View full text Add to dashboard Cite

Temporomandibular disorders (TMDs) predominantly affect reproductive female patients, with pain the most frequent complaint. Although estrogens are believed to play important roles in TMD pain, the mechanism underlying modulation of TMD pain by estrogens remains largely unknown. Accumulating evidence implies that the hippocampus is involved in sexual dimorphism of pain sensitivity. In this study, we investigated the hippocampal TRPV1 (transient receptor potential vanilloid 1) expression in ovariectomized rats that received 17-␤-estradiol substitution and found that 17-␤-estradiol enhanced the mechanical allodynia of inflamed temporomandibular joint (TMJ) induced by complete Freund's adjuvant. Real-time PCR and immunoblotting demonstrated that TMJ inflammation significantly induced hippocampal TRPV1 expression compared with the control group but failed to induce it in the ovariectomized rats that received no estradiol replacement. In addition, estradiol potentiated TMJ inflammation-induced hippocampal TRPV1 expression in a dose-dependent manner in the ovariectomized rats. In contrast, TRPV1 transcription in amygdala, prefrontal cortex, and thalamus was not affected by TMJ inflammation and estradiol. Immunostaining showed TRPV1 localized in the processes and cytoplasm of pyramidal neurons in CA1-CA3 regions of the hippocampus. Moreover, intrahippocampal injection of TRPV1 antagonists capsazepine and 5Ј-iodoresiniferatoxin into the CA1 region of the hippocampus significantly attenuated allodynia of inflamed TMJ in both nonovariectomized and ovariectomized rats that received estradiol replacement. Our results suggested that hippocampal TRPV1 can modulate central pain processing and estradiol may contribute to the sexual dimorphism of TMD pain sensitivity through upregulation of TRPV1 expression in the hippocampus.

show abstract

“…Abubaker et al (29) found ER α immunoreactivity in the articular disc of human TMJs; however, Campbell et al (5) found no such immunoreactivity in the articular disc of a TMJ obtained from a TMD patient. In our previous study (30), with the use of Western blotting and PCR amplification, we were able to demonstrate the novel detection of ER ß and confirmed presence of ER α in RAW 264.7 cells (representing macrophage-like type A synovial linning cells).…”

Section: Discussionmentioning

confidence: 99%

Effect of estrogen on bone resorption and inflammation in the temporomandibular joint cellular elements

Galal

Beialy²,

Deyama³

et al. 2008

Int J Mol Med

View full text Add to dashboard Cite

Abstract. 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.

show abstract

Estrogen and progesterone receptors in temporomandibular joint discs of symptomatic and asymptomatic persons: A preliminary study

Cited by 162 publications

References 35 publications

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

Expression of estrogen receptor α (ERα) in the rat temporomandibular joint

17- -Estradiol Enhanced Allodynia of Inflammatory Temporomandibular Joint through Upregulation of Hippocampal TRPV1 in Ovariectomized Rats

Effect of estrogen on bone resorption and inflammation in the temporomandibular joint cellular elements

Contact Info

Product

Resources

About