Modulation of temporomandibular joint nociception and inflammation in male rats after administering a physiological concentration of 17β-oestradiol.
BACKGROUND
Previous studies have shown 17β-estradiol will reduce temporomandibular joint (TMJ) inflammation and hypersensitivity in female rats. Although male rats contain significant amounts of oestradiol, it was unknown whether a physiological concentration of 17β-estradiol would attenuate male TMJ inflammation and nociception.


METHODS
Intact and castrated rats were given a physiological concentration of oestradiol to examine first, if oestradiol will affect male TMJ nociception/inflammation and, second, if administration of oestradiol would act synergistically with endogenous male hormones to attenuate TMJ nociception. The hormonally treated rats were given TMJ injections of complete Freund's adjuvant (CFA) and then nociception was measured using a validated method in which a lengthening in meal duration is directly correlated to the intensity of deep TMJ nociception. Inflammation was assayed by quantitating pro-inflammatory gene expression.


RESULTS
Meal duration was significantly lengthened after TMJ CFA injection and this lengthening was significantly attenuated in the castrated but not intact males after administering a physiological concentration of oestradiol. A physiological concentration of 17β-estradiol also significantly increased IL-6 expression in the inflamed TMJ of castrated males while 17β-estradiol did not alter IL-1β, CXCL2 and CCL20 expression. Castration increased pro-inflammatory mediators IL-6, IL-1β and CXCL2 suggesting male sex hormones were anti-inflammatory. Calcitonin gene-related peptide in the trigeminal ganglia was unchanged.


CONCLUSIONS
Similar to females, male rats with TMJ inflammation showed a reduced nociceptive response after treatment with a physiological concentration of oestradiol suggesting the effects of oestradiol treatment were not constrained by organizational processes in the males.
Department of Biomedical Sciences, Baylor College of Dentistry, Texas A&M Health Science Center, Dallas, USA. pkramer@bcd.tamhsc.edu
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D000818:Animals; D000893:Anti-Inflammatory Agents; D018925:Chemokines / Q000378:metabolism; D004343:Drug Implants; D004958:Estradiol / Q000097:blood / Q000627:therapeutic use*; D030762:Estrous Cycle / Q000187:drug effects; D005247:Feeding Behavior / Q000187:drug effects; D005260:Female; D005620:Freund's Adjuvant; D008297:Male; D059225:Nociception / Q000187:drug effects; D009919:Orchiectomy; D010147:Pain Measurement / Q000187:drug effects; D011359:Proestrus / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018015:Receptors, Calcitonin Gene-Related Peptide / Q000378:metabolism; D013705:Temporomandibular Joint Disorders / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology
D000893:Anti-Inflammatory Agents; D018925:Chemokines; D004343:Drug Implants; D018015:Receptors, Calcitonin Gene-Related Peptide; D004958:Estradiol; D005620:Freund's Adjuvant