As an approach to clarifying the molecular basis of pain and fatigue in muscles involved in temporomandibular disorders, the authors examined the activity of histidine decarboxylase (HOC), the enzyme which forms histamine, in the masseter muscles of mice. In the resting muscle, HOC activity was very low. Direct electrical stimulation of the muscle markedly elevated HOC activity. HOC activity rose within 3 hours of the electrical stimulation, peaked at 6 to 8 hours, and then gradually declined. Intraperitoneal injection of a small amount of interleukin-1 (IL-1) (from 1 to 10mcg/kg) produced a similar elevation of HOC activity in the masseter muscle. They also examined the effect of an antihistamine, chlorphenylamine (CP), on temporomandibular disorders in humans and compared it with that of an antiinflammatory analgesic, flurbiprofen (FB). Two groups received one or the other of the drugs daily for 7 days, and they were asked about their signs and symptoms before and after the treatment. A positive evaluation of their treatment was made by 74 percent of the CP group, but by only 48 percent of the FB group. Although the effects of CP on the limitation of mouth-opening and on joint noise were negligible, about 50 percent of the CP group answered positively concerning the drug's effect on spontaneous pain or pain induced by chewing or mouth-opening. The positive evaluation for CP (50 percent) in relieving associated symptoms (headache or shoulder stiffness) was significantly greater than for FB (13 percent). FB showed effectiveness similar to but sometimes weaker than that of CP on several symptoms. On the basis of these and previous results and the known actions of histamine, the authors propose that the histamine newly formed following the induction of HOC activity, which is itself mediated by IL-1, may be involved in inducing pain and, possibly, stiffness in muscles in temporomandibular disorders.
|Number of pages||1|
|Publication status||Published - 1999 Dec 1|
ASJC Scopus subject areas
- Clinical Neurology