Intermittent compressive force stimulates bone resorption in orthodontic treatment. This study examined the molecular mechanism in human periodontal ligament (PDL) cells stimulated by an intermittent force. PDL cells were subjected to compressive force (2.0 or 5.0 g/cm(2)) for 2-4 days. Continuous or intermittent force was applied all day or for 8 hrs per day, respectively. At days 3 and 4, cell damage was less with intermittent force than with continuous force. At day 4, RANKL and IL-1beta expressions were greater with intermittent force than with continuous force. An IL-1 receptor antagonist inhibited the compressive force-induced RANKL expression. These findings indicate that IL-1beta is an autocrine factor regulating compressive force-induced RANKL expression in PDL cells, and that intermittent force can effectively induce RANKL in PDL cells with less cell damage.
The neurons in the trigeminal ganglion (TG) are surrounded by satellite glial cells (SGCs), which passively support the function of the neurons, but little is known about the interactions between SGCs and TG neurons after peripheral nerve injury. To examine the effect of nerve injury on SGCs, we investigated the activation of SGCs after neuronal damage due to the extraction of the upper molars in rats. Three, 7, and 10 days after extraction, animals were fixed and the TG was removed. Cryosections of the ganglia were immunostained with antibodies against glial fibrillary acidic protein (GFAP), a marker of activated SGCs, and ATF3, a marker of damaged neurons. After tooth extraction, the number of ATF3-immunoreactive (IR) neurons enclosed by GFAP-IR SGCs had increased in a time-dependent manner in the maxillary nerve region of the TG. Although ATF3-IR neurons were not detected in the mandibular nerve region, the number of GFAP-IR SGCs increased in both the maxillary and mandibular nerve regions. Our results suggest that peripheral nerve injury affects the activation of TG neurons and the SGCs around the injured neurons. Moreover, our data suggest the existence of a neuronal interaction between maxillary and mandibular neurons via SGC activation.
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