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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.

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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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Nerve growth factor (NGF) plays a critical role in the trigeminal ganglion (TG) following peripheral nerve damage in the oral region. Although neurons in the TG are surrounded by satellite glial cells (SGCs) that passively support neural function, little is known regarding NGF expression and its interactions with TG neurons and SGCs. This study was performed to examine the expression of NGF in TG neurons and SGCs with nerve damage by experimental tooth movement. An elastic band was inserted between the first and second upper molars of rats. The TG was removed at 0–7 days after tooth movement. Using in situ hybridization, NGF mRNA was expressed in both neurons and SGCs. Immunostaining for NGF demonstrated that during tooth movement the number of NGF-immunoreactive SGCs increased significantly as compared with baseline and reached maximum levels at day 3. Furthermore, the administration of the gap junction inhibitor carbenoxolone at the TG during tooth movement significantly decreased the number of NGF-immunoreactive SGCs. These results suggested that peripheral nerve damage may induce signal transduction from neurons to SGCs via gap junctions, inducing NGF expression in SGCs around neurons, and released NGF may be involved in the restoration of damaged neurons.

Objective: To examine the effect of mouth breathing on chewing efficiency by evaluating masticatory variables. Materials and Methods: Ten adult nasal breathers with normal occlusion and no temporomandibular dysfunction were selected. Subjects were instructed to bite the chewing gum on the habitual side. While breathing through the mouth and nose, the glucide elution from the chewing gum, number of chewing strokes, duration of chewing, and electromyography (EMG) activity of the masseter muscle were evaluated as variables of masticatory efficiency. Results: The durations required for the chewing of 30, 60, 90, 120, 180, and 250 strokes were significantly (P , .05) longer while breathing through the mouth. There was no significant difference in the glucide elution rate (%) for each chewing stroke between nose and mouth breathings. The glucide elution rates for 1-and 3-minute chewing were significantly (P , .05) lower while breathing through the mouth. However, there was no significant difference in the glucide elution rate for 5-minute chewing between nose and mouth breathings. While chewing for 1, 3, and 5 minutes, the chewing stroke and EMG activity of the masseter muscle were significantly (P , .05) lower during mouth breathing. Conclusions: It takes a longer amount of time to complete chewing to obtain higher masticatory efficiency when breathing through the mouth. Therefore, mouth breathing will decrease the masticatory efficiency if the duration of chewing is restricted in everyday life. (Angle Orthod. 2016;86:227-234.)