Effects of mandibular nerve transection on trigeminal ganglion neurons and the activation of microglial cells in the medullary dorsal horn

Microglial cell activation is known to contribute to neuropathic pain following spinal sensory nerve injuries. In this study, I investigated its mechanisms in the case of trigeminal sensory nerve injuries by which microglial cell and p38 mitogen-activated protein kinase (p38 MAPK) activation in the medullary dorsal horn (MDH) would contribute to the facial pain hypersensitivity following mandibular nerve transection (MNT). And also investigated the changes of trigeminal ganglion neurons and ERK, p38 MAPK manifestations. Activation of microglial cells was monitored at 1, 3, 7, 14, 28 and 60 day using immunohistochemical analyses. Microglial cell activation was primarily observed in the superficial laminae of the MDH. Microglial cell activation was initiated at postoperative 1 day, maximal at 3 day, maintained until 14 day and gradually reduced and returned to the basal level by 60 days after MNT. Pain hypersensitivity was also initiated and attenuated almost in parallel with microglial cell activation pattern. To investigate the contribution of the microglial cell activation to the pain hypersensitivity, minocycline, an inhibitor of microglial cell activation by means of p38 MAPK inhibition, was administered. Minocycline dose-dependently attenuated the development of the pain hypersensitivity in parallel with inhibition of microglial cell and p38 MAPK activation following MNT. Mandibular nerve transection induced the activation of ERK, but did not p38 MAPK in the trigeminal ganglion. These results suggest that microglial cell activation in the MDH and p38 MAPK activation in the hyperactive microglial cells play an important role in the development of facial neuropathic pain following MNT. The results also suggest that ERK activation in the trigeminal ganglion contributes microglial cell activation and facial neuropathic pain.

Chronic suppuraive osteomyelitis of the mandible caused by periodontal disease: a case report / 대한치주과학회지

Osteomyelitis is an exhaustive disease whose main feature is an inflammation of inner part of bone, bone marrow. In oral and maxillofacial area, we have maxillary and mandibular osteomyelitis and the latter is dominant because of its impaired blood supply. The main cause of osteomyelitis is a bacterial infection and the ways of infections are by periapical odontogenic infection, fracture, post-operative complication, and periodontal disease. The predominant etiologic factor is periapical odontogenic infection mostly caused by advanced dental caries. It is generally believed that periodontal disease could be a cause of osteomyelitis. But periodontal disease is usually confined to the alveolar bone area and not extends to the underlying bone marrow. Accordingly periodontal infection per se rarely cause produce oseomyelitis. Even though osteomyeltis could be occurred by periodontal disease, its virulence of infection is milder than periapical odontogenic infection. So it usually provokes sclerosing or hyperplastic osteomyelitis rather than suppurative type. We had a case of suppurative osteomyelitis caused by periodontal disease and treated it with periodontal and oral and maxillofacial surgical method.