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Rapidly Progressing Osteomyelitis of the MandibleDOI: 10.1155/2013/249615 Abstract: Acute osteomyelitis exists as a refractory disease even now, which usually exhibits systemic symptoms such as fever or malaise and local redness or swelling. The present paper describes a case of acute osteomyelitis of the mandible that was rapidly progressing without typical symptoms. The patient had liver cirrhosis, which should be one of the systemic factors that affect immune surveillance and metabolism. Actinomycotic druses and filaments were detected from the sequestrum. These were considered to play a role in the rapid progression of osteomyelitis without typical symptoms. There has been no evidence of local recurrence 24 months after surgery. 1. Introduction Acute osteomyelitis of the jaws is not commonly seen in modern oral and maxillofacial surgery practice. Generally speaking, this can be related to our society having become more health conscious, resulting in an increased awareness of nutrition, as well as earlier and better access to health care than in the past [1, 2]. However, acute osteomyelitis exists as a refractory disease even now, which usually exhibits systemic symptoms such as fever, malaise or high levels of CRP and local redness, swelling, or pus discharge. It is known that osteomyelitis can be attributed to one or more of the predisposing systemic diseases [3]. In immune-compromised patients, it is easy to expect that acute inflammatory reactions are poor. Few case reports such as osteomyelitis of the jaws with poor acute inflammatory reactions and rapid progression have been documented. The present paper describes a case of acute osteomyelitis of the mandible, with liver cirrhosis, that was rapidly progressing without typical symptoms. 2. Case Report A 77-year-old man was referred to our hospital for postextraction hemorrhage and spontaneous pain in the socket of the left mandibular first molar. The patient had a 1-month history of spontaneous pain of the left mandibular first molar. At a nearby dental clinic, restorative treatment was performed. However, as the pain continued, the tooth was finally extracted on January 19, 2011. Next day he visited our hospital. When first examined, he had neither swelling in his cheek nor paresthesia in his lower lip. Postextraction hemorrhage of the mandibular first molar had already arrested. Instead, the clot was absent and the socket made the pale alveolar bone expose (Figure 1(a)). There was no redness or swelling in the regional gum and no mobility and percussion pain of the adjacent teeth. Panoramic radiograph showed neither abnormal consolidation nor ill-defined trabecular bone
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