Florid cemento‐osseous dysplasia (FCOD) is a benign, non‐neoplastic lesion characterized by multiple sclerosing masses only within jawbones. It is frequently confused with chronic diffuse sclerosing osteomyelitis (CDSO) in the literature. Two cases of FCOD are examined to determine the characteristics of their calcifying tissues. The first case was non‐infected, while the second case was severely infected, displaying the typical features of CDSO in clinico‐radiologic findings. The infected FCOD case showed large bacterial colonies in the main lesion with rare inflammatory reaction. The globular cementum‐like materials of FCOD looked like woven bone and showed increased positive reaction to Alcian blue stain, of which peripheral margin was strongly positive for the antibody of ameloblastin, and weakly positive for the antibodies of bone morphogenetic protein‐2 and ‐4. In the immunostains of matrix metalloprotein‐3, ‐9, ‐10, and transforming growth factor‐alpha, macrophage infiltration in the FCOD lesion were rarely observed. These data suggest that the cementum‐like materials of FCOD contain various matrix proteins, and that the cementum‐like materials are relevant to the overgrowth of the bacterial colonies by the inhibition of regional inflammatory reactions.

A 57 years old female received xenogenic bone graft for the extraction socket augmentation of right maxillary molars and for the sinus floor elevation six months ago. The bone graft sites were healed uneventfully and showed marked radiopacity in the postoperative X-ray view. Before dental implant insertion the bone biopsy was made using trephine bur and examined pathologically. The graft bones showed minimum new bone deposition with dysplastic epithelium. The epithelium was proliferative on the surface of graft bones forming epithelial strands and nests, similar to the odontogenic epithelium. The immunohistochemical study was performed using different antisera of odontogenic markers, growth factors, oncogenes, etc. The epithelial cells were strongly positive for pan-keratins, EGF, pAKT, and HSP-70, consistently positive for PCNA, p53, EGFR, 14-3-3, and survivin, slightly positive for ameloblastin, but rarely positive for amelogenin. Particularly the matrix of graft bone was slightly positive for EGF. Taken together, it is presumed that the abnormal epithelium on the graft bones was derived from odontogenic epithelial elements, Malassez epithelial rests, distributed at the periodontal tissue of maxillary molars, and that they might undergo dysplastic proliferation affected by the release of growth factors and osteogenic proteins from the graft bones. It is also suggested that the graft bone substitutes inserted for the dental implant possibly have a potential to induce the proliferation of odontogenic epithelial rests leading to the pathogenesis of odontogenic cysts and tumors.