Florid osseous dysplasia is the preferred name for a condition that has many other names, each reflecting a different opinion regarding the fundamental nature of the disease and the tissue of origin, bone or cementum. It is acquired during the early adult years, is non-neoplastic and non-inflammatory, is self-limiting and generally requires no treatment. The strong propensity that FOD exhibits for middle age African American females is unexplained, and the reason it affects the jaws and is unknown in the rest of the skeleton remains a mystery. The condition may be ushered in by painless expansion of the jaws but more commonly is silent and discovered on radiographs taken for other reasons.
Both the maxilla and mandible may be involved but variants are encountered in which one jaw or one quadrant of one jaw is involved. The mandible bears the brunt of the disease. Radiographically, FOD progresses over a period of years beginning as a purely radiolucent lesion and ending as solid, dense masses in the jaws. The intermediate stage appears as a mixed radiolucent-radiodense lesion involving much of the body of the bone. Confluent sclerotic masses surrounded by radiolucent areas form an image that is virtually pathognomic. The appearance of early lesions in the vicinity of dental root tips has led to speculation that the calcified, dense material is cementum rather than bone. This accounts for other names such as cemento-osseous dysplasia and sclerotic cemental masses of the jaws. As it progresses, lesions spread far beyond the teeth and fill the surrounding bone. Teeth are not resorbed nor displaced. Florid osseous dysplasia may be the ultimate expression of a spectrum of fibro-osseous disease, the minimal form of which is the common cementoma (periapical cemental dysplasia), which also shows a propensity for African American females. Cavities resembling traumatic bone cysts are encountered in some cases of FOD. The histologic features of FOD overlap other fibro-osseous lesions so that radiographic and clinical correlation is necessary. From benign, cellular fibrous connective tissue arise trabeculae of woven bone and droplet, acellular calcifications that resemble cementum. The latter may grow to form large, globular masses that are more basophilic than bone and have prominent reversal lines. The histologic and radiographic features mimic Paget's disease of bone to some extent but in FOD, serum calcium values and alkaline phosphatase are unaltered and extragnathic lesions do not exist. When FOD is localized, it may resemble ossifying fibroma radiographically and histologically. No treatment is required for florid osseous dysplasia.
However, clinicians should be aware that sclerotic bone, regardless of the cause, is more vulnerable to infection. Invasive dental procedures such as dental extractions should take this into account. Edentulous patients pose another problem. Slow but inexorable atrophy of the alveolar bone may alter denture fit so that friction ulcers develop. This creates a portal of entry for pathogens and heightens the risk of osteomyelitis.
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