Florid osseous dysplasia of the mandible: report of a case.

In 1986, a 60-year-old African American woman visited the Marquette University School of Dentistry with a complaint of a vague, dull pain in her lower left quadrant. Tooth No. 19 was extracted 10 years earlier because of extensive decay, and tooth No. 18 had received root canal therapy. A panoramic radiograph revealed the presence of ill-defined, multilocular, mixed (radiopaque-radiolucent) lesions present throughout the lower jaw. She was treated with antibiotics and scheduled for follow-up visits. When the symptoms persisted, tooth No. 18 was re-treated with root canal therapy and a representative biopsy was taken from the left mandibular area. The biopsy showed the presence of chronic osteomyelitis. The patient was treated with antibiotics and was scheduled for periodic check-up visits. In February 1995, she returned with the same symptoms in the left mandible. A panoramic radiograph showed persistence of the mixed radiopaque-radiolucent lesions throughout her mandible; however, the mass on the left side was more radiopaque and had assumed a "cotton wool" appearance. Tooth No. 18 was extracted and a biopsy was taken from the area. After correlating the clinical behavior, radiographic appearance, and histopathologic features, a diagnosis of florid osseous dysplasia with osteitis was made. This case represents a classic example of the difficulty in diagnosing fibro-osseous lesions using radiographic interpretation alone and the need to correlate the clinical, radiographic, and histopathologic features to reach a diagnosis. Additionally, the present case clearly shows treatment problems of an otherwise self-limiting condition when secondary involvement with osteomyelitis is also present. A brief description of the conditions that were included in the differential diagnosis and their management is presented.

Keratoameloblastoma of the maxilla. A case report and review of the literature.

The keratoameloblastoma is a rare histologic variant of the ameloblastoma. Review of the English language literature revealed five case reports of keratoameloblastoma. We report the sixth case of this tumor. The tumor developed in the right posterior maxilla of a 26-year-old African-American man and demonstrated aggressive clinical behavior, analogous to conventional ameloblastoma. The initial biopsy specimen showed extensive cyst formation, which histologically resembled odontogenic keratocyst. However, the lining epithelium varied in thickness and there was separation and edema between the basal cells and the rest of the epithelium. The basal cells were strongly adherent to the underlying stroma unlike the basal layer of the odontogenic keratocyst, where cleavage often occurs in this area. Additionally, although the basal cells were palisaded and demonstrated nuclear polarization in areas, they were cuboidal rather than columnar. The excision specimen revealed more of a solid ameloblastic component in addition to the cystic component seen on the initial biopsy. Nevertheless, it is possible that the ameloblastoma had developed in an odontogenic keratocyst. Alternatively, it can be postulated that the keratoameloblastoma consists of both cystic and solid components, the former being analogous to the cysts of the conventional ameloblastoma.

Arteriovenous malformation of the mandible: report of a case with a note on the differential diagnosis.

Arteriovenous malformations are extremely rare conditions that can result from congenital or acquired abnormalities in the structure of blood vessels; they are potentially fatal. Arteriovenous malformations may be asymptomatic or may show various signs and symptoms including soft tissue swelling, pain, changes in skin and mucosal color, erythematous and bleeding gingiva, bruit, and paresthesia. Radiographically, there are no pathognomonic features. The present case illustrates an arteriovenous malformation in a 16-year-old Hispanic female. The case report is unique because the malformation was previously interpreted as a pathosis of pulpal origin and was initially treated as such, although the tooth showed no gross or radiographic dental caries. A broad view of the diagnostic imaging, radiographic differential diagnosis, treatment, and histopathologic description is also presented.

Zinc deficiency produces time-related ultrastructural changes in rat cheek epithelium.

The subject of this study was whether the ultrastructural changes in cheek epithelium of zinc-deficient rats are time related. Weanling male Sprague Dawley rats were fed a zinc-deficient diet containing 0.4 ppm zinc (ZD) ad libitum and controls were pair-fed zinc adequate diet containing 40 ppm zinc. After 9, 18, and 27 days of zinc deficiency, specimens from cheek epithelium of both groups were processed for transmission electron microscopy. Partial conversion of the orthokeratinized cheek epithelium to parakeratinized was seen as early 9 days. An electron-lucent band surrounding the nucleus was observed in ZD cells. Mitochondria, tonofilaments, keratohyalin granules and ribosomes seemed to be increased with the increase in time of zinc deficiency. There was a thickening of the stratum corneum as well as hyperplasia and widening of the intercellular spaces of the spinous layer cells. Retention of a few membrane coating granules (MCGs) in the parakeratinized layer was seen after 9 days. Parakeratinization was further increased after 18 days of zinc deficiency, and the number of MCG profiles also increased. The epithelium was fully parakeratinized following 27 days of zinc deficiency, and the number of MCG profiles was increased. It was concluded that zinc deficiency affected cell proliferation and differentiation of the epithelium as early as 9 days, and caused a delay in loss of nuclei and MCGs in parakeratinized cells.

Time-related changes induced by zinc-deficient diet in the concentration of rat cheek epithelial membrane-coating granules.

Weanling male Sprague-Dawley rats were fed a diet containing 0.4 parts/10(6) zinc and controls were fed an identical diet supplemented with 40 parts/10(6) zinc. After 9, 18 and 27 days of zinc deficiency, specimens were excised from cheek epithelium and processed for transmission electron microscopy to study the concentration of membrane-coating granules (MCG). Their concentration was increased in the granular-cell layers of the zinc-deficient epithelium and became significantly greater after 18 and 27 days than 9 days of deficiency. MCGs appeared in the parakeratinized layers of zinc-deficient epithelium and their concentration became significantly greater after 27 days in comparison with 9 and 18 days of deficiency. Thus the intracellular retention of MCGs was increased in the granular and parakeratinized layers with the increase in time of zinc deficiency.