Oral Surgery, Oral Medicine, Oral Pathology最新文献

Multiple mechanisms are involved in the pathologic changes associated with formation of acute and chronic periradicular lesions. Mechanical injury to the periradicular tissues can cause activation of several pathways of inflammation and release of nonspecific mediators. Continuous irritation of periradicular tissues can cause activation of several pathways of inflammation and release of nonspecific mediators. Continuous egress of antigens from a pathologically involved root canal can also result in one or a combination of the various types of immunologic reactions. A number of these reactions participate in the destruction of periradicular tissues. Because of complex interactions between the various components of these systems, the dominance of any one pathway or substance may be difficult to establish.

Research conducted in the last 10 years has increased our knowledge on pain mechanisms substantially. Although many local tissue mediators, including neuropeptides, are known to exert pro-inflammatory effects, comparatively little is known about the actual tissue levels of these inflammatory mediators and their pharmacologic regulation. This article describes two new methods, clinical microdialysis and superfusion of dental pulp, which provide data on the pharmacology of peripheral neuropeptide and inflammatory mediator release. Collectively, these methods provide a biochemically based approach toward determining the mechanisms and management of orofacial pain.

Tongue necrosis is a rare complication in giant cell arteritis, an entity in which both temporal arteritis and rheumatic polymyalgia may be included as two different manifestations of the same pathologic process. The case of a 79-year-old patient who had tongue necrosis 3 hours after ingestion of 2 mg of ergotamine tartrate is presented. This complication was the basis for the diagnosis of temporal arteritis. We reviewed possible clinical manifestations of temporal arteritis and cases of tongue necrosis in the world literature. The possible existence of triggering factors that seemed to be present in 11 of the published cases was analyzed. In seven of these cases ingestion of ergotamine derivates had taken place.

Proliferative verrucous leukoplakia is a slow-growing but highly aggressive precancerous form of leukoplakia of unknown cause. Proliferative verrucous leukoplakia is thought to possess a continuous spectrum of clinical and histopathologic expression, ranging from simple hyperkeratosis to invasive squamous cell carcinoma. Early diagnosis is difficult because of an initial innocuous character, but multiple and rapid multifocal warty recurrences are common. This article reports four additional archival cases of proliferative verrucous leukoplakia to determine if flow cytometric analysis can be useful in the early diagnosis of proliferative verrucous leukoplakia. Flow cytometric analysis was performed on available formalin-fixed paraffin-embedded specimens (N = 27). Flow cytometric analysis results showed DNA aneuploid cell lines in each proliferative verrucous leukoplakia case studied (DNA index range, 1.1 to 2.6). In all four patients the abnormal cell line DNA index appeared to be maintained throughout the sampling period. The results suggest flow cytometric analysis could be a possible aid in early recognition of proliferative verrucous leukoplakia and might enable aggressive therapy at an earlier stage.

The bacteria present in infected root canals include a restricted group of species compared with the total flora of the oral cavity. Conditions exist in the root canal that permit the growth of anaerobic bacteria capable of fermenting amino acids and peptides, whereas bacteria that mainly obtain energy by fermenting carbohydrates are restricted by lack of available nutrients. During the course of infection interrelationships develop between microbial species and population shifts are produced as a result of these interactions. Strong associations between certain species are present. These associations are most likely based on nutritional demands and nutritional relationships. The pathogenicity of the polymicrobial root canal flora is dependent on bacterial synergy.

Eleven HIV-positive patients with chronic oral candidiasis were supplemented with 60 to 120 mg of beta-carotene daily for 3 to 7 months. Lymphocyte profiles were evaluated at intervals to help assess immune competence. Although there was a modest increase in some lymphocyte values at 2 months, there was a significant decrease in numbers of CD4 and CD8 cells and CD4 percentage of lymphocytes after 6 months of beta-carotene supplementation. Serum triglyceride and liver enzyme levels were not affected by the beta-carotene supplementation. No improvement was observed in the control of the oral candidiasis. Under the conditions of the study, there was no indication that daily beta-carotene supplements enhanced immune competence or was of benefit in managing oral candidiasis.

Necrosis that occurs in a salivary gland neoplasm is usually considered to be an ominous sign, suggesting malignant transformation, particularly in lesions that have had no prior manipulation such as fine-needle aspiration. We describe five pleomorphic adenomas and two canalicular adenomas of salivary gland origin that exhibited necrosis, yet were otherwise benign. All lesions displayed a distinctive histopathologic pattern characterized by a narrow rim of viable tumor tissue at the periphery of the neoplasm combined with a diffuse central region that demonstrated apparent ischemic necrosis. No invasion of adjacent normal tissue was identified, and no recurrence or metastasis has been seen with these lesions. Caution should be exercised in the evaluation of salivary gland neoplasms with central necrosis to avoid misdiagnosis of all such lesions as malignant.

Seventy-nine patients with oral leukoplakia that was histologically verified as either hyperkeratosis or epithelial dysplasia with hyperkeratosis were enrolled in an antioxidant supplementation program for the treatment of the oral lesions. The patients received 30 mg of beta-carotene, 1000 mg of ascorbic acid, and 800 IU of alpha-tocopherol per day for 9 months. Clinical improvement of the oral lesion was noted in 55.7% of the patients and was more likely to occur in patients who reduced their use of alcohol or tobacco (p = 0.0056). Although risk-factor reduction was important, approximately half of the patients who did not alter their exposure to either alcohol or tobacco showed clinical improvement. The antioxidant supplementation significantly increased serum and tissue levels of beta-carotene, ascorbic acid, and alpha-tocopherol, but these changes did not correlate strongly with clinical improvement.

Studies of the mechanisms of pathogenesis of periapical lesions were undertaken using a rat model of surgical pulp exposure. In this model, periapical lesions develop rapidly between days 0 and 15 (active phase) and more slowly thereafter (chronic phase). A Gram-negative anaerobic flora, similar to that seen in human beings, are quickly established. Lesions contain a mixed inflammatory cell infiltrate consisting of T cells, neutrophils, B cells, macrophages, and plasma cells. Helper T cells predominate during the active phase, whereas suppressor T cells are more frequent in the chronic phase. Extracts of periapical lesions contain bone-resorbing activity, the highest levels of which are present when lesions are actively expanding. Most bone-resorbing activity is mediated by the cytokine interleukin-1α, as determined by biochemical criteria and antibody neutralization studies. Prostaglandin₂ accounts for 10% to 15% of resorptive activity. Cells that express interleukin-1α were identified in pulp beginning on day 2 after exposure and in periapical tissue beginning on day 7, as determined by in situ hybridization and immunostaining. Macrophages, fibroblasts, neutrophils, and osteoclasts were positive for interleukin-1α mRNA and protein. Cells that express tumor necrosis factor α were also detected, whereas cells expressing interleukin-1β or tumor necrosis factor β were absent. Finally, periapical bone destruction was inhibited by 60% by treatment with interleukin-1 receptor antagonist. These studies establish a key role for interleukin-1α in the pathogenesis of periapical lesions in the rat model.