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Table of Contents for Dr. Bouquot's Abstracts |
Population Studies |
History of Oral Pathology |
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Epidemiology of carcinoma in situ of the upper aerodigestive tract. Bouquot J, Gnepp D. West Virginia University, Morgantown, WV, and St. Louis University, St. Louis, MO, U.S.A.
Reference: J Oral Pathol 1988; 17:433.
Epidemiological analyses of upper aerodigestive tract (UAT) carcinoma in situ are non-existent, hence only hospital records and surgical pathology resources are available for its descriptive characterization. The National Cancer Institute's Surveillance, Epidemiology and End Results investigation has, however, published valuable raw data pertaining to CIS of the UAT. This information is analyzed here and summarized for the first time, demonstrating the following: a male incidence rate which is 4 times greater than the female rate (0.8/1000,000 males versus 0.2/100,000 females); similar ages at diagnosis for both sexes (62.7 and 60.0 years of age for males and females, respectively); no significant urban/rural incidence differences; that CIS represents 2.8% of all UAT malignancies; that 2.0% of all CIS lesions in humans are found at UAT sites; and that CIS of the uterine cervix is not a good model for CIS of the UAT.
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Incidence, time trends and follow-up of oral/pharyngeal carcinoma in situ, 1935-1984. Bouquot JE, Kurland LT, Weiland LH. West Virginia University, Morgantown, WV; Mayo Clinic, Rochester, MN
Presented to the International Association
of Oral Pathologists in Toronto, Canada,
1986.
Reference: J Oral Pathol 1986; 15:395.
The dearth of epidemiologic studies relating to carcinoma in situ (CIS) of the mouth and pharynx has lead to the acceptance of clinicopathologic data for the descriptive characterization of this disease. Such data, however, cannot be said to represent any population beyond that of the particular hospital from which a study originated. Hence, our understanding of this disease is necessarily skewed to the more difficult or unusual cases. The present investigation is the first to offer a clinical characterization of CIS from a pool of patients known to represent virtually all cases of CIS and invasive carcinoma in a stable population (Rochester, Minnesota, 1935-84). The annual incidence of CIS in this population was 2.0/100,000 (3.7 for males; 0.7 for females), compared to a rate of 12.6 invasive carcinomas/100,000 (20.7 for males and 6.8 for females). Incidence of CIS increased with increasing age, to a maximum of 28.3/100,000 for males 75 years of age and older. Time trends of CIS incidence showed no significant change over 50 years. Clinical features and follow-up results will be reported.
This study was supported in part by NIH grand AM30582.
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Presented to the American Academy of Oral Pathology, May, 1986.
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Presented to the First International Conference on Smokeless Tobacco and Health, in Columbus, OH, May, 1991.
White oral mucosal changes resulting from chronic smokeless tobacco (ST) use are usually designated as leukoplakias, and the extensive precancer literature relative to leukoplakia is presumed to apply to them. ST keratosis is, however, considerably different from leukoplakia, and the purpose of the present study is to demonstrate those differences as reported in the literature. Although both are precancerous, the malignant potential for leukoplakia (4%) is several magnitudes greater than that for ST keratosis (0.5%). And while both are white surface changes, ST keratosis typically presents as a smooth (perhaps fissured) gray/white, opalescent, velvety macule and usually remains so indefinitely, regardless of lenth of St usage. Leukoplakia plaques become very definitely white, continue to expand laterally and may become nodular and/or "speckled" (erythroleukoplakia) over time. Leukoplakia, furthermore, lacks the intracellular edema of the superficial epithelial cells which is so characteristic of ST keratosis, a change recently called "surface etching." In fact, ST keratosis is more histologically similar to chronic cheek bite and leukoedema than to leukoplakia. An additional important difference is that ST keratosis occurs only at areas of ST contact and is usually completely reversible after habit cessation, while leukoplakia lacks such features. It is recommended that smokeless tobacco keratosis and leukoplakia be considered as and reported as separate lesions with different diagnostic criteria, different diagnostic names, and different biological behaviors.
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Presented to the 2nd International Congress on Oral Cancer, New Delhi, India, December, 1991
The object of this paper is to demonstrate the clinical and microscopic differences between the white oral mucosal changes resulting from chronic smokeless tobacco use (ST keratosis) and the WHO-defined leukoplakias. Although both are precancerous, the malignant potential for leukoplakia (4%) is several magnitudes greater than that for ST keratosis in the US population (0.5%). And while both are white surface changes, ST keratosis typically presents as a smooth a (perhaps fissured) gray-white, opalescent, velvety macule with a poorly-defined periphery. After its initial onset it usually remains similar indefinitely. Leukoplakia plaques become very definitely white, with distinct borders, and continue to expand laterally over time. They also tend to change appearances, i.e. become nodular and/or "speckled" (erythroleukoplakia) over time.
Leukoplakia lacks the intracellular edema of the superficial epithelial cells which is so characteristic of ST keratosis, a change recently called "surface etching." Epithelial dysplasia is exceeding uncommon in ST keratosis biopsy samples, but is noted in as many as 40% of leukoplakias. Also, ST keratosis occurs only at areas of ST contact and is usually completely reversible after habit cessation; leukoplakia lacks such features.
It is recommended that ST keratosis and leukoplakia be considered as and reported as separate diagnostic names, and different biological behaviors. Such a separation is similar to the one presently distinguishing another tobacco-induced lesion, nicotine palatinus, from leukoplakia.
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Presented to the annual meeting of the American Academy of Oral & Maxillofacial Pathology in Hawaii, 1999.
Problem: Leukoplakia is the most common oral precancer but there is a wide variety of estimated transformation rates in published follow-up studies. No study has attempted to reduce case-selection biases in order to assure that established rates are determined from a reasonably accurate sample of a particular population. Objective: To review medical records of an entire community in order to identify, over an extended time period, all cases of head & neck (H&N) leukoplakia, and to characterize the clinical presentation and follow-up experience. Study Design: Medical records of Rochester, MN residents diagnosed with any benign or malignant lesion of H&N mucosa between 1935 and 1988 were retrieved from all hospitals where residents may have gone for care. Physician-generated leukoplakia diagnoses were confirmed by clinical and histopathologic review, acceptable lesions were characterized and followed through the records and a mail survey. Results: 568 cases of leukoplakia were diagnosed during the period of observation and followed for a cumulative total of 6,720 person-years, with an average follow-up time of approximately 12 years (range: 1 month to 41 years). The most common locations were, in decreasing order of frequency: lip vermilion, vocal cords, buccal mucosa, gingiva, and tongue. The malignant transformation rate from this relatively unbiased patient cohort was 15.4% for males and 10.1% for females (oral: 11.2 & 9.5%, respectively; lip vermilion: 26.3 & 8.3%, respectively). Lesions near the pharyngeal tonsils were most likely to transform, followed by the oral floor, the lower lip vermilion, the vocal cords, lip mucosa and lateral/ventral tongue. Conclusion: When H&N leukoplakia patients are followed for long enough, the malignant transformation rate rises to more than 14%. Rates vary with gender and with different anatomic sites of involvement.
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