Leukoplakia buccalis

In these days of preventive medicine and cancer-detection clinics, it is quite natural that extra emphasis has been placed on the precancerous lesions. Also, the present hue and cry of tobacco as a major factor in the etiology of lung can cer has focused the attention of the lay populace and medical authorities alike' on the detrimental effects of smoking. Smokingalsoplaysan important rolein producing leukoplakia of the buccal mu cosa, a precancerous lesion,@' with which this report mainly concerns itself. There is, therefore, a suggestive parallelism be tween leukoplakia of the oral cavity and cancer of the lung. It is felt that the con tinuous exposure to chronic irritation pro duced by the products of combustion and heat of smoking is a definite causative factor in both the production of leuko plakiabuccalis and pulmonarycancer. Both leukoplakia and cancer of the lung occur predominantly in males and it is thought by many that the male species has an inherent susceptibility. However, Graham feels that the increased inci dence of pulmonary carcinoma in males is due to the fact that fewer women of cancer age smoke and that it is chiefly the teenagers and young women who are the heavy female smokers. He is of the opin ion that a statistical study in another ten to fifteen years will reveal a more pro portionate division. Evidence continues to accumulate on the role of smoking in cancer of the lung. For example, in Ice land, where cigarette consumption is markedly less than in the United States, primary cancer of the lung is still a rarity.' The maintwotypesofcancerofthe lung are the epidermoid or squamous type and the adenomatous type. It is specu lated that the adenomatous type arises from fetal bronchial buds and the squa mous-cell typeiscausedbya metaplasia of the adult bronchial epithelium owing to the action of carcinogenic agents, such as smoking. It is of special significance that only the squamous-cell type of can cer of the lung has shown such a marked increase in the past decade. The initial metaplasia of the bronchial epitheliuni and the leukoplakic lesion of the buccal mucosa can be produced by similar car cinogenic irritants with the ultimate pro gression of both lesions into the squamous cell type of cancer. Unfortunately, in can cer of the lung, the early histological changes are not visible, the patient is com pletely asymptomatic; and when symp toms, such as cough, weight loss, pain and hemoptysis, finally do appear, progression to the frank squamous-cell pathology has already occurred. The term“¿ leukoplakia― 12etymologi cally is derived from the Greek, leukos, white—and plax, plaque. The condition was first described by Bazin and others as a type of lingual psoriasis, but it was Schwimmer, in 1877, who differentiated it from psoriasis and described it under its present name. Leukoplakia of the oral cavity, other wise known as leukokeratosis, leukoplakia buccalis, orsmoker's patch, isarelatively common condition. When first seen, it ap pears on the buccal mucosa as a bluish white or bluish-red patch that is sensitive to chemical irritation and to hot and cold foods. Older lesions take on a dull grayish hue and are slightly raised, indurated, nontender, and somewhat rough to the touch. Upon removal of the grayish patch, bleeding will result. When these lesions show evidence of cracking, fissuring,