Oral submucous fibrosis is a chronic disease that can affect any part of the oral cavity. Due to the degeneration of fibrous tissue in the lamina propria and epithelial atrophy, it causes hardening of the mucosa and formation of striae, which ultimately leads to dentition, hinders the performance of various functions of the oral cavity and becomes a pre-cancerous state. the disease was first discovered in India in the early 1950s, and it occurs mainly in India, but also in Nepal, Thailand, Malaysia, Uganda and other countries, and there are also scattered cases reported in southern Africa and the United States. Xiangtan, Hunan Province and Taiwan are also the high incidence areas of this disease. Liu Shufan, Jian Xinchun et al. (1985) found that betel nut chewers in Xiangtan, Hunan Province, submucosal fibrous degeneration, heavy plate-like nodules, some families are susceptible to the disease. Symptoms and signs of the disease occur in 20 to 40 years of age, male and female gender differences are not significant, easy to occur in the cheek, soft palate, lips, tongue, floor of the mouth, pharynx and other parts. Early asymptomatic, later there is a burning sensation in the mouth, especially when eating irritating food more obvious. Most of the early appearance of blisters, rupture to form an ulcer. Some have spontaneous pain, dry mouth and loss of taste. In the later stage, there is difficulty in opening the mouth, inability to whistle and blow out candles, limited mouth opening, speech and swallowing difficulties. The oral mucosa becomes whitish, mildly opaque, hard on palpation, and fibrous striae may be found. Tongue lesions with atrophy of the tongue papillae and limited movement. Diet and health care should be light, eat more fruits and vegetables, reasonable combination of meals, pay attention to nutritional adequacy. I. Disease diagnosis 1, white spots: oral mucosal white spots are white or grayish-white plaques, soft to the touch, asymptomatic or mildly rough feeling. There are no plaques or fibrous strips on palpation, and no symptoms such as clenched teeth, restricted mouth opening and difficulty in swallowing. Pathologic examination can help differential diagnosis. 2.Flat moss: plaque-type flat moss is soft, if congestion, vesicles, irritating pain, no plaque or fibrous striae on palpation, no restriction of mouth opening, no teeth clenching, no dysphagia. Pathologic examination helps diagnosis. 3, white keratosis: there are obvious mechanical or chemical factors stimulation, remove the stimulus, lesions can be reduced or completely subside. White keratosis is grayish white, light white or white plaque, smooth and soft. There is no plaque-like or fibrous stripes when touched, not to mention limited mouth opening and difficulty in swallowing. Second, folding edit this paragraph examination method laboratory examination: the main change for the connective tissue occurs fibrous degeneration, can be divided into four stages: 1, the earliest stage: the appearance of some fine collagen fibers, and there is obvious edema, blood vessels are sometimes dilated and congested, and there are neutrophil infiltration; 2, early: immediately below the epithelium there is a band of vitreous degeneration of the collagen fibers, and then below the collagen fibers between the edema, with lymphocyte infiltration; 3.Mid-term: moderate vitreous degeneration of collagen fibers, mild edema, with lymphocyte and plasma cell infiltration; 4.Late-term: all vitreous degeneration of collagen fibers, with stenosis or occlusion of blood vessels. Epithelial atrophy, epithelial pinnae shortened or disappeared, some epithelial hyperplasia, pinnae hypertrophy, vacuoles in the epithelial cells, epithelium sometimes abnormal hyperplasia. In patients with severely impaired turgor, a large number of muscle fibers were seen to be necrotic. Electron microscopy showed a widening of the epithelial cell gap, and a large number of free bridging grains or cellular debris were seen. The number of mitochondria was significantly reduced, and some mitochondria were swollen, aberrant or disappeared in a vacuolated form. Collagen fibers proliferated in large quantities and were distributed in bundles, and some collagen fibers were arranged haphazardly. In severe lesions, the collagen fibers were degenerated, and the periodical transverse lines disappeared, or even showed focal disintegration.