What Is Oral Submucous Fibrosis?

Oral submucous fibrosis (OSF) is a chronic disease that can invade any part of the mouth. Due to the fibrous tissue degeneration and epithelial atrophy of the lamina propria, the mucosa hardens and forms a cord, which eventually causes the teeth to close tightly, hinder the various functions of the oral cavity, and become a precancerous state. The disease was first discovered in India in the early 1950s, mainly in India, and also found in countries such as Nepal, Thailand, Malaysia, Uganda, and scattered cases in southern Africa and the United States. China's Hunan Xiangtan and Taiwan regions are also high incidence areas of the disease. Liu Shufan, Tong Xinchun, et al. (1985) found that submucosal fibrosis occurred in those who chewed betel nut in Xiangtan area, Hunan province. In severe cases, there was sclerosis, and some families were susceptible to this disease.

Oral submucosal fibrosis

Oral cavity

The disease is prevalent in people between 20 and 40 years of age, and there is not much difference between men and women. It is easy to occur on cheeks, soft palate, lips, tongue, floor of mouth, and pharynx. It is asymptomatic in the early stage, and there is a burning sensation in the mouth later, especially when eating irritating food. Mostly blistering occurs early and ulcers form after ulceration. Some have spontaneous pain, dry mouth, and decreased taste. It is difficult to open mouth later, can not whistle and blow out candles, restrict mouth opening, and have difficulty speaking and swallowing. The oral mucosa becomes white, slightly opaque, hard on palpation, and fibrous strands can be found. Tongue papillary atrophy and restricted movement during tongue disease (Figures 1-13).

1. Vitamin E is 100mg / d for adults. Vitamin B and C can still be added.

2. Retinoic acid can reduce symptoms.

3. Cut the fiber strands and skin graft: suitable for patients with restricted mouth opening.

4. Traditional Chinese medicine treatment is mainly for promoting blood circulation and removing blood stasis, such as angelica, peach kernel, safflower, chuanxiong, bupleurum, red scallion, xiangfu, Wulingzhi, licorice and so on.

It should be light, eat more fruits and vegetables, match the diet reasonably, and pay sufficient nutrition.

There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease.

1. Genetic background Ling Tianhuan et al. Used BrdU-Giemsa staining to detect 27 patients with oral submucosal fibrosis (OSF) who had chewing betel nut habits in Xiangtan, Hunan, 14 healthy persons who had chewing betel nut habits but did not have OSF Peripheral blood lymphocyte sister chromatid exchange rate (SCE rate) of 44 normal people chewing betel nut habit. The results showed that the SCE frequency of those who chewed betel nut was significantly higher than that of those who did not chew betel nut (P <0.001); the SCF frequency of patients with OSF was significantly higher than that of healthy people (P <0.001). This study suggests that betel nut chews contain certain mutagenic or malignant components. Betel nut chewing habits can seriously affect the stability of chromosomes; the pathogenesis of OSF may have a certain genetic background or susceptibility. Foreign studies suggest that the expression frequencies of HLA A10, B7, D13, and DR3 sites are significantly increased. From India and South Africa, OSF occurred in the same family. In 60 cases in India, 7 were from brothers in three families. Some patients were not genetically predisposed to chewing betel nut.

2. Animal experiments of betel nut extract Huang Zhangao and Ling Tianyu used a combination of submucosal injection and surface coating of water soluble betel nut extract (AANE) to induce submucosal fibrosis (OSF) in the buccal cavity of SD rats. At 12, 16, 22, and 28 weeks of the experiment, buccal mucosa microscopy and ultrastructure observation were performed.

The results showed that the animals in the model group had different degrees of OSF-like changes in various periods, that is: epithelial atrophy, nail mutations were flat or disappeared; a large number of inflammatory cells infiltrate the lamina propria, collagen fibers were stacked, the arrangement was disordered, and the vitreous changes; the lesions further Development can spread to deep muscle layers. Six weeks after discontinuing the use of AANE, no significant reversal of the lesion was seen. No significant morphological changes were observed in the control group. OSF animal model can be established by using betel nut extract, and the etiology of OSF mentioned in the literature at home and abroad is more clearly determined to be related to chewing betel nut. On the above OSF animal model, the effect of mast cells on collagen metabolism was discussed. During the occurrence of CSF, mast cells were closely related to fibroblasts, and the number of mast cells was significantly increased. Compared with the control group at the same time, there was a significant difference. The stimulation time was prolonged and gradually increased; the buccal mucosa collagen fibers in the model group accumulated a lot, and the tissue hydroxyproline content was significantly higher than the control group in the same period, and increased with the extension of the stimulation time; the mast cell count and tissue hydroxyproline in the model group in each period The acid content was highly positively correlated; there was no significant difference in serum total hydroxyproline content between groups at each stage. Tip: Some water-soluble components of betel nut can induce OSF by stimulating the proliferation and activation of mast cells, and interfering with collagen metabolism in tissues.

Regarding the role of mast cells in the occurrence of OSF, Su Kui and Liu Shufan et al. Used isolated and purified human embryonic oral mucosal mast cell media and human embryonic oral mucosal fibroblasts cultured in vitro (experimental group). The growth curve, mitotic index, and 3H-TdR (3H thymidine) incorporation rate of fibroblasts were studied. The results showed that the number of fibroblasts in each phase of the experimental group was more than that in the control group without mast cell media, and the mitotic index and 3H-TdR incorporation rate of the fibroblasts in the experimental group increased significantly compared with the control group. It is suggested that the mast cell medium can promote the growth of fibroblasts, thereby promoting the development of oral submucosal fibrosis.

Transforming growth factor 1 may be involved in the pathogenesis of OSF as an intermediary. In-situ hybridization using digoxin-labeled probes such as Gao Yijun and Ling Tianyu on 25 cases of OSF and 5 cases of normal oral mucosa. Transforming growth factor 1 mRNA was detected in 10 cases of oral lichen planus keratinocytes. Transforming growth factor 1 (TGF1) expression was positive in 15 cases (60%) of OSF and tissue keratinocytes, which were distributed in early and intermediate OSF tissue keratinocytes. Five cases of normal oral mucosa and 10 cases of OLP tissue keratinocytes were negative. . It is suggested that keratinocytes of OSF can synthesize and secrete TGF1, and TGF1 may play an important role in the pathogenesis of OSF. This once again proves that TGF is closely related to tissue fibrosis.

4. Trace element and OSF onset Ling Tianyi and Tang Jieqing used atomic absorption spectrometry to compare and quantify the serum zinc, copper, iron, selenium, manganese and saliva zinc, copper, magnesium, lead, and iron in OSF patients and normal people. Measurement and analysis suggest that high blood zinc, lead, low iron, and selenium may be important factors for increased susceptibility to OSF. This is consistent with the increased susceptibility of OSF to iron deficiency anemia reported in foreign literature.

5. Decreased NK cell activity is related to OSF Ling Tianhuan, Gao Yijun used lactate dehydrogenase release method in 24 cases of chewing betel nut with oral submucosal fibrosis (OSF), 16 cases of chewing betel nut without OSF and Peripheral blood NK cell activity was measured in 10 normal people who did not chew betel nut, and the results showed that the NK cell activity in peripheral blood was significantly lower in those who chewed betel nut with OSF and in those who chewed betel nut without OSF (P <0.05). . It is suggested that chewing betel nut habit may inhibit the activity of NK cells, and the decrease of NK cell activity may be related to the occurrence of oral submucosal fibrosis.

6. Autoimmune disease scholars have proposed OSF as an autoimmune disease, and some scholars have proposed that OSF has many similarities with scleroderma. Histopathological increase of PAS positive substances and stroma heterostaining. Electron microscope changes are similar to rheumatoid arthritis and scleroderma. Some scholars have reported increased serum immunoglobulin and the presence of autoantibodies in patients with OSF. Wall cell antibodies, nucleoprotein antibodies. The authors explain that areca alkaloids can be used as a hapten to generate parietal cell antibodies.

1. White plaques White plaques of the oral mucosa are white or off-white plaques that are soft to touch, asymptomatic or mildly rough. There were no plaques or fiber strands on palpation, no closed teeth, restricted opening, and difficulty swallowing. Pathological examinations are helpful in differential diagnosis.

2. Lichen planus lichen planus is soft, if congested, erosive, irritating and painful, there is no plaque or fibrous cord, no open mouth is restricted, no teeth are closed, no swallowing difficulties. Pathological examination can help diagnosis.

3. White keratosis has obvious mechanical or chemical factors to stimulate. After removing the stimulating factors, the lesions can be reduced or completely subsided. Keratosis is grayish white, pale white, or white plaque, smooth and soft. There are no plaques or fibrous cords to touch, and there is no restriction on mouth opening and difficulty swallowing.

Laboratory inspection:

The main change is the occurrence of fibrosis in connective tissue, which can be divided into 4 stages: The earliest stage: the appearance of some small collagen fibers with obvious edema, the blood vessels sometimes dilated and congested, and neutrophil infiltration; early stage: immediately adjacent to the epithelium There is a hyalinization zone of collagen fibers below, and edema between collagen fibers below, with lymphocyte infiltration; middle stage: moderate hyalinization of collagen fibers, mild edema, lymphocyte and plasma cell infiltration; late stage: collagen All the fibers were vitreous, and the blood vessels were narrowed or occluded. Epithelial atrophy, epithelial nail mutations are short or disappear, some epithelial hyperplasia, hypertrophy of studs, vacuoles in epithelial cells, and sometimes epithelial hyperplasia. In patients with severely impaired openness, significant muscle fiber necrosis can be seen (Figures 14, 15).

Electron microscopy showed that the interstitial space of the epithelium was widened, and a large number of free desmosomes or cell debris were seen. The number of mitochondria was significantly reduced, and some mitochondria were swollen, distorted or disappeared, showing a vacuole shape. Collagen fibers proliferate in large numbers and are distributed in bundles, and some collagen fibers are arranged disorderly. In severe cases, collagen fibrosis is degenerative, periodic horizontal lines disappear, and even focal disintegration occurs.

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