Lichen planus is a distinctive skin and mucosal disease with a rash commonly consisting of polygonal flat papules that are purple, itchy, and occasionally have hypertrophic plaques, vesicles, or large sores that remain pigmented after the rash fades. There are characteristic changes in the pathologic tissue. The types of lichen planus damage include hypertrophic lichen planus (also known as warty lichen planus), sclerosing atrophic lichen planus (also known as scleroderma-like lichen planus), annular lichen planus, follicular lichen planus, linear lichen planus, vesicular or ulcerative lichen planus, photosynthetic lichen planus, pigmented lichen planus, lupus lichen planus, maculopapular lichen planus, and aspergillous lichen planus. The disease is commonly associated with skin damage, but a significant number of cases involve mucous membranes. It can occur on the skin or mucous membranes alone, at the same time, or sequentially. If it occurs on the skin, it is more likely to occur on the extremities, especially on the flexural side, especially on the flexural side of the wrist, around the ankle and the medial side of the femur. If it occurs in the trunk, it is common in the lumbar region. The face and fingernails or toenails, but less frequently. If it occurs on the scalp, it can cause permanent baldness. If it occurs on mucous membranes, it mainly damages the oral mucosa and glans, and rarely damages the conjunctiva, throat, female genitalia and anus, stomach, bladder and rectum. The incidence of lichen planus is about 3.5%, and the malignancy rate of mucosal damage is significantly higher than that of skin damage. Due to the limitation of time or text, this article only briefly discusses oral lichen planus of oral mucosa damage, the incidence of oral lichen planus is about 2.5%, more women than men. The incidence of oral lichen planus is about 2.5%, and there are more women than men. It occurs in the age group of 35-60 years old, and the onset of the disease is mostly seen in the mucosa of the cheek, tongue, gums and inner lip, especially in the buccal mucosa. The typical lesions are white or off-white streaks on the mucosa, with redness of the mucosa between the streaks, and the streaks are reticulate, linear, annular or dendritic, but reticulate is the most common, and the damage is often in the form of depressed flat papules. The cause of oral lichen planus (flat moss) is still unknown, but the known causative factors are often related to chemical irritation, dental materials, psychological factors, and bacterial or viral infections. Various types of lichen planus can affect the oral mucosa, but vesicular or ulcerative, sclerosing atrophic, canonical, and pemphigoid mosses are the most common. Patients have a family history of a certain percentage of cases, and in 50% of cases IgA is decreased and in 25% of cases IgM is decreased, suggesting that the disease is an autoimmune defect, together with dense lymphocytic infiltrative bands or ovoid gelatinous vesicles in the lamina propria of the mucosa as seen in histological pathology. These bases are sufficient to suggest that oral lichen planus has cancerous potential in the presence of immune deficiency. It can even be said that sclerosing atrophic moss, erosive or ulcerative mosses are precancerous lesions. Regarding the treatment of oral lichen planus, there is a lack of effective drugs in western medicine, and due to the lack of understanding of this disease, only vitamin supplements, corticosteroids or estrogen can be given. (The authors believe that if estrogen is used, it will instead aggravate the disease or accelerate the cancerous changes.) The author has treated more than 2,000 patients with oral lichen planus in his 32 years of medical practice. In 1997, he developed the immune theory of Qiheng’s internal organs, i.e. the “Rankin’s model of immune principle”, which believes that immune diseases originate from the metabolic dysfunction of Qiheng’s internal organs, which breaks the recognition function of the normal immune system of the human body and causes the human body to develop a certain organ or multiple systems or different parts of the body. It is believed that immune diseases originate from the metabolic disorder of the Qiheng internal organs, which breaks the recognition function of the normal immune system of the human body and causes the body to produce damage to an organ or multiple systems or different parts of the body. It is because Chinese medicine recognizes the etiology and pathogenesis of many difficult diseases that the theoretical doctrine of Qiheng’s internal organs has emerged, enriching the theory of Chinese medicine. The Qiheng’s internal organs expresses the principle of the relationship between the metabolism of the human body and its decline and prosperity, but in a different form than the immune principle of Western medicine. The most important basis is that the theory of Qiheng’s internal organs is far more effective in guiding clinical practice than Western medicine. The use of bland natural herbs has surprisingly given new life to millions of patients with difficult diseases. The effect we have achieved by using “Bengkuping” for the treatment of mucosal lesions such as oral lichen planus and oral leukoplakia is no exception, which is entirely due to the guidance of the immune principle of Qiheng’s internal organs, while the “immune effect” of western medicine is beyond our reach and cannot be helped. White spots are white patches that occur on the surface of mucous membranes and cannot be erased. Mucosal leukoplakia, also known as pre-cancerous leukoplakia keratosis, is mainly divided into oral leukoplakia and female pubic leukoplakia. Oral leukoplakia often occurs in people aged 40-65 years, with more male patients than female. Female pubic leukoplakia is mostly seen in middle-aged and elderly women, and is more common in obese people. The higher the incidence of labial and clitoral atrophy after menopause (endocrine dysfunction). At present, what the world medical science knows is similar to what the motherland medical science has known for a long time, all of them think that the occurrence of oral white spot is closely related to the diet of frying and barbecue and over-eating spices and thick, greasy and spicy taste, and the excessive smoking in recent times may also have a certain relationship. Especially in the past 20 years after the reform and opening up tends to progress in middle age, it is due to the large intake of fertilizers, hormones, antibiotics, pesticides and other food into the human body, resulting in immune dysfunction and weakened secretion, resulting in a significant increase in patients with mucosal leukoplakia. Oral leukoplakia can occur in the oral cavity, tongue, base of tongue, inner lip, hard palate, gums and alveolar ridge without teeth. The morphology and scope vary greatly, from dots to small or large patches, shiny white or gray-white patches with clear edges, relatively smooth like a thin film in the early stage, and thicken slightly above the mucosa in the later stage, and rough and uneven, with coarse and astringent sensation when licked by the tongue, interrupted by rupture or erosion. In the early stage, it is more sensitive to hot or irritating food. The incidence of oral leukoplakia is about 10%, and the cancer rate is about 6%. It is usually considered that leukoplakia is the only manifestation of tongue cancer or oral cancer. Female leukoplakia is confined to the clitoris, labia minora or inner labia majora and can occur on primary atrophy, sclerosing atrophic mossy lesions, damaged or completely normal mucosa. The lesions are one or several, well-defined, dead white or grayish hypertrophic patches or small irregular patches, smooth or rough to the touch. Self-perceived itchiness, painful if there are fissures, and fissures or rupture are symptoms of malignant change. Female leukoplakia is highly variable, it can increase suddenly or disappear suddenly, or it can vary greatly in a short period of time, some develop quickly and extensively, some can exist unchanged for many years, which is unpredictable. About 2% can develop into squamous carcinoma. Mucosal leukoplakia can be accompanied by histopathological changes, and the main pathological changes of leukoplakia are epithelial hyperplasia with hyperorthokeratosis or hyperincomplete keratinization, or both with mixed keratinization. Except for simple epithelial hyperplasia which is a benign lesion, the rest of epithelial warty hyperplasia (warty leukoplakia) and abnormal epithelial hyperplasia are non-benign leukoplakia. Especially when leukoplakia is accompanied by abnormal epithelial hyperplasia, the malignant potential increases significantly, although abnormal epithelial hyperplasia is usually classified as mild, moderate or severe, and any degree of abnormal hyperplasia implies an increased potential for carcinogenesis. Severe abnormal hyperplasia is actually carcinoma in situ, in which cells within the epithelial layer undergo malignant transformation. It is also common to see abnormal hyperplasia and infiltrating carcinoma together. When white spots are observed histologically to be cancerous, the keratinization of the epithelial surface layer appears as a hyper-hyperkeratotic layer, and its lesions are usually thicker than the epithelium of hyper-orthokeratotic lesions. Non-homogeneous leukoplakia is often associated with abnormal epithelial hyperplasia, carcinoma in situ or squamous cell carcinoma. The risk of malignancy is usually higher in non-homogeneous leukoplakia than in homogeneous leukoplakia. The location of leukoplakia also has an important relationship with malignancy, especially the leukoplakia occurring at the floor of the mouth (base of the tongue), the ventral part of the tongue and the lateral margin of the tongue are high-risk areas, and the cancer rate is higher than that of other parts of the oral cavity.