Vulvar leukoplakia is also known as vulvar white lesions, vulvar white changes, or vulvar malnutrition. So-called vulvar leukoplakia actually refers to a disease characterized by tissue atrophy and pigment change caused by local nerve and blood vessel malnutrition of the vulva. Clinically, the white and thickened or atrophic skin and mucosa of the vulva, or the diseases, are commonly referred to as 'vulvar leukoplakia'.
Clinical pathological examination of atypical cell hyperplasia belongs to the category of 'Yin Itch', 'Yin Pain', and 'Yin Sore' in traditional Chinese medicine. It is often caused by downward invasion of damp-heat in the liver meridian, or due to blood deficiency and liver hyperactivity, kidney-yin deficiency and kidney-yang deficiency, where the essence and blood cannot nourish the vulva. Vulvar itching may sometimes be accompanied by burning and pain sensations. Vulvar leukoplakia, also known as vulvar white lesions, is a chronic vulvar dystrophy disease. It includes primary vulvar atrophy, atrophic scleroderma, vulvar leukoplakia, leukoplakic vaginitis, and vulvar dryness. Clinical doctors usually refer to the vulva disease where the skin and mucosa become white and thickened, leading to atrophy, as vulvar leukoplakia. In traditional Chinese medicine, it is called Yin Xian, Yin Chuang, Yin Shi, and Yin Sore, and this disease is a precancerous lesion. Benign keratotic lesions in the vulvar area are called leukoplakic disease. Long-term non-healing leukoplakic disease can further develop into vulvar leukoplakia. The etiology is unclear and may be related to systemic factors, such as diabetes and endocrine disorders. Local environmental factors of the vulva, such as dampness and heat, can induce vulvar leukoplakia. Histopathological examination shows proliferative lesions of the mucosal epithelium or epidermis. Normally, the vulvar mucosa has no granular layer and stratum corneum. If leukoplakic disease or vulvar leukoplakia occurs, granular layer keratinization appears. If it occurs at the transition area between the skin and mucosa of the labia majora, there is significant hyperkeratosis, thickening of the granular layer, hypertrophy of the stratum spinosum, and about 80% of the lesions are benign leukoplakic disease, with no atypical keratinocytes in the stratum spinosum, generally no dyskeratotic cells, and chronic inflammatory cell infiltration below the epidermis. Vulvar leukoplakia disease, however, shows early dysplasia, where some keratinocytes appear atypical, with inconsistent nuclear size and cell size, disordered keratinocyte arrangement, and dyskeratotic cells in the superficial layer of keratinocytes, known as malignant dyskeratotic cells. There is varying degrees of inflammatory cell infiltration in the dermis, and collagen fibers in the superficial dermis show non-uniform degeneration.
Vulvar leukoplakia can occur at any age during women's various stages: infancy, adolescence, menopause, and old age, with the most reports occurring in women around 50 years old. The course of the disease varies, with some lasting for decades. The common locations are between the clitoris, the inner labia minora, and the inner labia majora, and sometimes occur in the vestibule, vagina, and urinary orifice, posterior symphysis, etc., often showing symmetry.