1. Etiology
Contact dermatitis is a dermatitis that occurs after the skin comes into contact with certain sensitizing or irritant substances, and it is mostly acute. It can be divided into two types according to the etiology: primary irritant dermatitis and allergic contact dermatitis.
Primary contact dermatitis is caused by strong irritants to the skin such as acids and bases, or other substances such as strong disinfectants, potassium permanganate that has not been completely dissolved during vaginal irrigation, and so on. Allergic contact dermatitis can be caused by exposure to sensitive substances by some individuals, such as vulvar contact with deodorant spray, contraceptives (condoms, birth control pills), dyed clothing, anesthetics, or locally applied antibiotics (especially penicillin) and other agents, which can all lead to dermatitis.
It is now known that there are more than 2800 allergens that can cause ACD, mainly including:
1. Animal: toxins, hair, down products, etc. of animals.
2. Plant: leaves, stems, flowers, fruits, seeds, and juice of plants. Common ones include lacquer, nettle, fig, ginkgo, mango, etc.
3. There are many chemical types, mainly including metal products such as nickel and chromium; household products such as detergents, brighteners, leather, plastics, and rubber products; cosmetics such as blush, perfume, hair dyes, etc.; and topical drugs. Common allergens in ACD of the female vulva include sanitary napkins, suppositories, perfumes, topical contraceptives, etc. Contact between couples can also lead to mutual sensitization.
Second, pathogenesis
1. In acute dermatitis, the histopathology shows edema between and within epidermal cells, up to spongiosis, vesicles, and bullae within the epidermis. There is infiltration of lymphocytes and neutrophils within the epidermis, with cells mainly concentrated within vesicles. The superficial connective tissue of the dermis is edematous, the blood vessels dilate, and there is focal infiltration of lymphocytes around small vessels, and sometimes a few neutrophils and eosinophils.
2. In subacute dermatitis, the histopathology shows edema and spongiosis in the epidermal cells, a few vesicles, mild epidermal thickening, and varying degrees of parakeratosis. There is a significant infiltration of lymphocytes around the blood vessels in the dermis.
3. In chronic dermatitis, the histopathology shows hyperplasia of the stratum spinosum, significant elongation of the epidermal papillae, and hyperkeratosis and parakeratosis. There may be mild intercellular edema in the epidermis, mild perivascular lymphocytic infiltration in the superficial dermis, and a small number of eosinophils and fibroblasts. The number of capillaries increases, and the endothelial cells swell and proliferate.
Primary Irritant Contact Dermatitis (ICD): The contact substance itself is strongly irritating to the skin, and anyone who contacts a certain concentration of the substance can develop a non-immunological skin inflammatory reaction. Primary irritation can be divided into two types: one is strongly irritating, with the disease developing shortly after contact, such as dermatitis caused by strong acids and alkalis; the other is weakly irritating, with the disease developing after a long period of contact, such as dermatitis caused by detergents, organic solvents, etc. Common causes of ICD in the vulva include highly concentrated disinfectants and preservatives, such as potassium permanganate solution, and some irritant topical drugs, such as podophyllotoxin, tretinoin, lactic acid, salicylic acid, etc. Factors affecting ICD include not only the physical and chemical properties, concentration, amount, contact time, and manner of the irritant itself, but also host factors such as age, gender, race, genetic background, and location, as well as local environmental factors such as temperature, humidity, friction, and pressure. Some literature reports that the A allele and AA genotype are significantly increased in the population prone to ICD.
Allergic Contact Dermatitis (ACD): The contact substance itself is non-irritating and non-toxic. Most people do not develop the disease after contact, but only a few sensitive individuals develop hypersensitivity reactions at the contact site of the skin and mucosa after a certain incubation period.
ACD is a delayed-type hypersensitivity mediated by T cells, in which T cells, keratinocytes, Langerhans cells, macrophages, vascular endothelial cells, and mast cells are involved. The pathogenesis is complex, and the following is a summary.
(1) Induction phase: The allergens that cause ACD are mostly haptens, which combine with carrier proteins on the cell membrane of epidermal cells to form complete antigens and obtain immunogenicity. The complete antigen is recognized, phagocytosed, and digested into peptide fragments by Langerhans cells (LC) in the epidermis, and then combined with MHC class II antigen molecules on the surface of LC to form antigen-MHC complexes. The LC carrying the antigen is transported to local lymph nodes through lymphatic drainage and presented to CD4+ T cells. As the LC migrate from the epidermis to local lymph nodes, their antigen processing activity gradually decreases while their immunostimulatory activity gradually increases. This maturation process of LC is considered a key factor in effectively inducing skin allergic reactions. This process is influenced by TNF-α, IL-1, and GM-CSF. In the process of presenting antigens to CD4+ T cells, the T cell receptor of CD4+ T cells must simultaneously recognize the antigen and the MHC class II antigen molecule complex to accept the antigen presented by LC and become activated, which is MHC restricted. In this process, LC also expresses ICAM-1, LFA-3, B7t, and other adhesion molecules, which bind to LFA-1, CD2, CD28 on the membrane of lymphocytes, respectively, to complete the sensitization reaction as the second signal.
(2) Activation phase: After sensitization, when the body is exposed to the same antigen again, after the induction phase, the antigen is transferred to specific CD4+ T cell sensitized cells. After CD4+ T cells recognize the antigen, they can cause cell differentiation and proliferation, and release a series of cytokines; IL-2, IFN-γ, GM-CSF, IL-3, IL-4, TNF, which promote T cell proliferation, expand the immune response, activate cytotoxic T cells, natural killer cells, and macrophages. This results in epidermal spongiosis and dermal inflammatory cell infiltration, capillary dilation, and increased permeability. Epidermal cells are damaged, leading to the acute dermatitis manifestation of papules, blisters, and even bullae.