Lichen planus (LP) is a chronic inflammatory condition that affects the skin, hair, nails, and mucous membranes. It is classified as an immune-mediated disorder where the body’s immune system mistakenly targets its own cells, though the precise cause remains unknown. This disorder is not contagious and is characterized by inflammation that causes distinctive lesions. A combination of genetic susceptibility and environmental factors is thought to be responsible for triggering the condition in susceptible individuals.
Understanding the Forms of Lichen Planus
Lichen planus presents in various clinical forms, with lesions commonly appearing on the skin or inside the mouth. Cutaneous LP frequently involves the flexor surfaces of the wrists, the ankles, and the lower back. These skin lesions are often described by their characteristic appearance, summarized as the “4 Ps”: purple, polygonal, pruritic (itchy) papules, which may coalesce into plaques.
On close examination, a fine, lacy, white network called Wickham’s striae can often be seen covering the surface of the lesions. This pattern is particularly recognizable when LP affects the oral mucosa, such as the inside of the cheeks or the sides of the tongue. Other variants include lichen planopilaris, which affects the scalp and can cause scarring hair loss, and nail LP, which may lead to ridging or nail loss.
Investigating Genetic Predisposition
Lichen planus is not considered a classically inherited disease, meaning it does not follow simple Mendelian inheritance patterns. However, a small percentage of cases demonstrate familial clustering, suggesting that genetics play a role in susceptibility. This observation indicates a genetic predisposition rather than a direct hereditary transmission of the disease itself.
Research has focused on the Human Leukocyte Antigen (HLA) system, which helps the immune system distinguish between the body’s own cells and foreign invaders. Specific HLA types are more frequently found in people with LP compared to the general population. For instance, certain alleles like HLA-DR1 and HLA-DQ1 have been associated with an increased likelihood of developing the condition.
The presence of these HLA markers does not guarantee that an individual will develop lichen planus, but it signifies an increased genetic susceptibility. Genetic factors likely influence the body’s immune regulation, making some people more prone to the aberrant immune response when exposed to an environmental trigger.
Autoimmune Response and Environmental Triggers
The accepted cause of Lichen Planus is an immune dysregulation known as a T-cell-mediated response. Specifically, cytotoxic T-lymphocytes (a type of white blood cell) mistakenly attack and destroy basal keratinocytes, the cells at the base of the skin’s outer layer. This targeted destruction results in the inflammation and characteristic lesions seen in the condition.
This aberrant immune response is often triggered by external factors in genetically susceptible individuals. One of the most recognized environmental associations is with the Hepatitis C virus (HCV) infection, particularly in cases of oral lichen planus. The virus may modify the self-antigens on the surface of the basal keratinocytes, leading the T-cells to perceive them as foreign.
Beyond infectious agents, certain contact allergens and specific medications are known to precipitate a lichenoid reaction, which is clinically and histologically similar to LP. Common pharmaceutical triggers include nonsteroidal anti-inflammatory drugs (NSAIDs) and certain blood pressure medications. Contact allergens, such as metals found in some dental restorative materials, can also serve as a trigger for lesions localized to the mouth.
Confirming the Diagnosis and Clinical Signs
The diagnosis of Lichen Planus is often suspected based on a clinical examination of the lesions. A medical professional looks for the characteristic purple, polygonal papules and the presence of Wickham’s striae, especially on the wrists, ankles, and oral mucosa. However, because many other skin conditions can mimic LP, a definitive diagnosis requires a tissue sample.
A small punch biopsy is performed to obtain a sample of the affected skin or mucosa for histopathological analysis. Under a microscope, the defining feature of LP is a dense, band-like inflammatory infiltrate composed primarily of T-lymphocytes, which is visible at the junction between the epidermis and the dermis. Other microscopic findings include the degeneration of the basal cell layer and the presence of Civatte bodies, which are dead or apoptotic keratinocytes. These specific microscopic findings are necessary to confirm the diagnosis and distinguish LP from other inflammatory skin disorders.