A Guide to Managing Lichen Planus with Homeopathic Remedies”

ABSTRACT

There is no known etiology for lichen planus (LP), an inflammatory skin and mucous membrane condition. It manifests as violaceous, itchy papules and plaques that are most frequently observed on the ankles, lower back, and wrists. Overlying the lesions is a lattice-like network of white lines known as Wickham striae, which are best seen on the buccal mucosa, where erosions may also be seen. Drug-induced lichen planus, or lichenoid drug eruption, is frequently photo distributed but may be indistinguishable from idiopathic LP. There are notable variations in the natural history of LP. Most patients with cutaneous lesions resolve on their own after a year or two of first appearing. Recurrences are common, though, and the skin often becomes persistently hyperpigmented as a result. Oral lichen planus, on the other hand, is a chronic illness.

INTRODUCTION

The cause of lichen planus (LP), an inflammatory condition affecting the skin and mucous membranes, remains unknown. Usually present on the wrists, lower back, and ankles, it manifests as itchy, violaceous papules and plaques. Overlying the lesions is a lattice-like network of white lines known as Wickham striae, which are easiest to see on the buccal mucosa, where erosions may also be seen. Although lichenoid drug eruption, also known as drug-induced lichen planus, is often photo distributed, it might be mistaken for idiopathic LP.
There are notable differences in the natural history of LP. Most patients with cutaneous lesions resolve on their own after a year or two of first appearing. [1] Recurrences, however, are frequent, and the skin often remains hyperpigmented. On the other hand, oral LP is a persistent condition that might or might not go away.[2]       When the causing drug is stopped, drug-induced LP progressively goes away. [3]

ETIOLOGY

Lichen planus is an idiopathic condition, and its exact pathogenesis remains unclear. However, it is believed to be a T-cell-mediated autoimmune disorder. The most widely accepted theory suggests that exposure to an external trigger, such as a virus, drug, or contact allergen, leads to changes in epidermal self-antigens. These alterations activate cytotoxic CD8+ T cells, which then cross-react with normal self-antigens present on basal keratinocytes, resulting in T-cell-mediated destruction and apoptosis of the affected cells.[4] Several factors have been linked to the development of lichen planus (LP), with a notable association to viral infections, particularly hepatitis C virus (HCV). Patients with LP are five times more likely to test positive for HCV compared to the general population, and those who are HCV-positive have a 2.5 to 4.5 times higher risk of developing LP. [5][6]
Oral lichen planus has been linked to allergic reactions to various metals commonly used in dental restorations, such as mercury, copper, and gold. Reports have shown that removing the offending metal often leads to the resolution of LP lesions.[7][8]  A variety of medications have been linked to the development of lichen planus, although recurrence of lesions after reintroducing the drug is uncommon. Drugs most frequently associated with LP include antimalarials, ACE inhibitors, thiazide diuretics, NSAIDs, quinidine, beta-blockers, tumor necrosis factor-alpha inhibitors, and gold.[3][9]

EPIDEMOLOGY

Global estimates suggest that 0.2% to 1% of adults are affected by cutaneous lichen planus (LP), while oral LP is more common, affecting 1% to 4% of the population. [10]  The condition is generally 1.5 times more prevalent in women than in men, with the majority of cases occurring between the ages of 30 and 60. LP is rare in children, accounting for less than 5% of all cases. [5] Although the racial predisposition for LP is still debated, some recent studies indicate that African Americans, as well as individuals of Indian and Arabian descent, may have a higher susceptibility. [11][12] Additionally, up to 10% of a patient’s first-degree relatives may be affected, suggesting a potential hereditary component. [13]

HISTOPATHOLOGY

In rare and severe cases, a skin biopsy and microscopic examination can help confirm the diagnosis of lichen planus (LP), as the histopathological features are consistent regardless of the lesion’s location or subtype. Key findings include irregular thickening of the stratum granulosum, destruction of the stratum basale, and changes in the rete ridges that create a sawtooth pattern. The stratum corneum may also show thickening without nuclei (hyperkeratosis without parakeratosis), and a dense band of lymphocytes typically infiltrates the dermis along the dermo-epidermal junction, a feature known as interface dermatitis. While eosinophils are rarely present in idiopathic LP, they may be observed in drug-induced forms of the condition. Additionally, apoptotic keratinocytes, or Civatte bodies, are commonly found near the basal layer. Immunofluorescence studies may reveal these colloid bodies with asymmetric IgA deposition. [14][15]

HISTORY

Lichen planus can present in various forms, but the most typical appearance is a group of polygonal, pruritic (itchy), violaceous (purple), flat-topped papules, usually a few millimeters in size. This classic presentation is referred to as the “Six Ps” of LP: purple, polygonal, planar, pruritic papules, and plaques. The lesions often have a shiny surface, marked by fine white lines called Wickham striae, and are firm to the touch. They can appear as solitary lesions, be scattered across the body, form plaques, or present in annular, linear, or actinic patterns. An isomorphic response may occur in LP, where new lesions develop along lines of trauma or scratching, similar to what is seen in psoriasis. The most commonly affected areas include the flexor wrists, dorsal hands, lower back, ankles, and shins. After the lesions heal, a grayish-brown hyperpigmentation may remain due to melanin deposition in the superficial dermis. [5][10]

Lichen planus (LP) can manifest in several subtypes, each with distinct patterns that differ from the classic presentation. Hypertrophic LP typically affects the shins and ankles, presenting as red, red-brown, or yellow-gray papules and plaques that merge into thickened or verrucous lesions. Ulcerative LP appears on the soles of the feet or between the toes, characterized by painful, erosive lesions that can make walking difficult. Bullous LP most commonly affects the legs, presenting as tense blisters filled with clear or pale-yellow fluid, ranging from small to large in size. Lichen planus pemphigoides combines features of LP with the formation of bullae both atop existing LP lesions and on unaffected skin. Lichen planus pigmentosus presents as macular or papular pigmented lesions, often arranged in linear, follicular, or Blashkoid patterns. Inverse LP is similar to inverse psoriasis, occurring in intertriginous areas and losing the typical appearance of LP. It features extensive erythematous lesions with lichenification and indistinct borders, commonly found in the axillae, inguinal folds, beneath the breasts, and in other skin folds. [16]

Mucosal involvement occurs in over half of all lichen planus (LP) cases and often presents as the initial symptom. While it is most commonly seen in the mouth, LP can also affect the lips, esophagus, glans penis, vulva, or vagina. There are six subtypes of oral LP: reticular, erosive, papular, plaque-like, atrophic, and bullous. Reticular LP is the most common subtype, characterized by asymptomatic white, lacy lines typically found on the bilateral buccal mucosa. Erosive and atrophic LP forms are frequently associated with burning pain, which worsens with hot or spicy foods. Lesions on the tongue or buccal mucosa can sometimes be confused with leukoplakia or candidiasis. Esophageal LP predominantly affects women and can lead to dysphagia (difficulty swallowing), strictures, and, in rare cases, an increased risk of squamous cell carcinoma. [17][18][7]
When lichen planus (LP) affects the glans penis, it often presents in an annular (ring-shaped) configuration. In contrast, when LP involves the vulva or vagina in women, the erosive variant is more commonly seen, with scarring and strictures being problematic long-term complications. When LP affects both the female genital and oral mucosa simultaneously, it is referred to as vulvovaginal-gingival syndrome. This severe, desquamative subtype has been linked to the HLA DQB1*0201 gene in 80% of patients, suggesting a genetic predisposition to its development.[19][20]

Nail involvement in lichen planus (LP) occurs in about 10% of patients, often affecting multiple nails without necessarily involving the surrounding skin. Early signs include thinning of the nail plate and longitudinal ridging. As the condition progresses, it can lead to scarring of the nail matrix, dorsal pterygium formation, sandpaper-like nails, and, in some cases, complete nail loss. A variant of LP known as twenty-nail dystrophy can present with these nail changes as the only manifestation of the disease, affecting all twenty nails. This subtype is more common in children than in adults.[21][22]
Lichen planus affecting the scalp and other hair-bearing areas is known as lichen planopilaris (LPP). It begins with small, red, follicular papules and macules at sites of inflammation, which gradually lead to scarring alopecia (hair loss). LPP may occur alone or alongside typical lichen planus lesions on other parts of the body. When LPP primarily affects the anterior scalp and eyebrows in older women, it is referred to as frontal fibrosing alopecia. A familial form of LPP, called Graham-Little-Piccardi-Lasseur syndrome, is characterized by scarring alopecia of the scalp, typical cutaneous or mucosal LP, and non-scarring hair loss from the pubic and axillary regions, accompanied by follicular papules.[23][24]
Lichenoid drug eruption typically does not appear in the classic locations for lichen planus. Instead, it is more commonly found in sun-exposed areas, tends to be symmetric, and is more widely distributed. The lesions often resemble eczema or psoriasis, and Wickham striae are rarely seen. There is usually a delay of several months to a year between the initiation of the drug and the onset of the eruption, making a thorough review of the patient’s medication history crucial for diagnosing drug-induced lichen planus.[3]

TREATMENT / MANAGEMENT

1. Apis Mellifica:

Indications: This product relieves itching and burning sensations, particularly in swollen, blistering lesions, and can be best used with cold applications.

2. Arsenicum Album:

Indications: The patient experiences intense itching and burning, especially with dry, scaly skin, which worsens in cold weather and improves with warmth.

3. Borax:

Indications: This medication is used for mouth blisters and ulcerations, often with a putrid taste, and is also prescribed for vulvar itching and skin eruptions.

4. Carcinosin:

Indications: This medication is effective in treating painful eruptions and oral lichen planus with offensive discharge, particularly in chronic cases with a history of illnesses.

5. Graphites:

Indications: Thick, honey-like discharges with rough, dry skin often improve with warmth.

6. Ignatia:

Indications: The individual experienced severe eruptions accompanied by emotional stress, significant itching, and sensitivity to air drafts.

7. Lycopodium:

Indications: The condition involves urticaria, characterized by urticaria and fissured eruptions, especially when the symptoms are more severe on the left side of the body.

8. Natrum Muriaticum:

Indications: Dry, raw skin eruptions, particularly in joint folds and scalp edges, are exacerbated by salt and sunlight.

9. Silicea:

Indications: The treatment aids in healing ulcers and painful lesions by addressing the weakness and sensitivity associated with chronic skin issues.

10. Sulphur:

Indications: The individual experiences dry, scaly skin that is susceptible to suppuration, with intense itching that worsens in the evening and with heat.[28][29][30][31]

DIFFERENTIAL DIAGNOSIS

Since lichen planus (LP) can be triggered by various exogenous factors, such as viruses, medications, or contact allergens, it’s important to identify and address any underlying causes before diagnosing idiopathic LP. Several conditions may resemble LP, including lupus erythematosus (LE), erythema dyschromicum perstans, psoriasis, secondary syphilis, pityriasis rosea, lichen nitidus, graft-versus-host disease, and keratosis lichenoides chronica. Hypertrophic LP can mimic lichen simplex chronicus, while vulvar LP may be difficult to distinguish from lichen sclerosis. Differentiating LP from LE can be especially challenging when lesions are confined to the scalp or oral mucosa, making biopsy with direct immunofluorescence (DIF) particularly helpful in these cases. Reports have documented the coexistence of both conditions, possibly linked to the use of antimalarial drugs in the treatment of LE. [27][32]

PROGNOSIS

Cutaneous lichen planus (LP) often resolves on its own within 1 to 2 years, although residual hyperpigmentation is common. Oral LP may also resolve spontaneously within 5 years, but it generally follows a chronic, relapsing-remitting course. Hair loss due to lichen planopilaris (LPP) is usually permanent. In cases of drug-induced LP, lesions tend to clear gradually after the offending medication is discontinued.

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