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 Table of Contents 
Year : 2019  |  Volume : 8  |  Issue : 11  |  Page : 3504-3517  

Oral lichen planus and associated comorbidities: An approach to holistic health

1 Department of Oral Medicine and Radiology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, India
2 Department of Periodontology, Darshan Dental College and Hospitals, Udaipur, Rajasthan, India
3 Department of Oral Medicine and Radiology, Institute of Dental Sciences, SOA University, Bhubaneswar, Odisha, India
4 Private Practitioner, Paravur, Ernakulum, Kerala, India
5 Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh, India

Date of Submission08-Sep-2019
Date of Decision08-Sep-2019
Date of Acceptance23-Sep-2019
Date of Web Publication15-Nov-2019

Correspondence Address:
Dr. Shazina Saeed
Amity Institute of Public Health, Amity University, Noida, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfmpc.jfmpc_749_19

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Lichen planus (LP) is a chronic inflammatory disorder with involvement of skin, oral and genital mucosa, scalp, and nail appendages. Oral lichen planus (OLP) lesions demonstrate a number of morphologic presentations, persist for a long time with rare self-resolution, and undergo malignant changes. OLP has been associated with numerous systemic connotations such as metabolic syndrome, diabetes mellitus, hypertension, thyroid diseases, psychosomatic ailments, chronic liver disease, gastrointestinal diseases, and genetic susceptibility to cancer. The oral health physician should be aware of these systemic associations and should work in close connect with the primary healthcare physicians to rule out the predisposing factors for the associated comorbidities. This article aims to highlight the various systemic associations of OLP and warrants the screening of these ailments in OLP for prevention and effective management.

Keywords: Diabetes mellitus, hepatitis C virus, lichen planus, oral lichen planus, psychosomatic diseases, systemic diseases

How to cite this article:
Hasan S, Ahmed S, Kiran R, Panigrahi R, Thachil JM, Saeed S. Oral lichen planus and associated comorbidities: An approach to holistic health. J Family Med Prim Care 2019;8:3504-17

How to cite this URL:
Hasan S, Ahmed S, Kiran R, Panigrahi R, Thachil JM, Saeed S. Oral lichen planus and associated comorbidities: An approach to holistic health. J Family Med Prim Care [serial online] 2019 [cited 2021 Sep 19];8:3504-17. Available from: https://www.jfmpc.com/text.asp?2019/8/11/3504/270947

  Introduction Top

Lichen planus (LP) is a chronic autoimmune mucocutaneous condition, primarily affecting the oral and genital mucous membrane, skin, nails, and scalp. Although the condition has an obscure etiopathogenesis, an underlying immune dysfunction and multifactorial predisposing factors also play a role.[1]

Oral lichen planus (OLP) is the mucosal analog of LP of skin, although the two demonstrate marked clinical variability. OLP exhibits a more persistent course, propensity for malignant alterations with seldom undergoing self-remission. Isolated OLP cases are frequently seen in the dental setup, with only 20% of the OLP cases presenting with cutaneous manifestations.[2]

OLP has demonstrated numerous systemic connotations such as diabetes mellitus (DM), hypertension, metabolic syndrome (MS), thyroid diseases, psychosomatic ailments, chronic liver disease, gastrointestinal diseases, and genetic susceptibility to cancer.[3] Therefore, OLP should be regarded as a systemic disorder, and the dental surgeon should be aware of the various systemic associations of LP and should work in close connection with primary healthcare physicians to rule out the predisposing factors for the associated comorbidities.[1]

  Etiopathogenesis Top

The exact etiology of OLP is not fully elucidated, although recent research suggests a key role of immunological mechanisms that may be implicated. LP is an autoimmune disease, mediated by T CD 8+ cells, macrophages, and Langerhan's cells. Immune mechanisms trigger apoptosis resulting in cell destruction and the appearance of characteristic histological changes.[2]

Systemic associations

Hepatitis C virus (HCV) infection: Prevalence of HCV infection in patients with OLP varies between 0.5% and 35% as reported by multiple authors for distinguished geographical areas.[4] Ulcerative/erosive OLP is most frequently seen in patients with chronic liver diseases.[5] Mokni et al.[6] were the first to suggest a possible link between chronic liver diseases and OLP.

A recent meta-analysis by Alaizari et al. ascertained the association between OLP and HCV infection and further necessitated the screening of patients with OLP for the timely diagnosis of HCV infection [Table 1].[7]
Table 1: Studies showing LP association with hepatitis C virus infection

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LP has a long-established relationship with a multitude of comorbidities including MS, DM, thyroid dysfunction (hypothyroidism), and dyslipidemia (a risk factor for cardiovascular diseases).[1] The association of LP with one or two of these comorbidities has been published in the literature.[8],[9],[10],[11],[12] Current published literature has emphasized that chronic inflammation, endocrine dysfunction, and oxidative stress, frequently associated with mucocutaneous disorders, may serve as potential predisposing risk factors for the development of the MS.[13] According to a recent study by Sadr Eshkevari et al., a majority of patients with LP presented with features of DM, hypertension, MS, and dyslipidemia [Table 2].[14]
Table 2: Studies showing association of LP and comorbidities

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Hence, patients with OLP entail exceptional surveillance from skilled health professionals and should be meticulously investigated to rule out the predisposing factors for cardiovascular diseases. This will aid to avert the possible complications and the associated comorbidities.[15]

The linkage between DM and OLP was first reported by Grinspan et al.[16] This association of DM and OLP may be highlighted by two facts: (a) impaired endocrine function in DM may result in immune dysregulation which may predispose to the development of OLP lesions [17] and (b) few antidiabetic medications in patients with DM may evoke an allergic reaction and result in an oral lichenoid lesion.[18] A meta-analysis study by Mozaffari et al. showed a statistically significant difference between the occurrences of OLP in patients with DM when compared with the controls (1.37% in patients with DM and 0.75% in the control population).[19] Otero Rey et al. conducted a recent systematic review with a two-fold objective, wherein they demonstrated the prevalence of DM in patients with OLP (1.6%–37.7% DM in OLP) and also the prevalence of OLP in DM (0.5%–6.1% OLP in DM) [Table 3].[20]
Table 3: Studies showing association of LP with DM

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The association of thyroid disease and OLP was first reported in 1994, and the published literature has strengthened this association.[21] The possible association of OLP and thyroid gland diseases (TGDs) can be partly strengthened by the fact that numerous autoimmune conditions tend to congregate with autoimmune TGDs.[10],[22],[23] A meta-analysis study by Li et al. showed a statistically significant difference in the prevalence of TGD between the OLP and the control population. The study showed that hypothyroidism and Hashimoto thyroiditis were the most common associated thyroid diseases with OLP [Table 4].[24]
Table 4: Studies showing association of LP with thyroid diseases

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A study by Dreiher et al. demonstrated that a majority of patients with OLP presented with dyslipidemia.[9] Studies by Arias-Santiago et al.[25] and Aniyan et al.[26] demonstrated a higher prevalence of dyslipidemia in both skin and oral LP patients. Chronic inflammatory components result in uncontrolled dyslipidemia, and thus, augment the atherosclerotic plaque formation and other predisposing factors for cardiovascular diseases [Table 5].
Table 5: Studies showing association of LP and dyslipidemia

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Bowel diseases occasionally described concomitant with OLP including celiac disease, ulcerative colitis, and Crohn's disease.[27] The relationship between Helicobacter pylori and OLP has been suggested by various studies. A statistically significant difference in Helicobacter pylori infection between patients with LP and control groups has been observed according to studies by Morravvej et al.[28] and Vainio et al.[29]

Psychological stress and anxiety

OLP is regarded as a psychosomatic disorder,[30] and an increased rate of depression, anxiety, and psychic ailments has been associated with patients with OLP.[31] Stress accounts as the major attribute to the acute exacerbations in patients with OLP.[32] The relationship between OLP and stress is well-documented by frequent depressive and anxiety episodes and an elevated salivary cortisol level in patients with OLP.[33] Elevated salivary/urinary cortisol levels correspond to increased anxiety and depressive states.[34] A recent study by Radwan-Oczko et al. assessed the psychological and psychopathological aspects of patients with OLP. The study confirmed the interrelationship between OLP and stress, depression, anxiety, and the resultant compromised quality of patient's life.[30] Another systematic review by Cerqueira et al. strengthened the linkage between the prevalence of OLP in patients with psychological disorders [Table 6].[35]
Table 6: Studies showing association of LP and psychosomatic disorders

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Pharmacological and/or psychotherapeutic stress management may prove as a valuable additional approach in OLP therapy. Psychological assessment of patients should be an integral approach in the comprehensive OLP diagnosis.[30]

Oral lichenoid reactions

Lichenoid reactions have a recognizable etiology, and clinically and histopathologically mimic OLP. Lichenoid lesions are characteristically unilateral [36] and erosive.[37] The inflammatory infiltrate is primarily composed of plasma cells, eosinophils, and neutrophils, and with numerous Civatte bodies.[36],[38]

Dental restorative materials: Amalgams, composite resins, cobalt, and gold are the chief contributors to oral lichenoid reaction (OLR). Flavoring agents and plastics also play a role in the pathogenesis and management of patients with OLR.[39]

Drug-induced OLR: The most common drugs associated with OLR are nonsteroidal anti-inflammatory agents (NSAIDs) and angiotensin-converting enzyme inhibitors (captopril, enalapril).[37] In 1994, Thompson and Skaehill showed strong evidence that drugs such as beta-blockers, methyldopa, penicillamine, and NSAIDS are linked with lichenoid eruptions.[40] Withdrawing the offending drugs results in the resolution of the lichenoid reaction and this aids the diagnosis of OLR.

Genetic predisposition: Documentation of several familial cases have suggested genetic predisposition in the pathogenesis of OLP.[41] Lowe et al. were the first to report a significantly higher HLA-A3 frequency in a British family with cutaneous LP.[42]

Predisposing factors

Mechanical trauma

Dental procedures, sharp cusps, uncountoured dental restorations, ill-fitting prosthesis, and deleterious oral habits are the possible predisposing factors.[43] Koebner's phenomenon refers to the development of lesions at sites subjected to trauma. This suggests a possible explanation for erosive lesions being more common in trauma-prone sites (buccal mucosa and lateral aspect of the tongue).[33]

Plaque and calculus

Erosive/atrophic LP patients, especially with desquamative gingivitis, face difficulty in tooth brushing because of gingival pain and bleeding. Gingival lesions of LP may be worsened by dental plaque and calculus.[44]

  Clinical Manifestations Top

OLP is a mucocutaneous disorder of unknown etiology. In a majority of cases, LP may affect only the oral cavity. The condition may also affect other mucosal sites such as skin, genitals, scalp, and nails.[45] OLP primarily affects perimenopausal females with a prevalence of 0.1%–4%. Most OLP patients are in the age range of 30–60 years; however, no age group is spared.[46]

Skin lesions: Cutaneous LP lesions are usually self-limiting, cause itching, and are delineated by the characteristic six P's – planar, polygonal, pruritic, purplish, papules, and plaques. The disease has an acute onset, and the commonly affected sites are flexor surfaces of the wrists, forearms, and legs. Interlacing, fine, reticular-white lines (Wickham striae) often surround the skin lesions [47] [Figure 1].
Figure 1: Solitary papular lesion on the dorsum of the leg

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Oral manifestations: Oral lesions have a chronic course with infrequent spontaneous remission and are potentially premalignant. In addition, oral lesions are difficult to treat, and hence, a source of morbidity.

Andreason classified OLP into six clinical types: reticular [Figure 2]a and [Figure 2]b, papular, plaque-like [Figure 3], atrophic [Figure 4], ulcerative [Figure 5], and bullous [Figure 6].[48] OLP was further classified into reticular (reticular, plaque-like, and papular), erythematous (atrophic), and erosive type (ulcerative, bullous).[49] However, according to a few authors, OLP is of two types: reticular (reticular, plaque-like) and erosive (atrophic, ulcerative, and bullous).[50]
Figure 2: (a and b) Reticular lichen planus. Wickham's striae on the (a) lower labial mucosa and (b) buccal mucosa

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Figure 3: Plaque-like lichen planus on the dorsum of the tongue

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Figure 4: Atrophic lichen planus on the buccal mucosa

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Figure 5: Ulcerated lichen planus on the lower lip

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Figure 6: Bullous lichen planus

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The reticular type is the most frequently encountered form and manifests as bilateral asymptomatic Wickham striae on the buccal mucosa, labial mucosa, tongue, palate, and gingiva. Atrophic and erythematous oral mucosa is seen in the atrophic LP. The vesicles filled with fluid are characteristically seen in bullous LP. Erosive LP presents as an ulcerated, erythematous, and painful lesion. These erosive lesions are frequently accompanied by secondary opportunistic candidal infections.[51]

Most of the OLP cases are seen on the buccal mucosa, followed by dorsum of tongue, gingiva, labial mucosa, and vermilion border of the lower lip.[33],[52] Exclusive gingival lesions are seen in about 10% of patients with OLP. Erythematous gingival lesions result in desquamative gingivitis, the most frequently seen form of gingival LP [Figure 7].[53] These lesions also manifest as a minute, raised, fine white interlacing papules or plaques and may mimic keratotic lesions (frictional keratosis or leukoplakia). Isolated OLP cases at sites other than the gingiva are rarely seen, although few isolated lip [54] or tongue [48] lesions have been reported.
Figure 7: Desquamative gingivitis in lichen planus

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Genital mucosa: Genital mucosa is the most commonly involved extraoral site in female patients, and about 20% of females with OLP develop genital lesions.[55] Vulvovaginal–gingival syndrome denotes the relationship of LP with the vulva, vagina, and gingiva.[56] Usually, genital lesions are primarily erosive. However, few patients may present with asymptomatic reticular genital lesions.[57]

The penogingival syndrome denotes the male analog of the vulvovaginal–gingival syndrome of LP.[58]

Skin appendages: Scaly, violaceous, pruritic papular lesions affecting the scalp are known as Lichen planopilaris. Untreated cases may result in scarring alopecia.[59]

Nails: Irregular, longitudinal grooving, ridging, and thinning of the nail plate are seen. This causes shedding of the nail plate with atrophy of the nail bed. Pterygium (i.e. cuticular overgrowth) is a characteristic finding.[60]

Esophageal LP may manifest as dysphagia, chronic pain, and strictures.[61]

  Diagnosis Top

Bilaterally, symmetrical, white interlacing striae, and/or popular lesion is the most peculiar clinical manifestation of OLP.[62] The presence of bilateral, often symmetrical reticular lesions was also considered as an essential clinical criterion.

The following histopathological features are fundamental for OLP diagnosis [Figure 8]:
Figure 8: Histopathology of lichen planus

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A distinct band-like lymphocytic infiltrate in the connective tissue zone.

Presence of epithelial basal layer liquefaction degeneration

No signs of atypia/epithelial dysplasia.[63]

Eisenberg [64] suggested the optional histologic diagnostic features, including saw-toothed rete ridges, colloid/civatte bodies, and parakeratotic epithelium.

Immunofluorescence shows a linear pattern of fibrin and shaggy fibrinogen deposits at the epithelial basement membrane or cytoid bodies (Russell bodies), or both in the absence of deposition of fibrinogen [Figure 9].[65]
Figure 9: Direct immunofluorescence showing shaggy bands of fibrinogen

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  Treatment Top

Currently, OLP treatment intends at minimizing the ulcerations and mucosal inflammation, diminish the flare-up of the lesions, and possibly enhance the disease-free period. However, no single therapeutic regimen has proven valuable in the management of OLP.[66]

Usually, no treatment is warranted for the benign/asymptomatic form (reticular OLP), and periodic observation and evaluation is usually sufficient in such cases.[67] Patient education and motivation for maintaining oral hygiene and corrective dentistry may play a pivotal role in OLP management.[68] Topical high-potency corticosteroids comprise the cornerstone therapeutic regimen in patients presenting with severe pain and burning sensation.[67]

A range of therapeutic regimen is used for the management of OLP, including corticosteroids (topical, intralesional, and systemic), immunosuppressive agents (tacrolimus, cyclosporin, mycophenolate mofetil, azathioprine), retinoids, and immunomodulatory agents (thalidomide and levamisole).[69]

Mouth is a mirror of systemic diseases and oral manifestations of systemic disease may serve as an initial clue in the diagnosis and management of the primary systemic pathology. OLP is associated with numerous systemic manifestations (MS, chronic viral hepatitis, diabetes, hypertension, dyslipidemia, and psychosomatic disorders). The primary healthcare providers play an important role in the management of patients who have oral consequences of systemic disease, as they are often likely to be the first clinicians to observe such abnormalities. They will ensure that any potential oral manifestation of systemic disease is managed quickly and appropriately to improve the patient's quality of life.[70]

  Conclusion Top

OLP has been associated with numerous systemic connotations and may necessitate a multidisciplinary treatment strategy. OLP should not be treated as an isolated entity, but utmost care should be taken to screen and treat the associated systemic manifestations. Hence, it is essential that the dental surgeon should be aware of the various systemic associations of LP and should work in close connect with physicians to rule out the predisposing factors for the associated comorbidities.

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Conflict of interest

There is no conflict of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]

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