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REVIEW ARTICLE

Oral : An Update on Etiology, Pathogenesis, Clinical Presentation, Diagnosis and Management Sonia Gupta, Manveen Kaur Jawanda1

Abstract From the Department of Oral The is a mirror of health or disease, a sentinel or early warning system. The oral Pathology, Swami Devi Dyal cavity might well be thought as a window to the body because oral manifestations accompany Hospital and Dental College, 1 many systemic diseases. In many instances, oral involvement precedes the appearance of other Golpura, Barwala, and Laxmibai Institute of Dental Sciences and symptoms or lesions at other locations. Oral lichen planus (OLP) is a chronic mucocutaneous Hospital, Patiala, Punjab, India disorder of stratified squamous of uncertain etiology that affects oral and genital mucous membranes, skin, nails, and scalp. LP is estimated to affect 0.5% to 2.0% of the general population. This disease has most often been reported in middle‑aged patients with Address for correspondence: 30‑60 years of age and is more common in females than in males. The disease seems to Dr. Sonia Gupta, #95/3, be mediated by an ‑specific mechanism, activating cytotoxic T cells, and non‑specific Adarsh Nagar, Dera Bassi, mechanisms like degranulation and matrix metalloproteinase activation. A proper Mohali, Punjab ‑ 140507, India. understanding of the pathogenesis, clinical presentation, diagnosis of the disease becomes E‑mail: Sonia. [email protected] important for providing the right treatment. This article discusses the prevalence, etiology, clinical features, oral manifestations, diagnosis, complications and treatment of oral LP.

Key Words: Degranulation, mucocutaneous, oral lichen planus, pathogenesis, stratified squamous

What was known? Lichen planus is one of mucocutaneous disorder in which oral involvement precedes the appearance of other symptoms or lesions at other locations. Etiology of lichen planus as such is not known clearly, but at present it has been linked to autoimmune disorder For a general practitioner it is very important to know the important clinical features, diagnosis and treatment plan for this disease to differentiate it from other lesions. Now a days novel drug therapy and use of custom trays are of special concern for a dentist in management of oral lichen planus lesions.

Introduction “leichen” means tree moss and Latin word “planus” [4] The mouth is a mirror of health or disease, a sentinel means flat. or early warning system. The oral cavity might well be thought as a window to the body because oral Historical Background manifestations accompany many systemic diseases. The designation and description of the pathology were In many instances, oral involvement precedes the first presented by the English physician Erasmus Wilson appearance of other symptoms or lesions at other in 1866.[5] He considered this to be the same disease locations.[1] Most of the is derived as “lichen ruber,” previously described by Hebra[6] and embryologically from an invagination of the ectoderm characterized the disease as “an eruption of pimples and perhaps not surprisingly, this, like other similar remarkable for their color, their figure, their structure, orifices, may become involved in disorders that are their habits of isolated and aggregated development.”[7] primarily associated with the skin. In 1892, Kaposi reported the first clinical variant of the disease, lichen ruber pemphigoides.[8] In 1895, Lichen planus (LP) is a chronic mucocutaneous disorder Wickham noted the characteristic reticulate white lines of the stratified squamous epithelium that affects oral on the surface of LP , today recognized as [2] and genital mucous membranes, skin, nails, and scalp. Wickham striae.[9] Darier is credited with the first formal Oral lichen planus (OLP) is the mucosal counterpart of [3] description of the histopathological changes associated cutaneous LP. It is derived from the Greek word with LP.[10]

Access this article online Epidemiology Quick Response Code: The exact incidence and prevalence of LP is unknown. Website: www.e‑ijd.org In 1895, Kaposi noted the disease as “rather frequent” with 25 to 30 cases presenting annually.[11] In the United States, the incidence of LP is reported to DOI: 10.4103/0019-5154.156315 be approximately 1% of all new patients seen at health care clinics.[12] The Indian subcontinent has a

Indian Journal of 2015; 60(3) 222 Gupta and Jawanda: Oral lichen planus particularly high incidence of disease.[13] LP is estimated studies reveal that there is an insignificant association to affect 0.5% to 2.0% of the general population,[14] between candida infection and OLP.[35,36] OLP has been the prevalence being ranging from 0.5% selectively in found to be associated with various viral agents such Japanese population, 1.9% in Swedish population, 2.6% as human papilloma virus (HPV),[37‑40] Epstein Barr in Indian population and 0.38% in Malaysia (relatively virus (EBV),[41] human herpes virus 6 (HHV‑6)[39] and uncommon).[15] The relative risk is 3.7% in people with human virus (HIV).[42] Epidemiological mixed oral habits, lowest (0.3%) in non‑users of tobacco evidences from various studies worldwide strongly and highest (13.7%) among those who smoked and suggest that hepatitis C virus (HCV) may be an etiologic chewed tobacco.[16] This disease has most often been factor in OLP.[43,44] In OLP, HCV replication has been reported in middle‑aged patients with 30‑60 years of age reported in the epithelial cells from mucosa of LP lesions and is more common in females than in males. OLP is by reverse transcription/polymerase chain reaction or also seen in children, although it is rare.[17] It affects all in‑situ hybridization; also, HCV‑specific CD4 and CD8 racial groups.[18] However, according to some literature lymphocytes were reported in the subepithelial band. white individuals are five and a half time more likely These probably suggest that HCV‑specific T lymphocytes to develop this disease compared to other races.[19] may play a role in the pathogenesis of OLP. The OLP occurs more frequently than the cutaneous form putative pathogenetic link between OLP and HCV still and tends to be more persistent and more resistant to remains controversial and needs a lot of prospective and treatment.[20] interventional studies for a better understanding.[45] Etiology Autoimmunity Although the exact etiology of this disease is still OLP may occasionally be associated with autoimmune unknown, but some factors are associated with it. These disorders such as primary biliary cirrhosis, chronic active are as follows: hepatitis, , myasthenia gravis, and thymoma.[46] Genetic background Familial cases are rare. An association has been observed Bowel disease with HLA‑A3, A11, A26, A28, B3, B5, B7, B8, DR1, and Bowel diseases occasionally described concomitant with DRW9.[21‑24] In Chinese patients, an increase in HLA‑DR9 OLP include , ulcerative colitis and Crohn’s and Te 22 has also been noted.[25] disease.[47] Dental materials Food A great many materials commonly used in restoration Food and some of food additives such as cinnamon treatments in the oral cavity have been identified as aldehyde have been found to be associated with OLP.[28] triggering elements for OLP, including silver amalgam, Stress gold, cobalt, palladium, chromium and even non‑metals such as epoxy resins (composite) and prolonged use of One of the factors responsible for the development of OLP denture wear.[26‑29] is anxiety and stress. Some of the studies in literature reveal the role of the psychological stress in the etiology Drugs of OLP.[48‑50] Oral lichenoid drug reactions may be triggered by systemic drugs including NSAIDs, beta blockers, sulfonylureas, Habits some angiotensin‑converting enzyme (ACE) inhibitors, Although most patients with OLP show no increased [51] and some antimalarials, contact including prevalence of cigarette smoking, it has been flavorings, especially cinnamates.[26,30] suggested to be an etiological factor in some Indian communities.[52] Betel nut chewing is also more prevalent Infectious agents in Indian patients with OLP than in those without.[53‑55] OLP has been suggested to be related to bacteria such as a Gram‑negative anaerobic bacillus and spirochetes Trauma but this has not been confirmed.[28] Some of the Trauma as such has not been quoted as an etiological studies reveal the role of Helicobacter pylori (HP) in the factor in LP, although it may be the mechanism by etiology of OLP.[31,32] However, no evidence of its role which other etiological factors exert their effects.[28] [33] has been detected in OLP in some recent studies. Diabetes and hypertension Recently, it has been found in some literature that few Studies have revealed that both diabetes mellitus (DM) periodontopathogenic microorganisms are also associated and high blood pressure are associated with OLP.[56‑59] with the patients of OLP.[34] Role of candida infection is controversial in OLP. Several studies have shown an (Greenspan syndrome: Triad of DM, hypertension and increased prevalence of candida species.[28] However, some OLP)

223 Indian Journal of Dermatology 2015; 60(3) Gupta and Jawanda: Oral lichen planus

Malignant neoplasms of the BM. Again, a non‑intact BM cannot send a cell LP has been observed on the skin and/or mucosae of survival signal. This sets in a vicious cycle which relates patients affected by a range of different neoplasms such to the chronic nature of the disease.[65] [28] as with breast cancer and metastatic . The matrix metalloproteinase (MMP) are principally Miscellaneous associations involved in tissue matrix protein degradation. MMP‑9, OLP has occasionally been associated with other which cleaves collagen 4, along with its activators is conditions, including , lichen sclerosis, upregulated in OLP lesional T cells, resulting in increased [66] urolithiasis, agents used to treat gall stones, Turner’s BM disruption. [28] syndrome, etc. RANTES (Regulated on Activation, Normal T‑cell Expressed and Secreted) is a member of the CC Pathogenesis chemokine family which plays a critical role in the OLP is a T‑cell mediated autoimmune disease in which recruitment of lymphocytes and mast cells in OLP. The the auto‑cytotoxic CD8 + T cells trigger apoptosis of the recruited mast cell undergoes degranulation under the [60] basal cells of the oral epithelium. influence of RANTES, which releases chymase and TNF‑α. An early event in the disease mechanism involves These substances upregulate RANTES secretion by OLP [67] keratinocyte antigen expression or unmasking of an lesional T cells. antigen that may be a self‑peptide or a heat shock Weak expression of transforming growth factor (TGF)‑β1 [61] protein. Following this, T cells (mostly CD8+, and has been found in OLP. TGF‑β1 deficiency may some CD4 + cells) migrate into the epithelium either predispose to autoimmune lymphocytic inflammation. due to random encounter of antigen during routine The balance between TGF‑β1 and IFN‑γ determines the surveillance or a chemokine‑mediated migration toward level of immunological activity in OLP lesions. Local basal keratinocytes. These migrated CD8 + cells are overproduction of IFN‑γ by CD4 + T cells in OLP lesions activated directly by an antigen binding to major downregulates the immunosuppressive effect of TGF‑β1 histocompatibility complex (MHC)‑1 on keratinocyte and upregulates keratinocyte MHC class II expression or through activated CD4 + lymphocytes. In addition, and CD8 + cytotoxic T‑cell activity.[68] the number of Langerhans cells in OLP lesions is increased along with upregulation of MHC‑II expression; Clinical Features subsequent antigen presentation to CD4 + cells and The cutaneous lesions of LP are characterized (IL)‑12 activates CD4 + T helper cells which by 5 ps: Purple, polygonal, pruritic papules and activate CD8 + T cells through receptor interaction, plaque.[14] Initially, LP is evident as a cutaneous and interferon γ (INF‑γ) and IL‑2. The activated CD8 + T mucosal eruption, though rarely it can manifest with cells in turn kill the basal keratinocytes through tumor only oral or findings. LP usually begins as discrete, necrosis factor (TNF)‑α, Fas–FasL‑mediated or granzyme flat‑topped papules that are 3 to 15 mm in diameter B‑activated apoptosis.[62] which may coalesce into larger plaques. Early in course A Cytokine‑Mediated Lymphocyte Homing of the disease they appear red, but soon they take on reddish purple or violaceous hue. The center of the Mechanism may be slightly umblicated and its surface is In OLP, there is increased expression of the vascular covered by characteristic, very fine grayish white lines, adhesion molecules (VAM), that is, CD62E, CD54, and called Wickham striae. The lesions can occur anywhere CD106, by the endothelial cells of the sub‑epithelial on the skin surface but often are located on the flexor vascular plexus. The infiltrating lymphocytes express surfaces of limbs, inner aspects of knees and thighs and reciprocal receptors (CD11a) to these VAM. Some of the trunk and also may appear on lines of trauma, reflecting cytokines that are responsible for the upregulation of the Köbner phenomenon.[7] The face frequently remains [63] the VAM are: TNF‑α, IFN‑γ and IL‑1. uninvolved. The primary symptom of LP is severe Nonspecific mechanisms like mast cell degranulation pruritis. The severity of pruritus varies.[16] Some patients and MMP‑1 activation further aggravate the T‑cell report genital involvement with features similar to skin accumulation, BM disruption by mast cell proteases lesions.[69] scalp involvement (lichen planopilaris), and and keratinocyte apoptosis.[64] The normal integrity of nail beds.[14] Rarely, there is laryngeal, esophageal and the BM is maintained by a living basal keratinocyte conjunctival involvement.[62] due to its secretion of collagen 4 and laminin 5 into the epithelial BM zone. In turn, keratinocytes require a Oral Manifestations BM‑derived cell survival signal to prevent the onset of In the oral cavity, the disease assumes somewhat its apoptosis. Apoptotic keratinocytes are no longer able different clinical appearance than on the skin, and is to perform this function, which results in disruption characterized by lesions consisting of radiating white,

Indian Journal of Dermatology 2015; 60(3) 224 Gupta and Jawanda: Oral lichen planus gray, velvety, thread‑like papules in a linear, annular Reticular and retiform arrangement forming typical lacy, reticular It is the most common clinical form of this disease patches, rings and streakes. A tiny white elevated dot and presents with fi ne, asymptomatic intertwined is present at the intersection of white lines known here lace-like pattern called “Wickham striae” in a bilateral symmetrical form and involves the posterior mucosa of as striae of Wickham as compared to Wickham striae the cheek in most cases. in skin.[16] The lesions are asymptomatic, bilaterally/ symmetrically anywhere in the oral cavity,[70] but most Erosive common on buccal mucosa, , , gingiva, floor of This is the most significant form of the disease because it shows symptomatic lesions often surrounded by fine mouth, and may appear weeks or months before radiant keratinized striae with a network appearance.[20] the appearance of cutaneous lesions. Atrophic OLP has six classical clinical presentations [Figures 1-6] It exhibits diffuse red lesions and it may resemble the described in the literature:[2] combination of two clinical forms, such as the presence • Reticular of white striae characteristic of the reticular type • Erosive surrounded by an erythematous area.[2] • Atrophic Plaque‑like • Plaque‑like This type shows whitish homogeneous irregularities • Papular similar to ; it mainly involves the dorsum of [2] • Bullous. the tongue and the mucosa of the cheek.

Figure 2: Erosive type lichen planus−ulcerated lesion in the buccal mucosa with Figure 1: Reticular type lichen planus−on the lips and mucosa of the cheek erythematous borders

Figure 3: Atrophic type lichen planus−sometimes representing as desquamative Figure 4: Plaque type lichen planus−lesion on tongue

225 Indian Journal of Dermatology 2015; 60(3) Gupta and Jawanda: Oral lichen planus

Papular This form is rarely observed and is normally followed by some other type of variant described. It presents with small white papules with fine striae in its periphery.[2] Bullous It is the most unusual clinical form, exhibiting that increase in size and tend to rupture, leaving the surface ulcerated and painful. Nikolsky’s sign may be positive. Gingival Involvement The gingival lesions in LP fall into one or more of the following categories [Figure 2]:[2] Figure 5: Papular type lichen planus−lateral border of tongue Keratotic lesions are usually present on the attached gingiva as small raised round white papules of pinhead size with a flattened surface. Vesiculo‑bullous lesions are other mucocutaneous disorders especially , , or linear IgA disease.[71] Atrophic and Erosive: Produce the . The triad constituted by desquamative or erosive LP involving the vulva, vagina and gingiva is termed as vulvovaginal–gingival syndrome.[72] Diagnosis The history, typical oral lesions and skin or nail involvement are usually sufficient to make a clinical Figure 6: Bullous type lichen planus−lesion on upper buccal mucosa diagnosis of OLP. However, a is the recommended procedure to differentiate it from other lesions. Histopathology The classic histopathologic features of OLP include liquefactive degeneration of the basal cell accompanied by apoptosis of the keratinocytes, a dense band‑like lymphocytic infiltrate [Figure 7] at the interface between the epithelium and the , focal areas of hyperkeratinized epithelium (which give rise to the clinically apparent Wickham’s striae) and occasional areas of atrophic epithelium where the rete pegs may be shortened and pointed (a characteristic known as saw tooth rete pegs). Eosinophilic colloid bodies (Civatte bodies), which represent degenerating keratinocytes, are often visible in the lower half of the surface epithelium.[14] Figure 7: of oral lichen planus Degeneration of the basal keratinocytes and disruption of the anchoring elements of the epithelial BM and basal keratinocytes (e.g. hemi desmosomes, filaments, fibrils) Direct Immunofluorescence weaken the epithelial connective tissue interface. As a Immunoglobulin or complement deposits are not a result, histologic clefts (Max–Joseph spaces) may form consistent feature of OLP. In some instances, fibrinogen and blisters on the oral mucosa (bullous LP) may be and fibrin are deposited in a linear pattern in the seen at clinical examination. B cells and plasma cells are BM zone. Colloid bodies contain fibrin, IgM, C3, C4, uncommon findings.[18] and . Laminin and fibronectin staining may be

Indian Journal of Dermatology 2015; 60(3) 226 Gupta and Jawanda: Oral lichen planus absent in areas of heavy fibrin deposition and colloid Management body formation. This finding suggests BM damage in The principal aims of current OLP therapy are the these areas. In OLP, electron microscopy (EM) is used resolution of painful symptoms, oral mucosal lesions, the principally as a research tool. The ultrastructure of reduction of the risk of , and the maintenance the colloid bodies suggests that they are apoptotic of good . Eliminate the local exacerbating keratinocytes, and recent studies using the end labeling factors as preventive measures. Up to now different method revealed DNA fragmentation in these cells. therapies are described for OLP including drug therapy, EM shows breaks, branches, and duplications of the surgery, psoralen with ultraviolet light A (PUVA), and [18] epithelial BM in OLP. laser. Use of novel drug therapy is the most common method for treatment of OLP. Different drugs have been Serology used in the form of topical and systemic application There are no consistent serological changes associated for the treatment of OLP.[77] Drugs used in topical form with OLP but some patients do present an elevated are , immunosuppressives, retinoids, and antinuclear antibody (ANA) titer. immunomodulators. Drugs which are used systemically are , metronidazole, griseofulvin, and Hematological Investigations hydroxychloroquine, some retinoids and corticosteroids. Blood biochemistry and full blood examination (FBE) Small and accessible erosive lesions located on the should also be included in the full patient workup. gingiva and palate can be treated by the use of an adherent paste in the form of a custom tray, which Cytology allows for accurate control over the contact time and Although cytological changes may be detected in OLP, ensures that the entire lesional surface is exposed to the the use of exfoliative cytology is not recommended.[62] drugs.[3] Some studies show an increased incidence of C. albicans Local drug delivery can provide a more targeted and infection in patients with OLP. Periodic acid–Schiff (PAS) efficient drug‑delivery option than systemic delivery staining of biopsy specimens and candidal cultures or for diseases of the oral mucosa. The main advantages [18] smears may be performed. of local drug delivery include (i) reduced systemic side effects, (ii) more efficient delivery as a smaller Differential Diagnosis amount of drug is wasted or lost elsewhere in the body, The differential diagnosis can include cheek and (iii) targeted delivery as drugs can be targeted to chewing/frictional keratosis, leukoplakia, lichenoid the diseased site more easily when delivered locally, reactions, leukoplakia, erythematous, , thereby reducing side effects.[78] However, potential for mucus membrane pemphigoid, para neoplastic novel drug delivery systems in dentistry has not yet pemphigus, erythematous and chronic been fully realized and further research is still needed in ulcerative , Graft vs. host disease.[3] order to improve treatment outcomes. Surgical excision, cryotherapy, CO laser, and ND:YAG Malignant Potential of OLP 2 laser have all been used in the treatment of OLP. Malignant transformation of OLP remains a very In general, surgery is reserved to remove high‑risk controversial issue.[62] At least some reported cases dysplastic areas. diagnosed originally as OLP on clinical and/or histological grounds were probably epithelial dysplasia (lichenoid Photo chemotherapy, a new method in which clinician dysplasia) that progressed subsequently to overt uses ultraviolet A (UVA) with wavelengths ranging from (SCC).[73] The OLP lesions are the 320 to 400 nm, after the injection of psoralen is consistently more persistent than the dermal lesions also used. Relaxation, meditation and hypnosis have and have been reported to carry a risk of malignant positive impact on many cutaneous diseases and help transformation to oral squamous cell carcinoma (OSCC) to calm and rebalance the inflammatory response which of 1‑2% (reported range of malignant transformation can ameliorate inflammatory skin disorders. 0– 12.5%).[74] Erythroplastic lesions may also occur in OLP. They develop in approximately 1% of the patients Conclusion and are sharp with slight reddish depressions.[2] In OLP is a very common oral dermatitis and is one of the most cases, malignant transformation to carcinoma most frequent mucosal pathoses encountered by dental in situ (28.5%) and in micro invasive carcinoma (30‑38%) practitioners. It is imperative that the lesion is identified is observed, less frequently stage I and II carcinoma. Oral precisely and proper treatment be administered at the cancer‑correlated OLP predisposes to the development of earliest. A proper understanding of the pathogenesis, multiple primary metachronous tumors of the oral cavity clinical presentation, diagnosis of the disease becomes and of metastases.[75,76] important for providing the right treatment.

227 Indian Journal of Dermatology 2015; 60(3) Gupta and Jawanda: Oral lichen planus

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