INTRODUCTION:

OLP is a chronic inflammatory disease that affects the mucous membrane of the oral cavity. It is a T cell mediated autoimmune disease in which the cytotoxic CD 8+ T cells trigger apoptosis of the basal cells of the oral epithelium. (1)The prevalence of OLP globally is 1 to 2 % while in the Indian scenario, it is 2.6%.The malignant transformation rate ranges from 0.4 to 5.3 %.(2)

Case Report

A 64 year old female patient reported to the Department of Oral Medicine and Radiology, Saveetha Dental College with a chief complaint of burning sensation of the oral cavity for the past 6 months. Her burning sensation was aggravated on the intake of hot and spicy foods and had relief on the intake of cold food substances, but felt that off late she had been experiencing burning sensation on the intake of all kinds of food substances. Her past medical history revealed that she is a hypertensive and diabetic patient and is under Aten 50 and Glide M for the same.

Her past dental history revealed that she had undergone extraction of her maxillary and mandibular anteriors (11, 12, 21, 22, 31, 32, 41 and 42) 2 years before due to periodontitis. Following which 6 months later she had a Fixed Partial Denture (FPD) prosthesis from 13 to 23 and 33 to 43. The patient felt that she had developed this burning sensation only after the prosthesis was done. The patient had visited a private dental clinic for the same problem 1 month before and she says she was given topical corticosteroids and had temporary relief only. No significant family history. She is a nurse by profession and she revealed that her workplace was stressful. She is a vegetarian by diet. She brushes her teeth once daily in horizontal motion using toothbrush and toothpaste. No adverse oral or parafunctional habits. General physical examination revealed that she was moderately built and nourished. A review of her systems was done and no abnormalities were seen. Extraorally her face was apparently symmetrical with no scars, sinuses or pigmentation. On intraoral examination, erythematous radiating white striae with ruptured vesicles were seen both in the right and left buccal mucosa, which were tender on palpation. Generalised desquamation of both the marginal and attatched gingival were seen across both the arches. The size of the gingival was inflamed, oedematous and enlarged. The scalloped contour was lost. Stippling was also absent. Gingival stripping was observed in the marginal gingival region of 12, 13 and 14. A generalized chronic periodontitis of the gingiva was observed. Correlating with the patient’s history and clinical findings, it was provisionally diagnosed as Erosive OLP. The other possible differential diagnoses included Mucous Membrane Pemphigoid or Pemphigus Vulgaris.

Figure 1: A case of Erosive OLP, during the initial visit. Areas of desquamation seen in both the marginal and attatched gingival across both the arches. Areasof erythema with ruptured vesicles seen in the buccal mucosa.

An incisional biopsy of the right buccal mucosa was taken in the region of 45, 46 and sent for histopathological examination. Histopathology revealed atrophic parakeratinised stratified squamous epithelium along with ulceration in one area and basal cell degeneration. The underlying connective tissue had sub epithelial band of lymphocytic infiltration with germinal center formation in an area and moderate vasculature. Skeletal muscle and adipose tissue were evident in deeper planes which was suggestive of Erosive OLP.

Figure 2: Photomicrograph reveals atrophic parakeratinised stratified squamous epithelium along with ulceration and basal cell degeneration. The underlying connective tissue reveals sub epithelial band of lymphocytic infiltration with germinal centre formation and moderate vasculature suggestive of Erosive OLP

Patient was treated with topical candid mouth paint,tenovate to be applied thrice daily, Betnesol 0.5 mg BID, Cap. Doxycycline 100 mg OD, T.Cetzine OD and Cap. Evion OD for one week. During the second visit, the patient showed good improvements in her condition.

Figure 3: A case of Erosive OLP during the second week of follow up

Following in the second visit, patient was instructed to use topical candid mouth paint, Betnesol 0.5 mg BID and Cap. Evion OD and asked to report after a week for review.

DISCUSSION:

The word lichen planus is derived from the Greek literature, ‘lichen’ meaning tree moss and ‘planus’ refers to flat. Lichen planus was first reported by Erasmus Wilson in 1869.Darier is credited with the first formal description of the histopathological changes associated with OLP.(3) Oral lesions of lichen planus were first described by Thiebergie. Wickham in 1895, described the appearance of whitish striae and punctuations that develop along the flat surfaced papules.(4) OLP is a chronic inflammatory disease that affects the mucous membrane of the oral cavity. It is a T cell mediated autoimmune disease in which the cytotoxic CD 8+ T cells trigger apoptosis of the basal cells of the oral epithelium. The etiopathogenesis of OLP can be attributed due to T cell mediation wherein there is an overproduction cytokines which leads to apoptosis. Autocytotoxic CD8 and T cells trigger apoptosis of oral epithelial cells. The immune system is triggered due to interactions among genetic, environmental and lifestyle factors.(5) Other possible theories include the genetic background where the weak association between HLA antigen and oral lichen planus.(6) Dental materials and infectious agents like gram negative aerobic bacillus, spirochetes and increased prevalence of candida species.(7) There is also a strong association of psychological factors like higher level of anxiety, greater depression and psychic disorders in patients with erosive OLP.(8) OLP may contain both red and white elements and provide together with the different textures, the basis for clinical classification of this disorder. The white and red components of the lesion can be a part of the different textures which include reticulum, characterised by fine white lines or striae. The striae may form a network but may also show annular (circular) patterns.(9) The striae often display a peripheral erythematous zone, which reflects the sub epithelial inflammation. Although the reticular OLP may be encountered in all regions of the oral mucosa, most frequently this form is observed bilaterally in the buccal mucosa and rarely on the mucosal side of the lips. It can be sometimes be observed in the vermillion border.(10) The other form is the papular type of OLP which is usually present in the initial phase of the disease. It is clinically characterised by small white dots, about 0.5mm which in most occasions intermingle with the reticular form.(11) The other form is the plaque like which shows a homogenous well demarcated white plaques often, but not always surrounded by striae, they clinically resemble homogenous oral leukoplakias. This is the most constant form, commonly encountered in smokers and on cessation the plaques may disappear and convert into reticular OLP.(12) Bullous form of OLP is another very unusual type of OLP and may appear as bullous structures surrounded by a network.(13) Erythematous or atrophic form of OLP is characterised by homogenous red area. When this type of OLP is present in the buccal mucosa or in the palate, striae are frequently found in the periphery. Some patients may experience erythematous OLP exclusively affecting the attatched gingiva. This form of lesion may occur without any papules or striae and presents as desquamative gingivitis. Therefore erythematous OLP requires a histopathological examination in order to arrive at a correct diagnosis.(14) Ulcerative form of OLP are lesions that are the most disabling form of OLP. Clinically, the fibrin-coated ulcers are surrounded by an erythematous zone frequently displaying radiating white striae. This appearance may reflect a gradient of the intensity of sub epithelial inflammation that is most prominent center of the lesion. A study using the combination of selenium-ACE combined with topical corticosteroids and an antifungal agent had been proven to provide symptomatic relief in patients with ulcerative oral lichen planus.(15)

Skin involvement in lichen planus:

Skin lesions are characteristically itchy and violaceous to brown papules very frequently distributed over the flexor aspect of the wrist or ankles, extensor aspect of the lower legs, skin of the lower central back and natal clefts. Scalp involvement results in loss of hair (alopecia) which is lichen planopilaris. Longitudinal ridging and grooves are seen over the nail (onychorrhexis). Other changes seen in the nail include distal splitting (onychoschizia), separation of the nail plate from nail bed (oncycholysis), permanent damaged nail matrix (pterygium) and finally permanent nail loss(anonychia).(16) Koebner’s phenomenon which is the appearance of lesions at the site of micro trauma is also well demonstrated in case of skin involvement as well demonstrated in oral lesions. Hence any mechanical trauma or irritation such as sharp filling margins or rough surfaces or ill fitting dentures should be evaluated and eliminated.(17)

Syndromes associated with OLP:

Grinspan syndrome is the association of OLP with diabetes mellitus and hypertension. Graham-Little syndrome and vulvovaginogingival syndrome are other syndromes associated with OLP in which there is mucosal involvement of gingival and genital region usually of erosive type.(18)

Differential Diagnosis:

Differential diagnosis of reticular/annular type of OLP includes lichenoid drug reaction, electrogalvanic white lesions and frictional keratosis and leukoplakia. Keratotic forms of lichen planus can be differentiated from leukoplakic plaque as the former is usually associated with burning sensation and association with etiologic factors in the latter. Hypertrophic form resembles hyperplastic candidiasis. Erosive lichen planus resembles lupus erythematosus. Oral lichenoid reactions clinically and histopathologically resemble OLP but have an identifiable etiology like drugs and dental restorative materials including amalgams, composite resins, cobalt and gold have been implicated as causes of lichenoid reactions. Erosive OLP should be differentiated from lichenoid reaction, graft versus host disease, discoid lupus erythematosus and speckled leukoplakia. The desquamation in the gingival of erosive OLP should be differentiated from other forms like pemphigus, pemphigoid and linear IgA disease. Erythematous lesions of OLP can be excluded from atrophic candidiasis by the presence of whitish striations at the periphery.(19)

Investigations:

A detailed case history and a thorough clinical examination can give an insight into the provisional diagnosis. An incisional biopsy can be taken from the site of the lesion and sent for histopathological examination. For gingival lichen planus, direct immunofluorescence assay can be done to detect the presence of autoantibodies. Histopathological features include essential features like the presence of a superficial band –like infiltrate of T lymphocytes, liquefactive degeneration of the basal cell layer, saw tooth and spindly rete ridges, colloid (civatte, hyaline and cytoid) bodies and epithelial separation from lamina propria. Degeneration of basal cell layer and basal keratinocyte anchoring elements in OLP produce weakness at the epithelial-connective tissue interface causing histological cleft formation (Max-Joseph spaces) and clinical blistering of the oral mucosa (bullous lichen planus). Immunofluorescence of perilesional mucosa reveal fibrin and shaggy fibrinogen in a linear pattern at the basement membrane zone and cytoids in the absence of deposition of fibrinogen.(20)

Modified diagnostic criteria for the diagnosis of OLP (WH0 2003):

It includes clinical criteria which are the presence of bilateral, more or less symmetrical lesion, presence of a lacelike network of slightly raised gray-white lines (reticular pattern), erosive, atrophic, bullous and plaque-type lesions are accepted only as a subtype in the presence of reticular lesions elsewhere in the oral mucosa. In all other lesions that resemble OLP but do not complete the aforementioned criteria, the term ‘clinically compatible’ should be used. The histopathological criteria include the presence of a well-defined bandlike zone of cellular infiltration that is confined to the superficial part of the connective tissue, consisting mainly of lymphocytes, signs of liquefaction degeneration in the basal layer, absence of epithelial dysplasia. When the histopathologic features are less obvious, the term ‘histopathologically compatible’ should be used. To achieve a final diagnosis, clinical as well as histopathological criteria should be included. (21)

Prognosis:

Cutaneous lesions are self limiting, oral lesions are chronic, rarely undergo spontaneous remission while erosive lesions are difficult to palliate. The reticular type of OLP has best prognosis since spontaneous remission occurs in 40% of the cases.

Management:

Management options should be done according to the clinical type, associated symptoms and age. Reticular OLP are asymptomatic and require no therapy but only regular follow up for any potential changes. Precipitating factors like mechanical irritants (sharp fillings, metallic restorations, ill fitting dentures) should be removed. Proper oral hygiene measures to promote gingival health should be advocated. Topical corticosteroids like triamcinolone acetonide 0.1 % in orabase, oral suspension of triamcinolone, high potency steroid mouthwashes like betamethasone valerate 0.1 %, fluocinolone acetonide 0.1 %, clobetasone propionate 0.05 % can be used. Systemic corticosteroids can be used for recalcitrant erosive or erythematous OLP, in case where topical approaches have failed or wide spread involvement of skin, genital. eosophageal or scalp involvement.40-80 mg of prednisolone can be tried for 5-7 days and can be tapered gradually 5-10 mg per day gradually over a 2-4 week period. For intractable erosive OLP, intralesional injections of triamcinolone acetonide (10-20mg/ml per vial) for 2-4 weeks. Hydrocortisone, methylprednisolone can also be given. Immunosuppressive agents like cyclosporine 100 mg/ml can be used as a mouth rinse or finger rub application using cyclosporine 48 mg/day which suppresses T cell cytokine production. Immunomodulators like levamisole 150 mg/day for 3 days along with prednisolone is useful in long term remission. Topicaltacrolimus 0.1 % is effective in erosive OLP. Topicalretinoids like isoretinoin gel 0.1 % acts by down regulation of fibroblast function can also be used. Psoralens and long wave ultraviolet A (PUVA) therapy with 8-methoxy psoralen and photochemotherapy can be used. Excision, CO₂ laser, cryosurgery are useful in persistent or dysplastic lesions. Antibiotics like 2 % aureomycin mouthwash, antimalarials like hydroxychloroquine sulfate, azathioprine, dapsone, interferonsin the form of topical (human fibroblast interferon beta and human fibroblast interferon alpha) and systemic (IFN alpha-3 to 10 million for 3 weeks) can be given. Thalidomide, 100-150 mg /day can be given.(22)

CONCLUSION:

The risk of oral carcinoma in patients with OLP can be minimized by advising the patients to quit adverse oral habits like smoking, tobacco and alcohol consumption, by lifestyle and diet modification by encouraging the patients to have an increased intake of more amount of nutritious food substances, fresh fruits and vegetables. The principal aims of oral lichen planus therapy are the resolution of painful symptoms, the resolution of oral mucosal lesions, the reduction of the risk of oral cancer, and the maintenance of good oral hygiene. Following which definitive treatment for symptomatic relief can be initiated with topical followed by systemic corticosteroids. Therefore, the elimination of mucosal erythema and ulceration with residual asymptomatic reticular or popular lesions, should be considered in the management of OLP.

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Received on 23.02.2019 Modified on 18.03.2019

Research J. Pharm. and Tech. 2019; 12(6):3007-3011.

DOI: 10.5958/0974-360X.2019.00508.0