Human papilloma virus in erosive oral lichen planus.

Several types of human papilloma viruses (HPV) have been associated with benign and malignant squamous cell tumours of mucosal epithelium. To identify HPV in erosive oral lichen planus (OLPe), considered as a premalignant lesion, tissues from 20 patients were examined by Southern blot hybridization with 32P-labeled HPV DNA probes. Type 11 was found in 6 of the lesions while HPV types 6, 16 and 18 were not detected in any of the tissues examined. Using a type-specific polymerase chain reaction (PCR) assay for HPV-6, 11, 16 and 18, HPV-11 was detected in 8 of the samples (all of those positive by Southern blot), and, in addition, HPV-6 was found in 5 samples and HPV-16 in 3 samples. Overall, by the more sensitive PCR assay, 65% of samples were positive for HPV DNA. The finding of HPV DNA in many of the samples using two different techniques indicates a high prevalence of HPV in the OLPe afflicted oral mucosa. However, the role of HPV in the pathogenesis of OLPe has yet to be determined.

Assessment of Langerhans' cells in oral lichen planus using monoclonal antibodies.

In order to demonstrate Langerhans' cells in epithelium of oral lichen planus, monoclonal antibodies were used as immunological markers in combination with immunohistochemistry. By the use of anti-Ia antibodies the Langerhans' cells were shown to express an increased number of Ia-like antigens in comparison to the amounts found in healthy oral mucosa. The subepithelial infiltrate of mononuclear cells expressed identical Ia-like antigens on their surfaces. With anti-T6 antibodies as immunological markers, the number of Langerhans' cells was found to be virtually identical in diseased and healthy epithelium. Treatment of oral lichen planus with tretinoin resulted in a decrease of epithelial Ia-like antigens compared with the number found in untreated lesions. However, treatment with tretinoin did not alter the frequency of Langerhans' cell marked with anti-T6 antibodies. The present data demonstrate an increased amount of Ia-like antigens per number of T6-positive Langerhans' cells in diseased oral mucosa compared to healthy conditions. The increased expression of Ia-like antigens on Langerhans' cells and the contemporary finding of Ia-like antigens on the subepithelial T-cells support the opinion that the pathogenesis of oral lichen planus is mainly a cell-mediated type of immunological reaction.

Oral lichen planus: hypersensitivity to dental restoration material.

67 patients with oral lichen planus of the atrophic-erosive or reticular plaque type were examined. Dental amalgam in contact with mucosal lesions was present in 64 patients, and gold fillings in 33. Patch testing with a standard procedure was performed with components of dental fillings. 11 patients (16%) reacted to at least one of the mercury compounds compared to 8% in a reference group. Most positive reactions were caused by elemental mercury and ammoniated mercury. No patient reacted to gold or copper. Readings at days 10-14 did not increase the number of responders. 13 patients were patch tested with palladium; all were negative. It is not clear whether in the mercury-positive patients allergy to dental amalgam is a causative or aggravating factor, or merely on epiphenomenon.

Incidence of liver disease in chronic lichen planus of the mouth.

Fifty-four patients with oral lichen planus were screened for chronic inflammatory liver disease utilizing standard biochemical parameters of liver function, serum levels of immunoglobulins G, A and M and circulating autoantibodies against mitochondriae, smooth muscle and cell nuclei. One patient had primary biliary cirrhosis, and another had cryptogenic cirrhosis. This study did not confirm previous observations of a frequent association of oral lichen planus and primary biliary cirrhosis or chronic active hepatitis.

Severe oral lichen planus: remission and maintenance with vitamin A analogues.

Twenty-five patients with chronic oral lichen planus, usually of the atrophic-erosive type, were treated for 2 months with Etretinate 0.6 mg/kg b.w./day, followed for 4 months by Etretinate 0.3 mg/kg/day, or 0.1% Tretinoin in an adhesive base. Complete resolution or improvement was seen in 85% of the lesions after first treatment. The number of patients with oral soreness and pain was significantly reduced (p less than 0.001). During the second treatment, the improvement was maintained or even increased in about 70% of the patients, irrespective of the mode of treatment. Treatment was discontinued in one patient owing to moderately increased serum transaminase levels. The number of drug-related drop-outs was significantly lower than in a previous study utilizing an etretinate dose of about 1 mg/kg/day (p less than 0.05). Other adverse effects were minor and tolerable. Retinoids offer an effective mode of therapy for severe oral lichen planus.

Severe oral lichen planus: treatment with an aromatic retinoid (etretinate).

A double-blind study of twenty-eight patients with severe oral lichen planus treated with etretinate (75 mg daily) or a placebo for 2 months, showed that the oral retinoid had a marked beneficial effect. Nine non-responders who had received only placebo then entered an open cross-over study and they responded well to etretinate. Etretinate thus provided effective symptomatic relief for severe oral lichen planus, but side-effects were common, and six patients stopped treatment because of them.

Topical tretinoin therapy and oral lichen planus.

The treatment of severe forms of oral lichen planus is still relatively unsatisfactory. In this controlled study, 0.1% tretinoin in an adhesive base was used in 23 patients. Fifteen other control patients were similarly treated with the vehicle alone. In the tretinoin-treated group, 71% of the atrophic-erosive lesions improved while 29% improved from the vehicle (P less than .05). Reticular-plaque lesions improved in 74% from tretinoin and in 15% from the vehicle (P less than .001). Irritation from tretinoin occurs and thorough usage information is mandatory.