Until definitive testing for laminin 332 antibodies becomes available, we recommend that patients with MMP in whom serum indirect immunofluorescence (IIF) studies reveal antibodies bound to the dermal side of basement membrane zone-split skin undergo age and gender appropriate cancer screening. Additional evaluation for malignancy should be performed as indicated based upon a review of symptoms, physical examination, and the results of age-appropriate screening. Cause
Autoantibodies targeted to components of the basement membrane zone have been identified as pathogenic in mucous membrane pemphigoid. Antigens include 180-kD bullous pemphigoid antigen (BP180), laminin 332, beta-4-integrin, and other antigens that are not fully discovered are identified against the basement membrane. Complication of D- penicillamine therapy may trigger and causes mucous membrane pemphigoid. It also occurs after acute severe ocular inflammation in patients with Stevens-Johnson syndrome. Pathophysiology
Autoantibodies target the basement membrane zone proteins which are responsible to promote adhesion within the basement membrane zone of the mucosa and the skin. The major basement membrane zone proteins identified include :

C-terminus of BP180
BP230
Laminin 332(also known as laminin 5 or epiligrin)
Alpha-6-beta-4 integrin Type VII collagen.In contrast to the target of the N-terminus of BP180 that is located in the hemidesmosomes and upper lamina lucida in bullous pemphigoid, the target antigen in MMP is the C-terminus of BP180 which is located in the lower lamina lucida and lamina densa. This results in a deeper separation that is more likely to scar as compared to a more superficial blister that is unlikely to scar in bullous pemphigoid.
Dental tray can also be fabricated to help in the application of topical steroids to lesional sites under occlusion for patients with gingival involvement. Furthermore, topical tacrolimus, a calcineurin inhibitor, has also shown to be effective to control the disease, including some patients who failed to respond well to topical corticosteroids. Topical tacrolimus 0.1% ointment is applied two to three times a day and tapered after improvement in healing of pemphigoid. Another method is to use intralesional corticosteroids (Triamcinolone acetonide, dilution of 5 to 10 mg/ml; repeated every 2–4 weeks). Intralesional therapy is used when the patient does not respond to local therapies. For moderate to severe disease (including the ones involving ocular, nasopharyngeal, or anogenital mucosa) and patient who did not respond to local therapy adequately, systemic agents should be used. Systemic corticosteroids and dapsone are used in such cases. The dose of dapsone ranges from 50 to 200 mg daily. Dapsone is shown to be effective in treating mucous membrane pemphigoid that does not respond to systemic corticosteroids. Whereas for systemic corticosteroids, 0.25 to 0.5 mg/kg of prednisolone is prescribed per day (twice-daily dosage is used during the acute stage and change to a single daily morning dose after new blister formation stops). Thereafter, the dosage of prednisolone is slowly tapered over the months in combination with topical therapy or glucocorticoid-sparing agent (e.g., dapsone, azathioprine). Patients with severe mucous membrane pemphigoid that cannot be controlled by the intervention above and would need aggressive immunosuppressive regimens and biologic therapies to control the lesions.