Patients who have received allogeneic or matched unrelated transplants are at risk of developing graft-versus-host disease (GVHD).[1,2] A related condition referred to as pseudo-GVHD is occasionally reported in autologous hematopoietic stem cell transplant recipients. GVHD can affect oral tissues and often mimics naturally occurring autoimmune diseases such as erosive lichen planus, pemphigus, scleroderma, and Sjögren syndrome. Oral GVHD has also been linked to oral precancerous and malignant lesions.
Acute GVHD can occur as early as 2 to 3 weeks posttransplant; mucosal erythema and erosion/ulceration are typical manifestations. Chronic oral GVHD changes can be recognized as early as day 70 posttransplant. The pattern and types of lesions seen in acute GVHD are also seen in chronic GVHD, but manifestations can also include raised white hyperkeratotic plaques and striae and persistent reduced salivary function. Oral symptoms of oral GVHD include xerostomia and increased sensitivity and pain with spices, alcohols, and flavoring agents (especially mint flavors in toothpaste and oral care products). Patients may also suffer from odynophagia and dysphagia due to gastrointestinal involvement. All of these symptoms of GVHD may lead to weight loss and malnutrition.
Nasopharyngeal cancer is a disease in which malignant (cancer) cells form in the tissues of the nasopharynx.
The nasopharynx is the upper part of the pharynx (throat) behind the nose. The pharynx is a hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes from the throat to the stomach). Air and food pass through the pharynx on the way to the trachea or the esophagus. The nostrils lead into the nasopharynx....
Biopsy of oral mucosa, including both surface epithelium and minor labial salivary glands, may be of value in establishing a final diagnosis.[7,8] Presence of a lymphocytic infiltrate (grade I) with epithelial cell necrosis (grade II) provides the diagnostic basis for oral GVHD. As clinical criteria for recognition of oral signs and symptoms of GVHD have become more established, dependance on the oral biopsy to diagnose oral involvement has lessened. In cases of equivocal examination findings, the biopsy can improve the recognition of oral involvement.
Topical management of mucosal lesions may include steroids, azathioprine, and/or oral psoralen and ultraviolet A (PUVA) therapy (refer to the list on Management of Oral GVHD).[4,9] While topical cyclosporin has been suggested as therapeutically beneficial, its effectiveness is less predictable than that of other treatments-which, when coupled with increased cost of care, usually decreases its utility. The use of FK506 and mycophenolate mofetil to topically treat oral GVHD remains anecdotal and of uncertain efficacy. Systemic therapy (e.g., prednisone, budesonide, cyclosporine, mycophenolate mofetil, and other immunosuppressive agents) is routinely necessary, primarily to treat the condition. Topical treatment can be used to specifically manage oral sensitivity and help heal ulcerations. Patients with clinically significant xerostomia may benefit from pilocarpine (5 mg 3 or 4 times a day) or cevimeline (10 mg 4 times a day) if native salivary gland function remains partially intact.