Oral Manifestations of Rheumatic Diseases
Oral abnormalities seen in rheumatologic disease are secondary to the pathophysiology of the disease process and result from the medications used to treat the disease. The oral manifestations of Sjögren disease can cause an exacerbation of the underlying illness and alter an individual’s quality of life. At the core of this problem is an alteration in salivary production and flow. An infiltration of lymphocytes into the salivary gland results in irreversible damage to the gland and decreased or absent saliva production.
Xerostomia, commonly known as dry mouth, results from the inability of the salivary glands to produce saliva following destruction or atrophy of the glands and is paramount in Sjögren disease. Saliva is critical to the maintenance of oral health; therefore; its absence results in mastication difficulties, increased dental caries, and oral infections. Changes in the diet to reduce acidity, avoid foods containing sugar, and increase noncaloric clear fluid irrigation may reduce the effects of a low-saliva state. Pharmacologic interventions including cevimeline or pilocarpine are somewhat effective in the stimulation of saliva production.
Decreased (hypogeusia) or disordered (dysgeusia) taste may be a consequence of xerostomia that further complicates Sjögren disease.
Systemic sclerosis is a progressive autoimmune connective tissue disease resulting in vascular damage and tissue fibrosis. Fibrosis of the salivary gland in the absence of inflammation results in the same salivary alterations seen with Sjögren syndrome. Immunosuppressive agents used to treat these diseases can result in an increase in oral infections such as candidiasis. In addition to the decreased saliva production, diminished interincisal distance, increased tooth loss, and periodontal disease are seen in progressive systemic sclerosis. Limitation of mouth opening is likely a result of periorbital tissue fibrosis, and changes in interincisal distance are complications of progressive systemic sclerosis.
Behçet syndrome is a systemic vasculitis of unknown etiology characterized by a triad of recurrent oral aphthous ulcers, genital ulcers, and uveitis. The mucocutaneous lesions are the hallmark of the disease, with oral ulcers occurring in 97% to 99% of patients. The oral lesions are visibly indistinguishable from canker sores, but they occur in multiples and recur frequently. They are small, ovid lesions with circumscribed margins and a yellow-gray base frequently surrounded by a rim of erythema. Minor aphthous ulcers are the most frequent oral lesion in Behçet syndrome; they are typically smaller, under a centimeter in diameter, and usually heal without scarring. In contrast to the major herpetiform ulcers that typically form scars following healing, the aphthous ulcers are most often seen on nonkeratinized mucosal surfaces, such as the labial and buccal mucosa and the floor of the mouth. Herpetiform ulcers are multiple and much smaller, usually 2 to 3 mm in diameter; however, they can coalesce to form a larger ulcer. They differ from herpetic ulcers by not being preceded by vesicles and by not containing viral particles.
Disseminated lupus erythematosus is a chronic inflammatory disease of unknown etiology that can affect any organ system. Oral lesions are present in about 15% of cases and consist of irregular red patches, which may become eroded, atrophic, and, later, scarred. White pinhead spots are discernible about the periphery. The sites of predilection are the cheeks, palate, and lips.