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.
