Oral Manifestations in Nutritional Deficiencies
The oral mucous membranes are exquisitely sensitive to nutritional deprivation; however, pathognomonic findings are seen in very few deficiency states. Clinically significant malnutrition has multiple causes, including dietary insufficiency, decreased absorption, and increased elimination or metabolic demand. Ariboflavinosis, as a clinical syndrome, presents with specific features that can be attributed to riboflavin deficiency.
The oral lesions in ariboflavinosis begin with pallor of the labial mucosa and the skin at the corner of the mouth, followed by maceration of the epithelium and the formation of fissures and crusts. The angular and vertical fissures and superficial ulcerations are termed cheilosis; they are seen at the corners of the lips and along the lips and mucous membranes. Loss of differentiation along the mucocutaneous border is typically seen in a deficiency of riboflavin. The association of conjunctivitis, corneal opacities and increased vascularization, photophobia and signs of dermatitis in the nasolabial regions, together with cheilosis, may be considered pathognomonic for ariboflavinosis, particularly so if signs of glossitis can be observed simultaneously. Although not a universal finding, the most striking features on the tongue are a purplish magenta discoloration and a pebbly appearance resulting from early edematous enlargement of the fungiform papillae. Atrophy of the filiform papillae is not limited to riboflavin deficiency but rather may extend to B complex deficiency. Ariboflavinosis is not restricted to tongue manifestations; the gingivae may be colored more deeply red than is normally seen in nondeficient states. Deficiencies in niacin and pyridoxine can result in a scalding sensation of the tongue, which is followed by reddening and hypertrophy of filiform papillae; it can ultimately produce a bald lingual surface that is beefy red in color.
Pellagra is presently thought to be a disease caused by lack of several vitamins of the B group but primarily of nicotinic acid and the essential amino acid tryptophan. Soreness of the tongue and mouth may be one of the initial signs, but the fully developed changes of pellagrous tongue appear at a later stage. The papillae of the lateral margins and tip are first affected, and the changes progress to involve the entire tongue and all mucous membranes. The color at this time is scarlet red. Increased soreness and salivation are accompanied by edema, with indentations from the teeth and, often, ulcerations. Later, the tongue becomes bald and more beefy red in color. The papillary changes involve, first, hypertrophy, flattening, and coalescence (producing furrows) and then atrophy.
Rose-colored gingivae complicated by frequent bleeding is one of the earliest signs of scurvy, or vitamin C (ascorbic acid) deficiency. In later stages, the gingival papillae become enlarged, bluish red, and spongy; the teeth become loose; salivation increases; and an oral fetor appears. The bleeding tendency of the gingivae is part of a generally increased capillary fragility, which may be ascertained by producing the Rumpel-Leede phenomenon (appearance of petechiae in an area following the application of vascular constriction).
Celiac sprue is characterized by small bowel malabsorption due to villous atrophy resulting from an antigenic reaction to ingesting wheat gluten or similar grains, which can produce oral symptoms. A burning of the oral mucosa and tongue appears after episodes of diarrhea. Numerous vesicles may form; a scarlet color and aphthous lesions and fissures make a “sprue tongue” closely resemble a pellagra tongue. Iron deficiency anemia results from poor absorption of iron; reduced iron stores, most often due to chronic blood loss and poor dietary intake of iro , can cause pallor of the lips and mucous membranes.