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.
