Gejala dari kekurangan riboflavin (ariboflavinosis) adalah glositis, angular cheilitis seborrheic dermatitis dan superficial vascularizing keratitis. Karakteristik dari glositis adalah warna keunguan dan atrophy dari papilla. Pada kasus ringan hingga sedang, dorsum exhibits a patchy atrophy of the lingual papillae and engorged fungiform papillae, which project as pebblelike elevations. In severe deficiency the entire dorsum is flat, with a dry and often fissured surface. Changes observe in riboflavin-deficiency mongkey include severe lesions of the gingival, periodontal tissues, and oral mucosa, including noma.

Angular cheilitis begins as an inflammation of the commissure of the lips, followed by the erosion, ulceration and fissuring. Riboflavin deficiency is not the only cause of the angular cheilitis. Loss of vertical dimension, together with drooling of saliva into the angles of the lips, may produce a condition similar to angular cheilitis. Candidiasis may developed in the commissure of debilitated persons; the lesion has been termed perleche. Supplemental riboflavin is ineffective to resolves cases of glossitis and angular cheilitis that are not caused by vitamin deficiency.

Nianic deficiency result in pellagra, which is characterize by dermatitis, gastrointestinal disturbances, neurologic and mental disturbances (dermatitis, diarrhea, dementia), glossitis, gingivitis and generalize stomatitis. This condition is rare but occasionally result from mal-absorption of alcoholism. Glossitis and stomatitis may earliest clinical sign of nianic deficiency. The gingival maybe involved in aniacinosis with or without tongue changes. The most common finding is NUG, usually in area of local irritation.

Oral manifestation of vit-B complex and nianic deficiency in experimental animal include black tongue and inflammation gingival, with destruction of gingival, periodontal ligament, and alveolar bone. Necrosis of the gingival and other oral tissue and leucopenia are terminal features of nianic deficiency in experimental animal.

Folic acid deficiency result in macrocytic anemia with megloblastic erythropoiesis, accompanied by oral changes, gastrointestinal lesion, diarrhea and intestinal mal-absorption. Folic acid deficiency animal demonstrate necrosis of the gingival, periodontal ligament, alveolar bone without inflammation. The absence of inflammation is the result of deficiency-induced granulocytopenia. In human with sprue and other folic acid deficiency states, generalize stomatitis occurs, which may be accompanied by ulcerated glossitis and cheilitis. Ulcerative stomatitis is an early indication of the toxic effect of folic acid antagonists used in the treatment of leukemia.

In a series of human studies, Vogel et al. reported a significant reduction of gingival inflammation after systemic or local use of local use local acid compared with placebo. This reduction occurred with no change in plaque accumulation. The authors also postulated that the gingival changes associated with pregnancy and oral contraception may be partly related to suboptimal levels of folic acid in the gingival. In the clinical study of pregnant women, a reduction in gingival inflammation occurred with the use of folate mouth rinse; no change was found with systemic folic acid. A relationship has also been suggested between phenytoin-induced gingival overgrowth and folic acid absorption and utilization of phenytoin. However, a more recent double-blind, randomize, placebo-controlled study of 20 institutionalized epileptic adults taking phenytion found no different in gingival condition (gingival overgrowth, health of plaque index) between the group taking 2 mg folic acid daily versus the placebo group at 4-week intervals over a 16-week period.