Oral Lesions Associated with Diet
Reina Ligeralde
Riverside Community College
Oral Lesions 1

Abstract
The aim of this paper was to identify the etiology, clinical manifestations, differential diagnoses, and treatment modalities of micronutrient deficiency as related to oral lesions identified in various research. A person’s better eating practices aid in preventative care and long-term oral health, especially in reducing the risk of oral premalignant lesions. Given the serious nature of many of the oral manifestations of dietary deficiency, maintaining a proper intake of fruits and vegetables is not only reasonable but also absolutely vital.

Oral Lesions Associated with Diet
The mouth gives clues that reflect underlying disorders elsewhere in the body. Part of that is due to the fact that nutritional habits affect the connection between the mouth and the body. Some dietary micronutrients have the potential to protect against cellular damage
(Maserejian, Giovannucci, Rosner, and Joshipura, 2006). The purpose of this paper is to present current research on the topic of oral lesions associated with diet in regards to etiology, clinical manifestations, a differential diagnosis, and treatment modalities.
Etiology
While the effects of a diet deficient in fruit and vegetable consumption are widespread, varied, and often specific to a particular vitamin being withheld, the consequences of failing to recognize the correlation between patient diet and oral health can be serious and dire.
Maserejian, Giovannucci, Rosner, Zavras, and Joshipura (2006) stated that epidemiologic studies determined that 16-40% of oral premalignant lesions (OPLs) become malignant. Lu and Wu
(2004) conducted a study that reflected the oral mucosa’s sensitivity to nutritional deficiency and concluded that in every case of glossitis, glossodynia, angular cheilitis, erythematous mucositis, oral candidiasis, recurrent oral ulcer, and burning mouth when there are no obvious causes, the dietary deficiency or anemia of chronic diseases should be suspected. Iron deficiency can contribute to impaired cellular activity, and vitamin B
12
and folate deficiency will affect DNA synthesis (Lu and Wu). Gorsky and Epstein (2002) declared that vitamin A regulates growth and cell differentiation, and its deficiency enhances carcinogenesis susceptibility.
Clinical Manifestations
The numerous oral manifestations of dietary deficiencies can be misleading and daunting.
The eligible OPLs in the study conducted by Maserejian, Giovannucci, Rosner, Zavras, et al.

(2006) included leukoplakia, erythroplakia, erythroleukoplakia, lichen planus, oral epithelial dysplasia, and oral squamous cell carcinoma. In the study handled by Lu and Wu (2004), patients presented with oral manifestations that lasted for several months to one year and included angular cheilitis, glossitis with different degrees of papillary atrophy, pale oral mucosa, oral candidiasis, recurrent aphthous stomatitis, erythematous mucositis, and burning mouth. Weinsier and Morgan (1998) discussed periodontal disease seen in scurvy due to a vitamin C deficiency
(Figure 1). Femiano et al. (2001) hold that systemic treatment of vitamin A analogues regressed or resolved many leukoplakias, but there were unwanted side effects and recurrences after therapy cessation.
A Differential Diagnosis
Part of diagnosing is attempting to narrow down the list of possible diagnoses until one emerges as the most probable. In the common dietary deficiency sign of leukoplakia, a differential diagnosis may include chronic hyperplastic candidiasis, plaque-type lichen planus, and frictional keratosis (Newland, Meiller, Wynn, and Crossley, 2005). Erythroplakias, often indicate a precancerous condition (Newland et al.). Newland et al. contains of a list of diseases that include red lesions, a few being angular cheilitis, atrophic glossitis, and fissured tongue.
Ulcerated lesions may indicate squamous cell carcinoma, a deep fungal infection, or a traumatic ulcerated granuloma (Newland et al.).
Treatment Modalities
Once dietary deficiency is determined as a root cause, applying a proper treatment plan is equally important. Femiano et al. (2001) affirmed that the objective for treatment is to identify and prevent malignant change, and the choice of treatment is based on the known nature of the disease, possible adverse effects, and expected levels of patient compliance. Management of

lesions has included waiting and watching, surgical excision, and medical therapies, with noninvasive therapies favored (Femiano et al.).
Thomas et al. (2003) found that high dosages of vitamins is part of the oral submucous fibrosis treatment modality since a combination of micronutrients (vitamins A, B complex, C, D, and E) and minerals (iron, calcium, copper, zinc, and magnesium) alleviate some oral submucous fibrosis symptoms. Maserejian, Giovannucci, Rosner, and Joshipura (2006) expressed that dietary micronutrients have potential chemopreventive features that can counteract or block reactive oxygen species and protect against cellular damage. Maserejian, Giovannucci, Rosner,
Zavras, et al. (2006) discovered that the risk of OPLs in men was significantly reduced with higher fruit consumption, especially with citrus fruits and citrus fruit juice, yet with vegetable consumption, there was no consistent association. Maserejian, Giovannucci, Rosner, and
Joshipura determined that an immediate and high consumption of dietary sources of vitamin C, not from supplements, was associated with a reduced risk of OPLs in men. Maserejian,
Giovannucci, Rosner, Zavras, et al. claimed that chemoprevention studies determined nutrient supplements commonly obtained from fruits and vegetables have increased the likelihood of leukoplakia regression.
Conclusion
While the signs and symptoms of dietary deficiency are extensive, assorted, and can often be attributed to other etiologies, the importance of not ruling out dietary deficiency as a direct cause is clear. Dietary recommendations to maintain proper fruit consumption, regardless of the presence of clinical manifestations, are appropriate for preventing oral precancer and cancer.
While an apple a day may keep the doctor away, the numerous manifestations of symptoms, lesions, and diseases are most important to keep at bay.

References
Femiano, F., Gombos, F., Scully, C., Battista, C., Belnome, G., & Esposito, V. (2001, October).
Oral leukoplakia: Open trial of topical therapy with calcipotriol compared with tretinoin.
International Journal of Oral & Maxillofacial Surgery, 30 (5), 402-406.
Gorsky, M., & Epstein, J. B. (2002, September). The effect of retinoids on premalignant oral lesions: Focus on topical therapy. Cancer, 95 (6), 1258-1264.
Lu, S., & Wu, H. (2004, December). Initial diagnosis of anemia from sore mouth and improved classification of anemias by MCV and RDW in 30 patients. Oral Surgery, Oral Medicine,
Oral Pathology, Oral Radiology & Endodontics , 98 (6), 679-685.
Maserejian, N. N., Giovannucci, E., Rosner, B., & Joshipura, K. (2006). Prospective study of vitamins C, E, and A and carotenoids and risk of oral premalignant lesions in men.
International Journal of Cancer , 120 , 970-977.
Maserejian, N. N., Giovannucci, E., Rosner, B., Zavras, A., & Joshipura, K. (2006, July).
Prospective study of fruits and vegetables and risk of oral premalignant lesions in men.
American Journal of Epidemiology , 164 (6), 556-566.
Newland, J. R., Meiller, T. F., Wynn, R. L., & Crossley, H. L. (2005). Oral soft tissue diseases:
A reference manual for diagnosis & management (3 rd ed.). Hudson, OH: Lexi-Comp, Inc.
Thomas, G., Hashibe, M., Jacob, B. J., Ramadas, K., Mathew, B., Sankaranarayanan, R., et al.
(2003). Risk factors for multiple oral premalignant lesions. International Journal of
Cancer , 107 , 285-291.
Weinsier, R. L., & Morgan, S. L. (1998). Fundamentals of clinical nutrition (2 nd
ed.). St. Louis,
MO: Mosby Year Book.

Appendix
Figure 1.
Periodontal disease seen in scurvy due to a vitamin C deficiency.
From Weinsier, R. L., & Morgan, S. L. (1998). Fundamentals of clinical nutrition (2 nd ed.). St.
Louis, MO: Mosby Year Book.