2. Two Approaches to the Diagnosis of Lesions of the Oral Mucosa

by William M. Carpenter, DDS, MS; Peter L. Jacobsen, PhD, DDS;
and Lewis R. Eversole, DDS, MS, MA

Abstract: This article describes two approaches to the classification of oral mucosal lesions. One is based on the etiopathogenesis of the lesion and the second on the clinical appearance. These two approaches are compared and contrasted, and their integration is described. Combining these two classification schemas allows an excellent understanding of the various lesions so than an expeditious and correct diagnosis can result. Appropriate management and treatment can then follow.

The establishment of a differential diagnosis for lesions of the oral mucosa is often problematic. This problem relates to the large number of lesions that may affect a patient and the fact that many occur only rarely. A systematic approach to nosology is crucial. Classically, oral pathology has been taught following the etiopathogenic approach. This approach, as most commonly used in general pathology, considers the basic disease processes or mechanism and the body’s response, along with the etiologic factors involved. To approach the classification of disease from this viewpoint is efficacious and allows for effective management decisions. Once the etiology is understood, the treatment can be instituted.

General pathology texts are usually divided into chapters on inflammation and immunology, neoplasia, genetic and developmental disorders, and diseases of the various organ systems (e.g., cardiovascular, gastrointestinal, and liver).^l-3 Oral pathology texts traditionally follow this same approach and include other categories specifically relating to oral lesions, such as odontogenic cysts and tumors, and salivary glands.^4-9

The general etiopathogenic categories can be condensed into four major areas that can be best remembered by the acronym MIND (M = metabolic, I = inflammation, N = neoplastic, D = developmental diseases). This mnemonic reminds the student and practitioner to use his or her MIND to arrive at a correct diagnosis. This approach is condensed and simplistic but provides a good starting point for cerebration and further amplification of this classification¹⁰. The MIND classification system can then be expanded.

Etiopathogenic Classifications

The “MIND” Paradigm

• Metabolic is a group of oral lesions occurring as a result of various systemic diseases. These diseases may be of either a hormonal or a nutritional nature. The oral cavity may be affected directly, as occurs in Addison’s disease, which leads to changes in oral pigmentations of the tongue secondary to hypovitaminosis B complex.
• Inflammatory lesions are the most common type and have many subcategories. Classically, these lesions may manifest the cardinal signs of inflammation: redness, swelling, heat, and pain. The subcategories include trauma, reactive, infectious diseases (viral, bacterial, fungal), and the immunologic lesions (allergic reactions, autoimmune and immunodeficiency diseases).
• Neoplastic lesions may represent a benign, premalignant or malignant process and therefore cover a large group of both epithelial and mesenchymal tissues that are growing uncontrollably.
• Developmental may be of a genetic (heritable) or acquired nature. Either of these may be of a congenital nature (present at birth) or exhibit an oral manifestation as the individual matures and develops. These maldevelopments may manifest as a number of clinical presentations, e.g., clefts and cysts.

Although most but not all areas of etiopathogenesis are included here, this simplified system will allow a quick and easy review by the practitioner as the four major areas are considered. This system lends itself well to cognitive retention because one learns mechanisms of disease that are mentally imprinted as pictures, that occur as links. Learning the underlying basis of disease this way involves cellular processes in conceptional learning and is far more cognitively retentive than memorizing long lists.

Table 1. The Mind Classification System Metabolic (systemic) Hormonal Nutritional Inflammatory Trauma Reactive Infectious Bacterial Fungal Viral Immunologic Hypersensitivity Endogenous allergen (autoimmune) Exogenous allergen Immunodeficiency Neoplasia Benign Premalignant Malignant Developmental Acquired Genetic (heritable)

Procurement of Data

The practitioner must then be able to recall the signs and symptoms of the various categories of disease as a pertinent medical history and physical examination are performed. Age, sex, race, and gender may be important factors in data collection. The medical history would include questions regarding the chief complaint, history of present illness (lesion), past medical history, social history, and family history. The lesional history should include duration, pain, periodicity, treatment, and location. As this data is collected and tabulated, various diseases will be considered and deductive reasoning employed.

Physical examination of the head, neck, oral cavity, and particularly of the lesion is then carried out, and several aspects of the lesion must be taken into consideration. The visual assessment and palpation of the lesion of the oral mucosa would include an evaluation of any surface changes in the normal color or texture, along with any alterations in the normal morphology, including swellings, blisters, and/or surface ulcerations. These clinical categories are seen in Table 2. Several oral pathology textbooks now include a clinical outline section.

Clinical Classification

Setting aside the etiopathogenesis approach to disease classification for a moment, one must consider more practical clinical classification schemes. The categories that follow represent the various tissue alterations or lesions that clinicians observe.

• White lesions of the oral mucosa appear so because they represent 1) a pseudomembrane (intrinsic or extrinsic); 2) a thickening of one or more thickened layers of the epithelium (stratum corneum or spinosum); 3) subepithelial inflammatory cell infiltrate; or 4) dense fibrosis. White lesions frequently occur as a result of trauma that can cause either an ulceration or a hyperkeratosis depending on the chronicity of the process. A good clinical test is to determine the wipeability of the white area. Other important factors include pain, distribution, and duration of the lesion. Social habits, including tobacco and alcohol use, should also be ascertained.
• Red lesions may represent erythema (increased vascularity) or a thinning of the layers of the epithelium (atrophy). Diascopy or blanching of the lesions may help to differentiate intravascular from extravascular blood. These lesions may also represent inflammation (vasodilation) but may be the earliest sign of an epithelial premalignant lesion (dysplasia).
• Pigmentation that presents as black, brown, or blue may represent intrinsic or extrinsic pigments. The common oral mucosal pigmentations are extrinsic pigments due to amalgam filling material or root canal sealers. These generally are gray to black. Intrinsic pigments are melanin and blood products (hemoglobin and hemosiderin). Melanin is usually brown but may occasionally appear blue or black. Hemoglobin is found in red blood cells and is usually blue to purple. Diascopy may also be helpful with these lesions.
• Ulcerations occur as a result of a loss of the epithelium and may represent a primary lesion or occur secondary to rupture of a pre-existing lesion (vesiculobullous lesion). Other important distinguishing characteristics of ulcerations are whether they are focal or multifocal, the recurrence pattern, and the location.
• Vesiculobullous lesions begin as blisters of varying sizes. Vesicles are less than 5 mm in diameter and are usually of a viral or allergic nature. Viral diseases are associated with a fever in the primary infection and patients are afebrile during the recurrent episodes. Bullae are larger than 5 mm and usually represent one of the mucocutaneous diseases that are of an allergic or autoimmune nature. Intact blisters of oral mucosa are rarely seen. Most oral bullae appear as diffuse or multifocal desquamations.
• Swellings are the final group of lesions and range from a smooth to roughened surface (papillary, verrucous, papular, or polypoid nature). The roughened surface lesions usually represent proliferations of the surface epithelium and are frequently of viral origin. The smooth surface lesions are due to a submucosal enlargement. Important parameters are the location, consistency, and presence or absence of pain. Certain swellings have a propensity for a particular certain anatomic site and all of the etiopathogenic factors from the MIND classification may present as swellings in this category. Examples of these are:
  • Metabolic - amyloidosis
  • Inflammatory - parulis (gum boil)
  • Neoplastic - adenoma
  • Developmental - exostosis (torus)

The clinical classification approach to differential diagnosis of oral soft tissue lesions can be correlated with histopathologic findings. As discussed for each clinical group of lesions, this correlation will allow the clinician to visualize and understand what is occur clinician integrates the clinical and etiopathogenic classification schemas, the various lesions become mentally manageable. Therefore a combination of these two approaches, if performed correctly, will lead to a limited differential or working diagnosis (Figure 1).

 In general, the first step is to place the disease in one of the clinical appearance or lesional categories and then entertain thoughts as to which diseases present with such an appearance, while subcategorizing them as metabolic, inflammatory, neoplastic, or developmental. It may be necessary at this time to perform a supplementary diagnostic test to better delineate the definitive diagnosis. This test may be microbiological, serological, biochemical, imaging modalities, or therapeutic trial or may include a tissue sampling procedure (biopsy). Often a biopsy is necessary to establish the final diagnosis. However, occasionally a biopsy is unnecessary such as for a positive radiographic finding in an amalgam tattoo, a positive candidal microbiological test, or a positive serologic test for syphilis in a mucous patch. Once the definitive diagnosis has been established, the clinician can then administer the proper treatment. The final consideration is follow-up and re-assessment. This is a very important step that allows for there-establishment of normalcy and ensures that a correct diagnosis was achieved and proper treatment rendered.

Table 2. Lesions of the Oral Mucosa (Clinical Classification) White Red Pigmented Brown Blue Black Ulcerative Vesiculobullous Swellings Smooth surface Papillary, popular and multiple polypoid

Authors

William M. Carpenter, DDS, MS, is professor and chairman in the Depart- ments of Pathology and Medicine at the University of the Pacific School of Dentistry.

Peter L. Jacobsen, PhD, DDS, is director of the Oral Medicine Clinic at the UOP School of Dentistry.

Lewis Roy Eversole, DDS, MSD, MA, is a professor of pathology and medicine at the UOP School of Dentistry and a head and neck pathology consultant to Pathology Consultants of New Mexico.

References

1. Chandrasoma P, Taylor CR, Concise Pathology, 2nd ed. Appleton & Lange, Norwalk, Conn, 1995.
2. McPhee SJ, Lingappa VR, et al, Pathaphysiology of Disease: An Introduction to Clinical Medicine, 1st ed. Appleton & Lange, Stamford, Conn, 1995.
3. Robbins, Pathologic Basis of Disease, 5th ed, WB Sounders Co, Philadelphia, 1994.
4. Cawson RA, Odell EW, Essentials of Oral Pathology and Oral Medicine, 6th ed. Churchill Livingstone, Edinburgh, 1998.
5. Gorlin RJ, Goldman HM. Thomas Oral Pathology, 6th ed. CV Mosby Co, St Louis, 2: 1970.
6. Shafer WG, Hine MK, Levy BM, A Textbook of Oral Pathology, 3rd ed. WB Sounders Co, Philadelphia, 1974.
7. Sapp PJ, Eversole LR, Wysocki GP, Contemporary Oral and Maxillofacial Pathology. Mosby-Year Book Inc, St Louis, 1997.
8. Thomas KH, Goldman HM, Oral Pathology, 5th ed. CV Mosby Co, St Louis, 1960.
9. Tiecke RW, Oral Pathology. McGraw-Hill Co, New York, 1965.
10. Jacobsen PL, Carpenter WM, How then shall we think? About oral pathology using your M.I.N.D. Dentistry Today in press.
11. Bhaskar SN, Synopsis of Oral Pathology, 7th ed. CV Mosby Co, St. Louis, 1987.
12. Neville BW, Damm DD, et al, Oral & Maxillofacial Pathology. WB Sounders Co, Philadelphia, 1995.
13. Regezi AR, Sciubba J, Oral Pathology Clinical-Pathologic Correlations, 3rd ed. WB Sounders Co, Philadelphia 1998.
14. Wood NK, Goaz PW, Differential Diagnosis of Oral and Maxillofacial Lesions, 5th ed. MosbyYear Book Inc, St Louis, 1997.
15. Eversole LR, Clinical Outline of Oral Pathology: Diagnosis and Treatment, 2nd ed. Lea & Febiger, Philadelphia, 1984.

Copyright CDA Journal. Vol. 27. No. 8. August 1999
Reprinted with permission