Two Approaches to the Diagnosis of Lesions of the Oral Mucosa
William M. Carpenter, DDS, MS; Peter L. Jacobsen, PhD, DDS; and Lewis R. Eversole, DDS, MS, MADr. Carpenter and Sol Silverman, DDS, will present "Oral Pathology and Medicine Update" at the CDA Scientific Session in San Francisco. Their presentation will be from 10 a.m. to 5 p.m. on Friday, Sept. 17, in Room 103 of the Moscone Convention Center.
Copyright 1999 Journal of the California Dental Association.
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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.
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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).1-3 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
classification.10 The MIND classification system can then be expanded
(Table 1).
Table 1.The MIND Classification System |
|
Metabolic (systemic) |
A. Hormonal |
B. Nutritional |
|
Inflammatory |
A. Trauma |
B. Reactive |
C. Infectious |
1. Bacterial |
2. Fungal |
3. Viral |
D. Immunologic |
1. Hypersensitivity |
a. Endogenous allergen (autoimmune) |
b. Exogenous allergen |
2. Immunodeficiency |
|
Neoplasia |
A. Benign |
B. Premalignant |
C. Malignant |
|
Developmental |
A. Acquired |
B. Genetic (heritable) |
Etiopathogenic Classification
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.
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.11-15
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Table 2.
Lesions of the Oral Mucosa |
|
1. White |
|
|
|
3. Pigmented |
A. Brown |
B. Blue |
C. Black |
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4. Ulcerative |
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5. Vesiculobullous |
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6. Swellings |
A. Smooth surface |
B. Papillary, papular and multiple polypoid |
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)
 Figure 1. The clinical and etiopathogenic classification schemas can be combined to lead to a limited differential or working diagnosis. |
Authors/
William M. Carpenter, DDS, MS, is professor and chairman in the Departments 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/
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To request a printed copy of this article, please contact/William M. Carpenter, DDS, MS, 2155 Webster St., Suite 400, San Francisco, CA 94115.
