COMMON ORAL LESIONS
Clinicians unfamiliar with the mouth frequently regard the diagnosis of oral lesions as a daunting task. In reality, though, the approach to oral diagnostic problems is no different than that for any other tissue or organ. It begins with a full and accurate description of the detected “abnormality”, followed by a gathering of relevant clinical and historical data. In most instances, clinical findings alone comprise sufficient data upon which a diagnosis may be rendered. However, most complicated problems often mandate generation of a differential diagnosis, preceded or followed by acquisition of additional clinical, radiographic, or laboratory information. Ultimately, a definitive diagnosis is established. Oral mucosal tissue is subject to the same spectrum of pathological processes as may be encountered in other anatomic sites. These processes may be broadly classified as:
1. Developmental (congenital, genetic, environmental) disturbances
2. Inflammatory or reactive
4. Neoplastic (benign, malignant)
5. Oral manifestations of systemic disease.
In the approach to oral diagnostic challenges, three basic maxims should be borne in mind:
• Common things occur commonly
This is a key principle in that the majority of oral lesions encountered in daily practice represent benign reactions to low-grade, usually local inflammatory stimuli. Such etiologic agents are readily identified, in most instances, through history-taking and thorough examination. Other common findings include innocuous developmental variations of normal anatomy. Clinicians should become familiar with the range of common developmental anomalies and recognize them as such, in order to avoid unnecessary treatment. Thus, the second principle:
• Individual lesions or diseases possess distinguishing, classic features
In particular, the location (and, if relevant, distribution), surface features, size, texture, and borders of the lesions, along with the history, symptoms, and data from diagnostic tests (if necessary or available) comprise the essential elements of differential diagnosis. Nonetheless:
• Things that look alike are not necessarily the same
Superficial similarities among diverse conditions may lead to diagnostic confusion unless an organized and discriminating approach is taken. The clinician must adopt a systematic, thorough, and logical method of diagnostic data-gathering and processing in order to avoid jumping to conclusions and thus risking diagnostic errors. First and foremost in this scheme is the performance of a well organized proper oral examination. It is well to note that a wealth of useful diagnostic information is derived from the oral examination alone.
The Oral Examination
No thorough physical examination is complete without a proper examination of the oral cavity. Yet, even experienced physicians are sometimes reluctant to look in the mouth and fail to include oral examination as a routine component of periodic physical examinations. A good oral examination alone can generate most of the information about the lesions.
VARIATIONS OF NORMAL ANATOMY
The trick to detecting common benign anatomic variations is to be aware of their possibility and their classic clinical features.
• Torus (tori)
These are developmental exostoses (benign bony growths projecting outward from the surface of a bone, characteristically capped by cartilage) that arise early in life and are generally detected by the time the patient has reached young adulthood. They present as either a raised sessile mass or nodule on the midline of the hard palate (torus palatinus) or as bilaterally symmetrical nodules on the lingual aspect of the mandible in the premolar area (mandibular tori). Tori are characterized by smooth, intact surfaces, and may be uni- or multilobar. Tori are bony, hard and painless and may continue to increase in size until the individual’s full growth potential is realized.
• Fordyce granules
These are ectopic sebaceous glands, typically found on the buccal mucosa, vermilion border of the lips, and labial commissures. They appear as small, white-yellow, smooth-surfaced, painless papules arranged in clusters.
• Linea alba
Although not strictly a developmental anomaly, line alba is usually evident early in life, after the teeth have emerged. Linea alba appears as a white, non-wipeable “line” that bisects the buccal mucosa horizontally, at the level of the interocclusal plane, and is often bilateral. The condition is caused by the low-grade, chronic, normal friction of the teeth against the buccal mucosa, which stimulates a benign hyperplastic (protective) epithelial response. Characteristically a painless, slightly raised, keratotic (hence, nonewipeable) plaque, linea alba extends backward from the labial commissure to the posterior buccal mucosa.
COMMON FINDINGS OF THE TONGUE
• Benign migratory glossitis (geographic tongue)
This interesting, common condition is characterized by polymorphous changes in the appearance of the tongue’s surface over time. It typically involves the dorsal and lateral aspects of the tongue with migratory serpiginous (having a wavy or much indented margin) or annular-appearing white keratotic plaques and papules encircling relatively atrophic mucosa, which, in turn, is surrounded by annular erythema. Affected surfaces demonstrate relative hyperpapillation alternating with atrophy of filiform papillae (The microscopic appearance of geographic tongue resembles that of cutaneous psoriasis. However, these respective conditions are apparently unrelated.) Patients occasionally experience mild discomfort or sensitivity in predominantly atrophic-type lesions. Rarely, similar lesions may occur on the ventral surface of the tongue,or on other intraoral mucosal surfaces; these lesions are termed “erythema migrans”.
• Fissured (“scrotal”) tongue
This anatomic variation consists of permanent developmental furrows and clefts usually involving dorsal and lateral tongue surfaces, often associated with benign migratory glossitis. Patients may voice transient complaints of mild discomfort related to entrapment or accumulation of superficial debris within surface fissures.
• Median rhomboid glossitis
This term describes a fairly well-delineated atrophic, slightly lobulated, often fissured, erythematous patch of mucosa on the dorsal tongue surface, roughly at the junction of the middle and posterior thirds. This lesion is often asymptomatic, but like geographic or fissured tongue, it may be associated with mild discomfort on occasion.
• Black or “hairy” tongue
Unusually elongated filiform papillae are responsible for the “hairy” lingual appearance, which is most prominent on the dorsal mid-posterior third of tongue. The papillae may appear brown or black due to extrinsic staining by foods, tobacco, or chromogenic oral microflora. The condition may be pronounced in instances of xerostomia, in conjunction with or following antibiotic therapy, or as a consequence of the excessive use of undiluted proprietary antibacterial mouth rinses.
• Lingual tonsils
Typically found at the posterior-lateral aspect of the tongue, these aggregates of lymphoid tissue comprise a portion of Waldeyer’s ring and are detected by extending and turning the tongue for visual inspection. They appear as smooth-surfaced papillary projections with deep crypts, sometimes plugged with white or yellow debris. Although lingual tonsils are usually orange-pink in color, erythema may accompany local irritation or oropharyngeal infection. Other foci in which ectopic lymphoid tissue may be found include the anterior floor of the mouth and the soft palate.
• Circumvallate (‘vallate”) papillae
These are actually normal structures found on the posterior third of the dorsal tongue surface. Characteristically distributed in a linear, chevron-like formation, there are usually about 12 “vallate” papillae. They appear as large, round, evenly spaced, reddish pink papules surrounded by normal filiform papillae.
Exuberant Reactive Hyperplasias
Exuberant reactive hyperplastic responses to low-grade chronic irritation or injury comprise the largest group of mucosal lesions encountered during routine oral examination. Such lesions are usually painless and exophytic and arise in areas impinged on or aggravated by injurious agents. Hyperplastic responses are by nature benign, with no inherent predilection to transform to malignancy. Unlike benign neoplasms, reactive hyperplastic lesions develop in response to tissue stimulation by persistent, frequently identifiable causative agents. Characteristically, if the stimulus is removed, then the hyperplastic reaction ceases to progress and, in some instances, may actually regress or resolve. Typical sources of irritation or trauma associated with oral mucosal hyperplastic responses include cheek biting, sharp or fractured teeth, poorly contoured dental restorations, ill fitting or broken removable denture prostheses, broken partial denture clasps, orthodontic appliances, bacterial plaque, and calculus (tartar).
• Fibrous hyperplasia (traumatic fibroma)
A classic, common example of reactive hyperplasia, traumatic fibroma presents as a smooth-surfaced sessile or pedunculated mass of fibrous connective tissue arising on an injury-prone or chronically traumatized site. On palpation, it is soft to firm or rubbery and well-defined though not encapsulated. The surface of the fibroma may become ulcerated or exhibit a white, rough (keratotic) appearance if constantly subjected to friction.
• Papillary hyperplasia
This condition is classically found on soft tissue surfaces covered by ill-fitting removable denture prosthesis or occlusal appliances. It corresponds to the shape and extent of the irritating denture base. Often, there is a history of constant or prolonged contact of the denture base with underlying mucosa (i.e. without daily removal for cleansing). The lesion is red, with a fine pebbly or fissured surface; the surface coincides precisely with the tissue contact of the offending denture base. In most instances, papillary hyperplasia is painless; however, there may be superimposed, mildly symptomatic candididasis.
• Epulis fissuratum
This disorder appears as extensive folded or corrugated, bulbous, redundant soft tissue in the maxillary or mandibular buccal and/or labial or mandibular lingual vestibules. The borders of the lesion correspond to the flanges (external edges) of ill-fitting, unstable, removable dentures. Deep fissures and ulcers may enfold the denture flange. Epulis fissuratum is painless; the lesions are usually red or the color of normal mucosa.
• Pyogenic granuloma and peripheral giant cell granuloma (lesions of exuberant
inflammatory vascular hyperplasia)
Pyogenic granuloma assumes a red, exophytic, sessile or pedunculated raspberry-like appearance, while peripheral giant cell granuloma usually appears blue-red or brown, with a smooth surface. The most common intraoral location of both is on attached gingiva or the interdental papilla of a periodontally compromised tooth. Either lesion may exhibit ulceration and a tendency to bleed upon provocation. Pyogenic granuloma often arises on the gingiva during pregnancy as an exaggerated response to common local inflammatory stimuli, such a plaque and calculus (“pregnancy tumor”) , or during adolescence in association with puberty-related gingivitis.
• Mucocele (mucous escape or retention “cyst”)
Mucoceles develop secondary to either traumatic rupture of a minor salivary gland duct or lobule, which permits free mucin extravasation into the stroma, or as a result of obstruction within the ductal system, eventuating in mucus retention and, hence, ductal distention and hypertrophy, inflammatory atrophy, or fibrosis of the glandular parenchyma. These lesions most often arise in the submucosa of the lower lip (a site easily injured by inadvertent biting) or sublingually, in the floor of the mouth. They are dome-shaped, fluctuant, often bluish swellings that are themselves subject to repeated trauma and may become secondarily ulcerated. Usually there is a minor degree of discomfort. Small mucoceles frequently resolve spontaneously within several weeks’ time. Larger lesions involving extensive mucin spillage, secondary trauma, and fibrosis often require surgical excision.
Complete disruptions of the oral surface are common. They may be attributed to a variety of factors, intrinsic or extrinsic, which span the spectrum of pathologic processes. When an ulcer is detected, a diagnostically meaningful description must include the following:
1. Location (and, if relevant, the distribution) of the lesion
2. Clinical appearance (symmetry, borders, depth, presence of necrosis, erythema) and texture (firm, soft, indurated)
3. Symptoms (painful, painless, paresthesia)
4. Pertinent history (trauma, recurrence, tobacco use, alcohol use)
In general, the majority of intraoral ulcers are benign in nature and typically resolve within 10 or 14 days (unless they are extremely wide, deep, secondarily infected, or repeatedly traumatized, or the patient’s ability to heal is systemically compromised). Any ulcer that persists for more than 2 weeks, especially if there is a positive history of smoking or alcohol use, and if the lesion is located on a known cancer-prone intraoral site (lateral, ventral, and posterior surfaces of the tongue, floor of the mouth, retromolar trigone- soft palate - tonsillar pillar complex) must be considered suspicious, and malignancy or other unusual disease must be ruled out by tissue biopsy. The differential diagnostic considerations for oral ulcers are:
• Traumatic ulcers
Trauma is by far the most common cause of oral ulceration. On questioning, patients may recount a history of injury preceding the lesion. Traumatic ulcers are typically found on trauma-prone sites which include the labial and buccal mucosae, gingivae, alveolar mucosa, the hard palate, and the anterior dorsal and anterolateral tongue surfaces. The patient is usually aware of lesional onset and often will report associated discomfort or pain. When an ulcer is detected on a relatively protected area, like the floor of the mouth or the ventral or postero-lateral surface of the tongue, particularly if there is no reported history of trauma, carcinoma must be considered as a serious diagnostic possibility. Ulceration, induration, lack of pain, chronicity, and red and white, velvety, poorly defined surface changes strongly suggest malignancy and mandate biopsy.
• Recurrent aphthous ulcers (RAU, aphthous stomatitis, “cancer sores”)
This extremely common ulcerative condition affects a fairly large segment of the general population. It is estimated that from 20 - 60 % of individuals between childhood and roughly age 50 have experienced aphthous ulcers. The condition is characterized by painful, recurrent ulcers that arise on moveable, nonkeratinizing oral mucosal surfaces (with the exception of attached gingiva and hard palate) and the dorsal aspect of the tongue. The lesions are slightly raised, round, symmetric ulcers with white-yellow necrotic centers surrounded by an erythematous halo. Aphthae frequently occur in clusters “herpetiform” aphthae) and coalesce, resulting in large surface lesions. Individual ulcers range in diameter from 0.5 cm or less (minor aphthous ulcers to larger lesions (major aphthous ulcers, periodenitis mucosa necrotica recurrens, PMNAR), Sutton’s aphthae. Although the precise etiology remains unclear, evidence largely favors both cellular and humoral autoimmunity, rather than infection or trauma. Unlike the ulcers associated with herpes virus-induced lesions, aphthous ulcers are not preceded by vesicles. Minor aphthae usually run their natural course within approximately 2 weeks time. Major aphthae, however, tend to run a protracted course, take several additional weeks to resolve, and often heal with scarring. Regardless of size, aphthous ulcers are highly symptomatic. In some patients, overlapping episodes may compromise speech, mastication, and the ability to eat comfortably for weeks or months at a time.
• Herpetic ulcers
Mucocutaneous lesions of primary or reactivated infection with herpes virus simplex (predominately HSV-1 in oral lesions) or varicella zoster are vesicular. Intraorally, the vesicles rupture readily leaving painful, coalescing ulcerations surrounded by edema and erythema. In primary herpetic gingivostomatitis, all intraoral mucosal surfaces and the labial skin and vermilion borders may be involved with vesiculoulcerative lesions. A protean manifestation is concomitant acute, generalized, extremely painful gingivitis.
Constitutional signs of systemic infection (malaise, low-grade fever, lymphadenopathy) are notable and precede the onset of actual oral lesions. Severe discomfort frequently impairs the ability to drink or eat. In young children (classic primary herpes patients) this may be problematic, for the risk of dehydration is considerable. Unless there is underlying
immunosuppression, in otherwise healthy individuals the primary disease resolves within
about 2 weeks’ time. Reactivated (“recurrent”) herpes simplex lesions are also vesicular but occur relatively infrequently on oral mucosa (both features in contrast to those of aphthous ulcers). Rather, they more typically arise on the skin and vermilion of the lips (“cold sores”). However, although less common, when they do occur, recurrent intraoral herpetic lesions are localized, vesicular, croplike, painful eruptions that readily ulcerate. They affect keratinizing, “bound down” mucosa (i.e. the hard palate and attached gingiva) and are often preceded by trauma, such as dental or intraoral surgical procedures, or other stressful circumstances.
Primary infection with varicella zoster virus (varicella, “chickenpox”) may include relatively minor oral mucosal involvement with isolated, scattered vesicles and ulcers. However, in unusual instances of reactivated infection (herpes zoster, “shingles”) involving all or all branches of the trigeminal nerve, there may be striking peri- and intraoral involvement with unilateral, massive crops of coalescing vesicles and ulcers distributed linearly. The lesions are generally preceded and accompanied by edema and severe pain or paresthesia (zoster-related neuralgia), which may persist for long periods following resolution of the clinical vesiculoulcerative changes.
White Lesions: General Diagnostic Considerations
The oral mucosa appears white when the reflection of the underlying vascular bed is insulated from the observer’s eye by (1) the presence of surface debris, (2) diminished submucosal vascularity or an increase in stromal thickness, or (3) increased keratinization or width of the surface epithelium. It is often possible to distinguish among these phenomena clinically. Debris is usually “wipeable” (i.e. it can be swept or scraped away using gauze or a wooden tongue blade). White (or pale) lesions caused by decreased vascularity typically are smooth-surfaced and often feel firm on palpation. Keratotic (epithelial) white lesions are characteristically nonwipeable and generally show a roughened surface. The latter lesions comprise the entire spectrum of oral stratified squamous epithelial responses to myriad stimuli, ranging from benign physical irritants
to chemical carcinogens. Histologically, epithelial white lesions include various expressions of reactive hyperkeratosis and other benign conditions (i.e. lichen planus, lupus-related keratoses, verruca vulgaris, squamous papillomas), lesions of an epithelial maturation disturbance like atypia (which may represent an unusual reaction to irritation or emerging dysplasia), dysplasia, or carcinoma in situ (both of which are precancerous) and frank, squamous cell (epidermoid) carcinoma.
• Benign reactive epithelial hyperplasia (hyperkeratosis)
By far, the majority of oral keratotic lesions represent exuberant, reactive hyperkeratoses or benign epithelial hyperplastic responses secondary to irritation. Classically, such lesions are found on trauma-prone sites or in conjunction with an obvious low-grade irritant. They sometimes may regress following removal of the alleged irritant. In contrast, a keratotic white lesion whose presence cannot be explained as a result of chronic irritation or as a manifestation of lichen planus or other benign conditions (especially in a patient with a concomitant carcinogen history) is considered to be “leukoplakia”. Specific diagnosis for such lesions is required.
The term “leukoplakia”, often used incorrectly as a generic term for any white oral lesion, is actually a provisional clinical designation for a keratotic white mucosal lesion that cannot be scraped away, and for which a diagnosis cannot be determined clinically. Hence, wipeable white lesions indicative of surface debris, pseudomembranous candidiasis or necrosis, avascular submucosal processes, due to clinically obvious local physical irritants (namely, benign reactive hyperkeratoses, such as linea alba) are not considered leukoplakias. On the other hand, white keratotic lesions that are not preceded by a history of trauma, those on “protected mucosal sites (i.e. sites where trauma is unlikely to have occurred), and, in particular, those white lesions on known cancer-prone surfaces (especially in tobacco and/or alcohol users) do constitute leukoplakias. Diagnosis of such lesions requires tissue biopsy and microscopic evaluation. Dysplasia in a leukoplakic oral lesion must be regarded as a premalignant change. Exfoliative cytology is not an accurate or reliable means of establishing a diagnosis for keratotic white oral lesions.
• Hairy leukoplakias
Biopsy is particularly helpful in cases of suspected “hairy leukoplakia”. this exclusively oral entity, first described in 1984 in association with HIV infection (and subsequently noted in conjunction with several other non-HIV-related conditions involving immunosuppression), is by no means common. Nonetheless, its diagnostic specificity and prognostic significance, especially with regard to HIV infection, render it important for differential diagnostic consideration. Hairy leukoplakia has highly suggestive histological features on conventional microscopy; these include hairlike parakeratosis, koilocytic-like changes in superficial epithelial cells, acanthosis with a normal stratification pattern, and absence of stromal inflammation. Diagnosis is confirmed through disclosure of the presence of Epstein-Barr virus (EBV) in tissue or cells from a suspected lesion. the lesions of hairy leukoplakia are uniquely ascribed to opportunistic infection with EBV secondary to cell-mediated immune depletion. Thus, hairy leukoplakia may be the very first clinical sign of emerging immune suppression in an otherwise asymptomatic, known HIV-antibody-positive individual. Or, it may alert suspicion of possible HIV infection in an individual with unknown HIV status, and thus warrant HIV testing. Because it is painless, hairy leukoplakia is usually discovered as an incidental finding on oral examination. the lesions are white, hairlike, vertically oriented plaques with a preference for the lateral and dorsal surfaces of the tongue. They occur bilaterally and are nonwipeable. These lesions, despite their location, harbor no inherent predisposition for malignant transformation.