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Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023
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Image courtesy of Medscape.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
The above image shows exposed, necrotic bone in the left anterior maxilla of a patient with medication-related osteonecrosis of the jaws (MRONJ).
A systematic evaluation of the oral hard and soft tissues can provide clinicians with much information regarding a patient's health. Although the primary objective of an oral examination is to distinguish between health and disease, a comprehensive oral examination—in conjunction with a thorough medical and dental history—can also provide valuable insight into a patient's overall health and well-being.[1,2]
Image courtesy of Medscape.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Medication-Related Osteonecrosis of the Jaws
Shown is a case of stage 1 MRONJ of the right mylohyoid ridge area. MRONJ can be seen in patients taking a range of medications, including anti-resorptive and anti-angiogenic agents, that are given for cancer therapy and osteoporosis. The most well-known class of causative drugs is the bisphosphonates, particularly those given intravenously. These drugs inhibit osteoclast function and disturb bone remodeling. The osteoporotic agents denosumab, which is a receptor activator of nuclear factor kappa-B ligand (RANKL), and romosozumab are also implicated in MRONJ.[3] Patients usually present with exposed bone, halitosis, and pain. Pathologic fractures and infections can also be seen.
Prevention involves liaison between oral healthcare professionals, and it is usually recommended that invasive dental treatment be carried out prior to the administration of the next dose of the medication.[3] Treatment of MRONJ includes the use of topical and systemic antibacterials and antifungals. Nonvital bone sequestra may be removed surgically in patients with advanced MRONJ.[3,4]
Image courtesy of Medscape.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Radiation- and Chemotherapy-Induced Oral Ulcers
Shown is an ulcerative oral mucositis lesion on the buccal mucosa.
Oral presentations induced by radiation or chemotherapy may range from erosions or erythema to large painful ulcers that make eating very difficult (and thus contribute to malnourishment, further exacerbating the patient's condition). These ulcers may also be accompanied by xerostomia and herpetic and candidal infections, which may be fatal in patients with immunosuppression.
The mainstay of management is symptomatic and includes strict oral hygiene measures. Current targeted treatment strategies include cryotherapy with ice chips, low-level laser therapy, anti-inflammatory treatment, and anti-microbial treatment, in addition to growth factors, such as palifermin, to enhance the healing of oral mucosal lesions. The use of anti-oxidants has also been explored, but currently there is no consensus on their employment in preventing oral mucositis.[5]
Image courtesy of the CDC | Robert E. Sumpter.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Congenital Syphilis
An increase in the incidence of all stages of syphilis (74%) and congenital syphilis (303%) was reported in the United States from 2017 to 2021.[6] Patients with congenital syphilis have incisors with a straight-edge screwdriver shape and a notch in the middle of the incisal surface (called Hutchinson incisors). The molars have numerous globular projections, resulting in abnormal occlusal anatomy (called mulberry molars) with a narrow occlusal table. In addition, a short maxilla and a high-arched palate contribute to malocclusion.[2,7]
Image courtesy of Sheldon Mintz, DDS.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Herpetic Gingivostomatitis
Typical signs of herpetic gingivostomatitis are small vesicles that rupture easily and form shallow, punctate ulcers (shown). As these lesions develop, they form a central area of shallow ulceration with yellow fibrin in the middle. This is accompanied by fever, malaise, and lymphadenopathy. Patients with herpetic gingivostomatitis may present with lesions on the lips, buccal mucosa, tongue, and hard palate. In recurrent herpes simplex infections, the keratinized mucosa is usually affected. It is unusual for immunocompetent individuals to have recurrent herpetic gingivostomatitis. Instead, local trauma may predispose to reactivation and the development of localized crops of ulcers in the affected mucosa. The lesions usually resolve within 1 week.[8]
Image courtesy of the CDC | Emory University, Dr Sellers.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Epstein-Barr Virus
The majority of the population has asymptomatic subclinical infection with Epstein-Barr virus. Symptomatic patients present with prolonged fatigue, malaise, sore throat, nausea, and anorexia. On examination, patients infected with Epstein-Barr virus commonly have prominent lymphadenopathy, along with pharyngitis, palatine petechiae (shown), lingual tonsillar enlargement, and, less commonly but more specifically, edema of the uvula. On occasion, surface exudate is present on the tonsils. Rare complications include hyperplastic circumvallate papillae, which can compromise the airway. Petechiae on the hard or soft palate can be present. Airways should be monitored in patients with severe enlargement of the tonsils. Many of the signs/symptoms of Epstein-Barr virus last 4-6 weeks.[9]
Image courtesy of Wikimedia Commons | Shawn C.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Coxsackievirus
Ulcerous lesions of hand-foot-and-mouth disease are shown.
Coxsackievirus A16 is the most frequent cause of hand-foot-and-mouth disease. The most commonly involved oral sites are the tongue, palate, buccal mucosa, and labial mucosa. Signs/symptoms include sore throat, dysphagia, and low-grade fever. The lesions start as erythematous macules that develop into small vesicles that later ulcerate. Although oral vesicles do not typically appear in the oropharyngeal area and are generally confined to the anterior region of the mouth, ulcerous lesions can appear on the soft palate and oropharynx (above). The size of the oral lesions in hand-foot-and-mouth disease typically ranges from 2-3 mm, although they can be as large as 1 cm. The disease is self-limited, lasting 1-2 weeks; no treatment is necessary.[10,11]
Image courtesy of the CDC | Sol Silverman, Jr, DDS.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Kaposi Sarcoma
Kaposi sarcoma lesions (shown) are typically located on the hard and soft palates; occasionally, they may occur on the maxillary gingiva. They are reddish to blue-purple, nodular or macular lesions that are found bilaterally.[12] These lesions can be seen in immunocompromised patients; in the early 1990s, when the acquired immunodeficiency syndrome (AIDS) epidemic was at its peak, patients with the human immunodeficiency virus (HIV) had a 1 in 2 chance of developing Kaposi sarcoma. With currently available HIV treatment, however, only six patients with HIV per million in the United States will ever develop Kaposi sarcoma.[13] Importantly, 1 in 200 transplant patients may also develop Kaposi sarcoma.[13] The treatment for HIV-related Kaposi sarcoma is antiretroviral therapy (ART).[14] The patient in this image is HIV positive and has candidiasis overlying the intraoral Kaposi sarcoma lesion (arrow).
Image courtesy of Medscape.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Peutz-Jeghers Syndrome
The oral lesions of Peutz-Jeghers syndrome (shown) usually develop in early childhood and are often mistaken for freckles. Intraoral pigmented lesions primarily affect the buccal mucosa and tongue. In addition, the pigmentation spots can cross the vermilion border of the lips and extend into the perioral regions. Patients with Peutz-Jeghers syndrome should be monitored for intestinal tumors, polyps, and intussusception, as they are 15 times more likely to develop intestinal cancer than the general population.[15,16]
Image courtesy of the CDC | Drs. J. Lieberman and Freideen Farzin.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Pemphigus Vulgaris
Oral lesions are present in 50-70% of patients with pemphigus vulgaris. Superficial, ragged erosions with ulcerations occur on the oral mucosa (shown), with the buccal and labial mucosae, soft palate, and gingivae being common sites. Areas exposed to chronic abrasion during tooth brushing and constant frictional activity can develop more symptomatic erosive lesions. The oral mucosal lesions will most often arise prior to the development of cutaneous lesions. The blisters formed in pemphigus vulgaris are associated with the binding of immunoglobulin G (IgG) to keratinocyte adhesion molecules desmoglein 1 and 3, resulting in loss of cell-to-cell adhesion. At times, mucosal lesions may be the only clinical manifestation of pemphigus vulgaris. The mortality rate is 5-10%.[17] Prompt ophthalmologic assessment is important due to the risk of scarring and blindness.[2]
Image courtesy of Medscape.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Lichen Planus
Lichen planus is a chronic immune-mediated inflammatory disease in which the triggering antigen is unknown. The most common pattern of oral lichen planus is the reticular form, which consists of interlacing raised, thin, white lines known as Wickham striae. Variations in these lesions include appearance as papules or plaques (shown), and in erosive lichen planus they often manifest as painful lesions. Oral lichen planus is typically symmetrical and occurs primarily on the buccal mucosa, buccal vestibule, tongue, and gingiva.[18] There are a number of oral and systemic conditions that share common clinical features with lichen planus, such as lichenoid lesions in graft versus host disease, lupus erythematosus, and chronic ulcerative stomatitis, and biopsy is essential for diagnosis.[18,19] Malignant transformation of oral lichen planus can be seen in less than 0.5% of cases, occurring particularly in persons with the erosive type,[20] though malignant transformation rates may be higher in lichenoid lesions caused by drug reactions or contact hypersensitivity reactions.[2,18,20]
Image courtesy of Medscape.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Drug-Induced Gingival Hyperplasia
In drug-induced gingival hyperplasia, disruption of normal gingival collagen degradation results in enlargement of the gingiva. The gingival enlargement typically begins in the interdental area and continues until the crown is obscured (shown). Painful erythematous edges can manifest, depending on the medically compromised state of the patient. The main culprits in drug-induced gingival hyperplasia are anticonvulsant agents (eg, carbamazepine, phenobarbital, phenytoin), calcium-channel blockers (eg, nicardipine, nifedipine, verapamil), immunosuppressants in transplant protocols (such as cyclosporine), oral contraceptives, and erythromycin. In general, changing the medication regimen may resolve the gingival hyperplasia. However, laser or conventional scalpel gingivectomy/gingivoplasty is often necessary if the enlargement is not resolved after medication is reduced, proper oral hygiene is maintained, or a short regimen of antibiotics is administered.[21]
Image courtesy of Wikimedia Commons | Dozenist.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Methamphetamine Use
Methamphetamine use (the suspected source of decay in the above image) can cause carious lesions, which initially affect the facial smooth and interproximal regions of the tooth (arrows) and eventually lead to destruction of the entire crown. The pattern is also known as "meth mouth" or "crank decay." The severity of the tooth decay is most likely a result of both psychological and physiologic changes. Stimulation of the central nervous system can cause extreme xerostomia and result in patients consuming great quantities of sugary and acidic drinks. Periodontal disease and tooth loss can be seen at higher rates in methamphetamine users compared with non-users. If the patient is receptive to treatment, recommend topical fluorides and encourage consumption of water rather than sugary, carbonated drinks.[22]
Image courtesy of Matthew C. Lambiase, DO.
Clues in the Oral Cavity: Are You Missing the Diagnosis?
Willard J. Peng, DDS, MS; Claudia Camelia Cotca, DDS, MPH | October 30, 2023 | Contributor Information
Pseudomembranous Candidiasis (Thrush)
Candida albicans causes pseudomembranous candidiasis (thrush) when normal host immunity or normal host flora is disturbed. A superficial layer of white curds (shown here on the underside of the tongue) will appear on various intraoral sites; the white coating/patches can be easily removed with a tongue depressor or a piece of gauze, and the underlying mucosa may appear normal or erythematous. An impaired or altered immune system, as from chemotherapy or conditions such as Sjögren syndrome, HIV infection (see slide 8, on Kaposi sarcoma), or diabetes mellitus, may induce the formation of thrush. In addition, the use of broad-spectrum antibiotics can eliminate competing bacteria, thereby allowing overgrowth of C albicans.[23]
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Contributor Information
Authors
Willard J. Peng, DDS, MS
Dentist
Scripps Poway Dental Care
San Diego, CA
Disclosure: Willard J. Peng, DDS, MS, has disclosed no relevant financial relationships.
Claudia Camelia Cotca, DDS, MPH @dclaserdentist
Washington Institute for Dentistry & Laser Surgery
Chevy Chase, MD
Disclosure: Claudia C. Cotca, DDS, MPH, has disclosed no relevant financial relationships.
Editor
Lars Grimm, MD, MHS
Associate Professor
Department of Diagnostic Radiology
Duke University Medical Center
Durham, NC
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Reviewer
Muhammed Yakin, BDS MMedSci DClinDent FHEA FPFA
Associate Professor Oral and Maxillofacial Pathology
Adelaide Dental School
Faculty of Health & Medical Sciences
The University of Adelaide
Adelaide, Australia
Disclosure: Muhammed Yakin, BDS MMedSci DClinDent FHEA FPFA, has disclosed no relevant financial relationships.
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