Examination of the oral cavity is an integral component of primary care. It provides a valuable opportunity to assess dental and oral health, to identify symptomatic lesions which may interfere with oral function, to detect asymptomatic lesions with malignant potential, to identify detrimental effects of substance abuse on oral tissues, and to detect oralmanifestations of systemic disease and medical therapy. The American Cancer Society estimates that nearly 39,400 individuals will be diagnosed with oropharyngeal cancer in 2011, for 7,900 of whom the disease will prove fatal. High risk sites for oral cancer include the floor of the mouth, the posterolateral and ventral tongue as well as soft palatal complex. Significant racial disparities among adults with oral cancer have been noted, with black males having a higher incidence, more advanced stage of disease at diagnosis and worse survival rates compared to whites.
Although multifactorial in etiology, the main risk factors are abuse of tobacco and alcohol. Oral cancer also affects men more than women. Substance abusers from low socioeconomic groups with poor access to oral health suffer particularly poor prognosis, as disease is often discovered late, leading to mortality or greater morbidity due to aggressive therapy. Nevertheless, oral cancer also affects individuals who do not smoke or drink. In fact, a rise in the incidence of oral cancer among younger adults without the typical risk factors has been noted in recent years. A role for oral human papillomavirus (HPV) infection as a risk factor for a subset of these patients has been suggested. Therefore, all patients, irrespective of their social history, should undergo periodic screening for oral cancer. Primary care providers have the potential to positively impact the morbidity and survival outcome associated with oral cancer through patient education, regular oral surveillance as well as early detection of pre-malignant and cancerous lesions.
A thorough examination of the oral cavity involves both visual inspection and palpation, and can be accomplished in about five minutes. To perform the procedure properly, the clinician requires adequate lighting, a disposable mouth mirror or tongue blade and a 2x2 gauze. The patient should remove any oral prosthesis to allow examination of the oral tissues underneath. Also, it is advisable to develop a routine for the examination to avoid leaving any anatomical area unexamined. The anatomical regions to be examined include lip vermillion, upper and lower labial mucosa, right and left buccal mucosa, the floor of the mouth, ventral and dorsal tongue surfaces, right and left lateral borders of the tongue, hard and soft palatal mucosa, facial and lingual gingivae. In addition, the posterior oral cavity should be visually inspected and the floor of the mouth bimanually palpated. Any alteration in the color (leukoplakia, erythroplakia, erythro-leukoplakia, abnormal pigmentations) or texture (thickening, mucosal overgrowth, submucosal lumps, induration) of oral mucosa noted during the examination should be documented, followed to ensure resolution and if the abnormality persists, referred for further evaluation including biopsy (Figures 5-10).
|Case 2: HIV-associated salivary gland disease & Xerostomia
Mahnaz Fatahzadeh, BSc,DMD,MSD,Dip ABOM NewJersey Dental School, UMDNJ
A 45-year-old African-American male was referred for evaluation of xerostomia and oral burning to patient’s internist during his oral screening.
The patient stated that his oral dryness had progressively worsened and interfered with eating, mastication and swallowing. He admitted to drinking several cans of soda throughout the day to alleviate oral dryness and to help with oral lubrication at mealtimes. His teeth were also extremely temperature-sensitive on intake of foods and fluids. His last dental visit was over five years ago when he had several unrestorable teeth extracted. He admitted not brushing on a regular basis and complained of halitosis causing him embarrassment in social situations.
His past medical history was significant for HIV infection, Hepatitis C and type 2 diabetes. His medications included efavirenz/emtricitabine/ tenofovir disoproxil fumarate and glyburide. He was not receiving treatment for Hepatitis C. He had a 20 pack-year history of tobacco smoking and was a former alcoholic but had stopped drinking 5 years ago. His risk factor for HIV and Hepatitis C was IVDU which he had stopped years ago. On review of systems, he denied skin or ocular dryness and rheumatologic disorders. Review of blood work within the past three months revealed CD4 cell count = 300 cell/mm3, viral load = 500 copies/mm3, ANC = 5,000 cells/mm3, plt = 130,000 cells/mm3, HBA1C = 8.2%.
On extraoral examination, there was bilateral facial swelling affecting the parotid region (Figures 11 & 12). Swelling was palpable and non-tender. There were no lymphadenopathy or facial lesions. Intraorally, the patient’s oral hygiene was very poor and an offensive odor emanated from his mouth. Removable white plaques resembling food debris, tissue slough or fungal infection were also present throughout the oral cavity (Figure 13). Oral mucosa was dry and a tongue depressor applied to the soft tissue adhered upon attempts to lift it away. There was minimal salivary pooling on the floor of the mouth.Digital palpation of parotids and submandibular glands yielded minimal discharge from Stenson’s and Wharton’s ductal orifices. Expressed saliva was clear, viscous and free of pus or blood. Sialometry revealed resting secretion of less than 0.1ml/min and stimulated secretion = 0.6 ml/min, both of which were consistent with hyposalivation. Examination of dentition revealed generalized plaque and gingival inflammation, tobacco staining, cervical decalcification and multiple broken, carious teeth. There were no periodontal pockets but there was generalized bleeding on probing.
Differential diagnosis of bilateral parotid swellings included parotitis secondary to HIV or hepatitis C, diabetic sialadenosis, sarcoidosis,Sjögren's syndrome and Warthin’s tumors, for all of which except the latter xerostomia could be a common complaint. The patient’s HIV medications could also have contributed to oral dryness although a temporal relation between the start of his medications and onset xerostomia was absent. He was referred to an otolaryngologist for diagnostic evaluation of his salivary gland enlargement. A tongue blade was used to sample removable white plaques and prepare a smear on a glass slide. Microscopic examination of the specimen revealed presence of numerous fungal hyphae in the cytologic smear (Figure 14) and confirmed diagnosis of oral candidiasis possibly caused by a combination of systemic and local factors such as HIV-parotitis, diabetes and oral dryness.
The patient was prescribed a two week course of nystatin oral solution 100,000 units/ml to swish in the mouth for two minutes and then swallow three times daily to address oral candidiasis. He was also advised to sip water throughout the day and particularly during mealtimes, and use over the counter moisturizing gel or artificial saliva spray to palliate oral dryness and help with mastication and swallowing. In addition, the patient was advised to reduce intake of tea, coffee and alcohol to avoid dehydration of oral mucosa, and to use a humidifier in his bedroom to alleviate his symptoms while sleeping. Dental treatment plan included debridement and dental prophylaxis, extraction of non-restorable teeth, application of desensitizing agents and multiple restorations to be executed over the upcoming dental visits. He was educated about the increased risk of dental caries with hyposalivation and significance of preventive measures to maintain his remaining teeth caries free. An alcohol-free antimicrobial mouthrinse was prescribed for daily use to reduce bacterial load and assist with oral hygiene. Custom made oral trays were fabricated and patient was instructed on regular use of topical fluoride gel within these oral trays at bed time.
During the follow-up visit, the patient reported alleviation of oral burning within the first week of using the antifungal oral solution. He had found the recommended oral moisturizing agents beneficial in lubricating his mouth and facilitating oral functions. On examination, oral mucosa was still dry but oral hygiene, gingival inflammation and halitosis had improved and fungal infection had resolved. The result of work up by the patient’s otolaryngologist confirmed HIV-associated salivary gland disease as the etiology of his parotid swelling and ultimately his oral dryness. The patient reported his symptoms were manageable with recommended measures. He declined a trial course of a pharmacologic sialogouge, such as pilocarpine, bethanechol, or cevimeline, which would stimulate salivary output and provide further palliation.
Xerostomia refers to the subjective complaint of dry mouth which may reflect a true decrease in salivary output or distorted oral perception. Clinical evaluation of xerostomia should include:
- A review of the patient’s medications/treatments and inquiring about the start of therapies known to cause drymouth and onset of xerostomia, (i.e.,antidepressants, diuretics, antihistamines, radiotherapy, chemotherapy, protease inhibitors, NNRTIs,etc.). If xerostomia appears related to a specific medication, it may be warranted to ask the physician to consider a substitute with less oral xerostomic side effect or altering the dose or frequency of the offending medication, if possible.
- A focused review of systems inquiring about cutaneous, ocular, nasal and vaginal dryness to determine if the problem is of local or systemic nature followed by a referral to a physician for evaluation when indicated.
- A review of past medical history is also necessary to exclude systemic conditions with oral manifestation of xerostomia, (i.e., Sjögren's syndrome, diabetes, or sarcoidosis). If dryness appears related to an underlying systemic disease, primary management should be directed at the etiology.
- Evaluation of major salivary glands for enlargement, pain and tenderness on palpation, expression of saliva from ductal orifices upon digital palpation and noting the clarity and viscosity of secretions. Salivary output (sialometry) should also be measured objectively to confirm or exclude hyposalivation as the etiology of xerostomia. In clinical practice, whole unstimulated saliva (WUS) representing total discharge from all salivary glands is measured by asking the patient to spit or drool into a collecting cup for 10-15 minutes. Whole stimulated saliva (WSS) is measured in the same manner following a gustatory or masticatory stimulation such as application of lemon juice on the patient’s tongue or chewing on paraffin gum for about one minute. Although there is large variability in the normal values reported for UWS or SWS in the literature, WUS <0.1ml/min andWSS<0.7ml/min are considered abnormal and consistent with hyposalivation.
In addition to the clinical evaluation outlined in Case 2 above, the dentist has a role in palliation of xerostomia and prevention of oral disease (soft and hard tissue) secondary to xerostomia.
The management strategies for xerostomia are numerous and should be tailored to the patient’s needs. Examples include:
- Frequent sips of water throughout the day.
- Oral moisturizing gels and rinses as needed.
- Using humidifiers in the sleeping area to help with oral dryness at night.
- Gustatory or masticatory sialogouges (chewing sugar-free gumor candy).
- Avoiding alcohol containing mouth rinses which dehydrate oral mucosa.
- Avoiding strong flavorings whichmay irritate dry, sensitive oral mucosa.
- Watching for and treating oral fungal infections, if any.
- Meticulous oral hygiene.
- Frequent preventative recalls.
- Low cariogenic diet (relatively high amounts of protein, calcium and phosphorus,minimal fat and carbohydrate and high concentration of foods with pH greater than 6).
- Fabrication of customoral trays for topical application of fluoride at home.
- Prescribing systemic sialogouges, such as pilocarpine (Salagen®), cevimeline (Evoxac®) [if no contraindication].