Little is known about the oral manifestations of DN.⁵ A recent study of patients who have type 2 DM noted that 18 percent had burning mouth syndrome, or BMS, compared with 7 percent of nondiabetic patients within the control group.¹ Furthermore, peripheral neuropathy was noted in 42 percent of patients from the diabetic group and none from the control group. There seems to be no apparent difference in the prevalence of DN between patients who have type 1 DM and those who have type 2 DM.⁴

BMS, also known as glossodynia, is another relatively common neuropathic pain condition. Essential BMS refers to oral burning symptoms without discoverable etiology; these symptoms include allergy, oral autoimmune disease, xerostomia, nutritional deficiency, candidiasis, referred pain, complex regional pain syndrome type 1 or diabetic peripheral neuropathy. In making a diagnosis for patients who have BMS symptoms, it is necessary to establish a differential diagnosis that includes DN.⁶

	CASE REPORT

TOP ABSTRACT CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
A 54-year-old woman reported for an oral evaluation at the Howard University College of Dentistry Graduate Residency Program clinic. Her medical history was positive for hypertension, type 2 DM, asthma, hiatal hernia, sinusitis and von Willebrand’s disease, for which she was taking nifedipine, pravastatin, glibenclamide and albuterol. The patient neither smoked cigarettes nor drank alcohol.

The patient had a chief complaint of "burning tongue," which she had had for approximately several days to one week. The patient had rinsed with full-strength hydrogen peroxide but discontinued rinsing several days before her appointment, as there was no change in the condition.

An oral and maxillofacial surgeon (L.G.) and an oral medicine clinician (R.S.B.) were called in for a consultation examination. The examination revealed no lymphadenopathy. None of the major salivary glands demonstrated function. The tongue and all other oral tissues appeared to be within normal limits. The differential diagnosis was glossodynia/BMS, diabetic peripheral neuropathy, relative xerostomia and nutritional deficiency. The patient was referred to her physician for specific blood studies, including complete blood count and differential, glycosylated hemoglobin, or HbA_1c; serum glucose; iron, folate; B₁₂; antinuclear antibody; rheumatoid factor; Sjögren’s syndrome A and B; and an ery throcyte sedimentation rate.

With a diagnosis of diabetic neuropathy, the first line of treatment is diabetic control.

Ten days later, the patient returned to the dental clinic for a follow-up visit. The blood studies showed an elevated serum glucose level of 395 and an elevated HbA_1c level of 14.1. All of the other blood studies were within or very close to normal limits. The dental clinicians confirmed that the blood study results demonstrated that the diagnosis of DN was most probable, as the patient’s diabetic condition had been out of control. The patient’s physician had come to the same conclusion and confirmed the diagnosis of DN and the potential benefits of diabetic control. The patient became more compliant in taking her diabetic medication, maintaining a balanced diet and exercising. She reported that her oral burning symptoms had improved vastly. At follow-up appointments over the next two years, she remained pain free.

	DISCUSSION

TOP ABSTRACT CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
Glossodynia/BMS is a relatively common condition, particularly in postmenopausal women. Its prevalence rate in this population is between 0.7 and 2.6 percent.⁷ DM also is a relatively common condition in this same population. The differential diagnosis for our patient and patients in general who have oral burning symptomatology included essential BMS, DN, oral vesicularbullous disease, candidiasis, xerostomia and nutritional deficiency. The determination of the diagnosis of BMS is dependent on ruling in or out the various entities within the differential diagnosis. Conditions are ruled in or out on the basis of the patient’s history, the clinical examination and the laboratory study results.

Our patient’s medical and family history noted a correlation with DM, as she reported having a history of type 2 DM. Furthermore, her history was consistent with less than adequate management of her diabetic condition. Our clinical examination ruled out the likelihood of such diagnoses as oral vesicularbullous disease and candidiasis. These clinical entities usually are obvious, though sometimes they can manifest as more difficult to diagnose subclinical varieties. Laboratory studies within the diagnostic protocol for BMS include blood serum studies for diabetes (serum glucose, HbA_1c or both) and anemia.⁶ Our patient’s laboratory values for these assays correlated with a diagnosis of burning symptoms secondary to an orofacial diabetic peripheral neuropathy.

Xerostomia is another potential etiology for oral burning symptoms. Xerostomia may be associated with DM, nutritional deficiency, Sjögren’s syndrome, caffeine or alcohol use, drug-induced xerostomia or dehydration.⁶ With the exception of DM, however, the laboratory studies did not confirm a correlation with these other etiologic possibilities.

With a diagnosis of DN, the first line of treatment is diabetic control. If it is insufficient, various chronic pain strategies may be implemented, including tricyclic antidepressant, or TCAs, and other pharmacological therapies for neuropathic pain. In the case we report, fortunately diabetic control alone was sufficient. In the treatment of DN, however, adjuvant chronic analgesic therapy often is necessary.^4,5 Therapeutic strategies for the treatment of DN have demonstrated TCAs to be effective in the control of neuropathic pain.^8,9 A long-term concept for chronic neuropathic pain control states that anticonvulsant drugs such as carbamazepine and phenytoin are most effective for controlling lancinating pain and that antidepressants such as amitriptyline are most effective for controlling burning pain.⁴ However, this philosophy is not supported by recent studies.^8,10 Furthermore, there has been considerable controversy regarding the antidepressant effects of low-dose TCAs in the treatment of chronic pain. However, studies have repeatedly demonstrated that the analgesic benefit of TCAs is independent of any antidepressant effect.^8,9,11

Numbers needed to treat, or NNT, to obtain one patient with more than 50 percent pain relief rates analgesic pain control for neuropathic pain. This rating system is used to compare efficacy; the lower the NNT, the better the efficacy. In a systematic review, McQuay and colleagues⁸ found that in six of 13 DN studies TCAs demonstrated a significant benefit compared with placebo with NNTs between 2.4 and 4.3. No particular TCA has demonstrated a significant advantage compared with other TCAs; however, TCAs demonstrate improved pain control when compared with selective serotonin reuptake inhibitors, or SSRIs.^8,9 With regard to the treatment of DN, Sindrup and Jensen⁹ reported an NNT of 1.4 to 2.4 for TCAs, 6.7 for SSRIs, 3.3 for carbamazepine, 1.9 for dextromethorphan, 3.7 for gabapentin, 3.4 for tramadol, 5.9 for capsaicin and 10.0 for mexiletine.

	CONCLUSION

TOP ABSTRACT CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
We established a diagnosis of DN in a patient who was experiencing oral burning. It is important to consider DN as part of the differential diagnosis in patients who have symptoms compatible with BMS. Treatment for DN begins with attention to diabetic control. If necessary, adjuvant pharmacotherapy for neuropathic pain control can be initiated.

View larger version (127K): [in this window] [in a new window]   Dr. Getter is a professor and the chair, Department of Oral and Maxillofacial Surgery, Howard University College of Dentistry, Washington.

View larger version (138K): [in this window] [in a new window]   Dr. Brown is an associate professor, Department of Oral and Maxillofacial Pathology and Department of Oral Diagnosis and Radiology, Howard University College of Dentistry, Washington; and a clinical associate professor, Department of Otolaryngology, Georgetown University Medical Center, Washington. Address reprint requests to Dr. Brown at 600 W Street, N.W., Washington, D.C. 20059, e-mail "rbrown{at}howard.edu".