Leprosy and its dental management guidelines.

OBJECTIVES: Leprosy is a chronic, non-fatal disease caused by Mycobacterium leprae. It can cause cutaneous lesions, peripheral nerve lesions and orofacial manifestations, including destruction of the alveolar premaxillary process associated with loss of the maxillary incisors. The aims of this study were to assess orofacial manifestations of disease in patients attending the Bombay Leprosy Project clinics and develop clinical guidelines for dentists. MATERIALS AND METHODS: A cross-sectional questionnaire based study was administered to 43 diagnosed leprosy patients. This included questions on perceived oral health status and oral hygiene habits. An extra-oral and intra-oral examination was also performed. RESULTS: Eighty-four per cent of patients were male with a mean age of 35.9 years. Forty-nine per cent had extra-oral cutaneous lesions. Twenty-eight per cent had intra-oral lesions including hyperpigmented patches. Twenty-one per cent had cranial nerve involvement and the trigeminal nerve was most commonly affected. CONCLUSIONS: From this data a clinical dental pathway protocol for managing patients with leprosy was developed. It highlights dental issues when managing leprosy patients. Nerve involvement may mean patients are unable to give an accurate account of their symptoms. Special tests should include cranial nerve examination and swabs of intra-oral ulcers. Low rates of infectivity means that normal infection control measures can be taken when treating these patients.

Facial sensory loss in multi-bacillary leprosy patients.

Sensation over the face was estimated using the Semmes-Weinstein's monofilament (target force 0-05 gms) in a cohort of multi-bacillary (MB) patients whose clinical and ocular characteristics were available at the time of leprosy diagnosis. Among the 190 MB patients examined, 56 (30%) had areas of sensory impairment somewhere on the face and 43 (23%) had sensory deficit over the lids and/or the malar area. Lagophthalmos (adjusted OR 8.96, 95% CI 0.96-83.50), Type 1 reaction (aOR 2.47, 95% CI 1.11-5-52), history of reactions (aOR 6.36, 95% CI 2.40-16.85) and glove and stocking anaesthesia (aOR 3.49, 95% CI 1-40-8.70) were associated with impaired facial sensation. Hypoesthesia restricted to areas over the lids and/or malar area showed a stronger association with lagophthalmos (aOR 17.5, 95% CI 1.98-154.36). Loss of facial sensation appears to be associated with lagophthalmos in MB patients.

Hypopigmented face patches; their distribution and relevance to ocular complications in leprosy.

Eighty-two leprosy patients with hypopigmented patches over the face (cases) and an equal number of age-, sex-, and classification-matched leprosy patients without any hypopigmented patches over the face (controls) were examined for the distribution of hypopigmented facial patches, areas of anesthesia over the face, and eye complications. The hypopigmented patches did not follow any pattern and overlapped in the areas of sensation supplied by the three branches of the trigeminal nerve. Anesthesia over the face, evaluated by a Semmes-Weinstein monofilament which exerted a force of 0.05 grams, was present in 19.5% of the cases and 15.9% of the controls. Patients with hypopigmented facial patches were found to have more corneal hypoesthesia than patients who did not have hypopigmented facial patches. The risk of having impaired corneal sensation was three to four times higher in patients with hypopigmented facial patches. This feature can be used to identify decreased corneal sensation among leprosy patients under field conditions where direct estimation of corneal sensation is not advocated.

Dacryocystographic examination does not identify early seventh nerve failure in leprosy patients.

Dacryocystographic examination was performed in two groups of patients: patients having leprosy and those not having leprosy, in order to look for early failure of the facial nerve. The results of this study show that this kind of examination does not improve diagnosis of leprosy.

Cervical branch of the facial nerve in leprosy.

This study demonstrates that the platysma is occasionally palsied in leprosy and that this only occurs when the facial nerve already has some other palsy. That there needs to be a facial palsy before there can be a platysma palsy is strongly suggested, in that there was no case of an isolated platysma palsy. Patients, regardless of age or other factors, could mimic a platysma contraction. This obviates the need for electrical testing to examine for a platysma palsy. It also means that a nonfunctioning platysma on clinical examination is, in fact, a palsied platysma. While lagophthalmos is regularly examined for, and any obvious facial paresis would be noticed, less severe forms of facial muscle paresis will only be found if formally examined for. The mechanism whereby the facial nerve is involved in leprosy is not clarified, but our findings suggest that proximal spread of a lesion that began in the zygomatico-temporal branches and reaches to the facial nerve trunk is more likely than new lesions developing de novo in other peripheral facial nerve branches. That the primary lesion is within the facial nerve trunk in all cases but we only see the frequent zygomatic sequelae due to secondary factors is not excluded.

The significance of facial patches and type I reaction for the development of facial nerve damage in leprosy. A retrospective study among 1226 paucibacillary leprosy patients.

Charts of 1226 paucibacillary leprosy patients, registered between 1982 and 1987 were reviewed for recent facial nerve damage, facial patches and the presence of Type I reaction. Twenty-six (2.1%) patients with recent lagophthalmos were identified. In a great majority (85%) patients with recent lagophthalmos showed significant patches over the malar region or around the eye, at the same side as the nerve damage together with clinical signs of Type I reaction. This combination of significant patches in certain locations and Type I reaction seems to be a pre-condition for facial nerve damage. The clinical implication is that a small group of patients may be identified, who are at risk of facial nerve damage. By examining these patients more carefully it will be possible to detect nerve damage early and to prevent permanent damage of the facial nerve by timely treatment with an appropriate steroid regimen.

Treatment of recent facial nerve damage with lagophthalmos, using a semistandardized steroid regimen.

Twenty-seven patients with borderline leprosy and facial nerve damage of less than or equal to 6 months duration (36 eyes) were treated with a semistandardized regimen of steroids (the average starting dose was 25-30 mg, duration 5-6 months) on an outpatient basis. Red and raised reactive patches were usually present in the upper malar area or around the eye(s) in patients with recent lagophthalmos. The lid gap was measured in millimetres during gentle and strong closure. After completion of the steroid course 75% of the eyes had complete closure or only a slight gap of less than or equal to 2 mm on gentle closure. Steroids were found to be beneficial and safe, in the dosage that we prescribed.