SRM Journal of Research in Dental Sciences

: 2022  |  Volume : 13  |  Issue : 4  |  Page : 185--189

An overview of leprosy with its oral manifestations: A comprehensive review

Manisha Singh, Hemant Sawhney, Richa Mishra, Jayant Kumar 
 Department of Oral Medicine and Radiology, School of Dental Sciences, Sharda University, Greater Noida, Uttar Pradesh, India

Correspondence Address:
Dr. Manisha Singh
Department of Oral Medicine and Radiology, School of Dental Sciences, Sharda University, Greater Noida, Uttar Pradesh


Background: Leprosy is caused by Mycobacterium leprae which most commonly affects the skin and peripheral nerves. The other sites of leprosy include the liver, kidneys, eyes, oral mucosa, lymph nodes, bones and joints, and gonads. The oral involvement in leprosy includes the tongue, lips, hard palate, buccal mucosa, uvula, faucial pillars, and involvement of gums. Aim: The aim of this comprehensive review is to create the awareness among dental professionals about the classification, pathogenesis, clinical features, diagnosis and management, reactions of leprosy, and oral aspects of leprosy. The awareness among dental professionals will help in the early detection and treatment of leprosy patients. Methods: The comprehensive data were obtained based on the electronic data search about the classification, pathogenesis, clinical features, and oral aspects of leprosy on Google Scholar and PubMed. Results: A total of 14 articles were selected for the purpose of classification, pathogenesis, clinical features, and oral aspects of leprosy. Conclusion: The oral examination of these patients will be helpful in the early diagnosis and treatment of leprosy patients.

How to cite this article:
Singh M, Sawhney H, Mishra R, Kumar J. An overview of leprosy with its oral manifestations: A comprehensive review.SRM J Res Dent Sci 2022;13:185-189

How to cite this URL:
Singh M, Sawhney H, Mishra R, Kumar J. An overview of leprosy with its oral manifestations: A comprehensive review. SRM J Res Dent Sci [serial online] 2022 [cited 2023 Mar 20 ];13:185-189
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The other name for leprosy is Hansen's disease. The average incubation period of this virus varies from 3 years to 10 years. The infection mostly spread due to prolonged contact with infected patients with leprosy. Leprosy is in two clinical forms: tuberculoid leprosy and lepromatous leprosy. They are immunologically stable forms, whereas borderline and indeterminate forms are immunologically unstable.[1] The classification is given by Ridley and Jopling, 1966 which established the different forms of leprosy based on clinical characteristics as well as a host immune response.[2]

Another classification depends on the involvement of skin lesions in the paucibacillary form and multibacillary form of Leprosy.[3] Tuberculoid leprosy is a paucibacillary form of the disease which involves 5 or <5 skin lesions. Paucibacillary leprosy may involve one nerve trunk being affected by the sensory loss.[4] A lepromatous leprosy is a multibacillary form of the disease which involves more than five skin lesions. A lepromatous leprosy may involve two or more nerve trunks being affected with sensory loss.[4]

This review article discusses the classification, pathogenesis, clinical features, diagnosis and management, reactions of leprosy, and oral aspects of leprosy. The oral manifestations are generally associated with lepromatous leprosy. The awareness among dental professionals about the classification, pathogenesis, clinical features, diagnosis and management, and reactions of leprosy will improve the treatment plan for leprosy patients. This review article focuses on improving the understanding of oral manifestations of leprosy among dental professionals. These patients should be examined for oral manifestations and should be further sent to dermatologists for the examination of other body parts.


The comprehensive data were obtained based on the electronic data search about the classification, pathogenesis, clinical features, diagnosis and management, and reactions of leprosy and oral aspects of leprosy on Google Scholar and PubMed. The inclusion criteria include the studies involving the oral manifestations of leprosy from January 1, 2000 to December 31, 2020. The studies which include the classification, pathogenesis, clinical features, diagnosis and management, and reactions of leprosy were also selected. Review articles, case reports, and short communication were not selected for the study.


A total of 14 articles were selected for the purpose of classification, pathogenesis, clinical features, diagnosis and management, and reactions of leprosy. Recent studies which showed oral manifestations of leprosy were selected for the study.


When the bacilli enter the body, it releases inflammatory cytokines resulting in the proliferation of T-helper lymphocytes 1 and 2.[1] T-helper lymphocytes will help in promoting immune response toward Mycobacterium leprae. This will result in the clinical characteristics of tuberculoid leprosy and lepromatous leprosy.[5]

The cellular immune response toward M. leprae is with tuberculoid leprosy due to which lesser proliferation of M. leprae is seen.[1],[6] This constitutes fewer bacilli counts with fewer skin lesions and nerve involvement. CD4+ T cells of Th1 pattern are predominant in tuberculoid Leprosy with high levels of interferon-gamma (IFN-γ), interleukin-2 (IL-2), and tumor necrosis factor-alpha (TNF-α).[7]

The humoral immunity with the decreased cellular immune response toward M. leprae is with Lepromatous Leprosy.[1],[6] This results in increased susceptibility to the development of disease. This constitutes diffuse skin lesions and a higher degree of involvement of peripheral nerve lesions. CD8+ T cells of Th2 pattern are predominant in lepromatous leprosy with high levels of interleukin-4, interleukin-5, interleukin-10, and low levels of IFN-γ.[8]

Clinical forms of leprosy

Tuberculoid leprosy

The presentation of tuberculoid leprosy varies from annular erythematous plaques, hypopigmentation, and elevated external borders which may be single skin lesions or multiple asymmetric lesions.[1],[9] They are generally large lesions, and the lepromin test is positive for this leprosy.[9] The lepromin test indicates the cell-mediated immune response of patients toward M. leprae. They may be associated with alopecia and anhidrosis when skin lesions are involved. Thickening of the nerve sheath is seen with sensations absent when associated with nerve involvement in patients with tuberculoid leprosy.[2] Other features include hypoesthesia, muscle weakness, and facial paralysis when the facial nerve is involved.

Lepromatous leprosy

The presentation of lepromatous leprosy varies from erythematous brown spots, hypochromic spots, indefinite borders, and dry skin.[1] They are many in number, small, and symmetrical and the lepromin test is negative for this leprosy.[9] The sites which are more common are the face and auricle. Other features are no loss of sensations, edema of the legs, formation of lepromas, and leonine facies including infiltrated face with loss of eyelashes.[1],[10] Earlobes are affected, resulting in saddle nose deformity when the nose is involved.

Indeterminate leprosy

This leprosy is associated with hypochromic spots, no loss of sensation, and no thickening of the nerve sheath.[1],[9]

Borderline leprosy

This leprosy is classified as borderline tuberculoid, midborderline, and borderline lepromatous.[1],[2] The presentation of borderline tuberculoid leprosy is like tuberculoid leprosy. Skin lesions are large with loss of sensations and thickening of the nerve sheath.[1] Midborderline leprosy is characterized by brown erythematous plaques and foveal spots. The presentation of midborderline can exhibit both characteristics of lepromatous leprosy and tuberculoid leprosy. The lepromin test is weakly positive for borderline tuberculoid leprosy and negative for midborderline leprosy and borderline lepromatous leprosy.[9] The presentation of borderline lepromatous leprosy is like lepromatous leprosy. These patients are seen with many hypochromic macules and extensive involvement of peripheral nerves.

Oral manifestations of leprosy

Lepromatous leprosy is the most common involving oral and facial manifestations. The prevalence of oral lesions of leprosy in patients is 19%–60%.[11] When a nasal route is involved in leprosy patients, mouth breathing is seen in these patients. The oral lesions are generally seen in the late stage of this disease.[5] When these oral lesions are left untreated, it will result in facial deformities which will have a negative impact on patients. Most patients with leprosy do not maintain their oral hygiene and hence will result in dental caries, periodontal diseases, and tooth mobility.

Pallagatti et al., 2012 classified leprosy into leprosy-specific and nonspecific lesions.[12] The most common site involved in the oral cavity is the anterior part of the hard palate. The oral lesions included are hyperpigmentation of the oral mucous membrane, macrocheilia, microstomia, lepromas of the lips, and palate, nodules present on the face, uvula, buccal mucosa, and plaques associated with leprosy may involve the upper lip and lower lip [Figure 1]. Rawlani et al., 2011 mentioned dental caries, destruction of the anterior maxilla, teeth with periodontal disease, tooth loss, and increased bone loss due to the advanced stage of the disease as the dental problems associated with Leprosy.[13]{Figure 1}

Taheri et al., 2012 described facial nerve paralysis, facial deformity, visual impairment, and eye injury including lagophthalmos and keratitis to be associated with leprosy[14] [Figure 2]. On extraoral examination, the patient revealed nodules on the face, thickening of earlobes, nodules on the external ear, involvement of nasal structure, nasal obstruction, bleeding, atrophy of the nasal spine, and loss of eyebrows.[15]{Figure 2}

Pathogenesis of facial and oral manifestations of leprosy

Facial features are seen as sagged ears, saddle nose deformity, scanty eyelashes, scanty eyebrows, and nodular skin eruptions.[16] Lepra bacilli have an affinity towards the nasal mucosa due to low-temperature sites in the body. This results in saddle nose deformity and destruction of alar and nasal cartilage. Further, the continued destruction of the anterior face affects the facial esthetics and infection spreads to the maxillary region.[17] Sagging of ears is due to infiltration of ear lobules with lepra bacilli which results in the thinning and sagging of the ears. Degenerative changes in the cartilaginous tissues of the ear may result in ear deformities.[16]

When the infection of the nasal mucosa spreads locally, starting from the anterior nasal spine to the upper incisor region resulting in progressive bone loss with maxillary incisors. Missing maxillary anterior teeth, saddle nose deformity, and loss of anterior nasal spine will give an unaesthetic appearance to the face. Nodules and lepromas of the face are generally associated with later stages of the disease.

M. leprae infects the cooler areas of the body including peripheral nerves and nasal mucosa. Mouth breathing is common in patients with Leprosy with nasal obstruction and stuffiness. The most common oral sites of Leprosy are the hard palate, tongue, buccal mucosa, lips, soft palate, labial maxillary gingival tissues, buccal maxillary gingival tissues and labial mandibular gingival tissues. These oral sites have lower mean temperatures which are more prone to involvement in the disease. As the mean temperature of the oral site decreases, the frequency of sites of oral involvement becomes higher.

Other involvement of the oral mucosal site is due to the invasion of M. leprae. Initially, there is the formation of nodules in the oral cavity, and later stages of fibrosis and other functional deformities are noted. When the lips are involved in Leprosy they appear as microstomia, and macrocheilia, the presence of flat-topped nodules on lips. The later stages of the disease may involve the anterior part of the tongue, hard palate, and buccal mucosa which results in infiltration, nodule formation, and scarring.

Studies carried out on oral manifestations of leprosy

Castellano et al., 2020 stated the most common locations of leprosy include the hard palate and upper lip and leprotic lesions are in the form of plaques and lepromas. They concluded the most common oral leprosy lesions are seen in lepromatous leprosy, borderline lepromatous leprosy, and erythema nodosum leprosum.[18]

Vohra et al., 2019 concluded most patients with leprosy showed oral manifestations. The oral manifestations of Leprosy are seen in 70% of Leprosy patients. The leprotic oral lesions are atrophy of the tongue papillae, fissured tongue, chronic generalized periodontitis, loss of taste sensation, melanosis of the oral mucosa, candidiasis, and oral submucous fibrosis, and aphthous ulcers, depigmentation, and smoker's palate.[19]

Raja et al., 2016 evaluated gingival recession, tooth loss, chronic pulpitis, tooth mobility, dental caries, periodontitis, and attrition as other oral manifestations seen in patients with Leprosy.[20]

Babu et al., 2015 included four groups of Leprosy patients based on the duration of exposure to the disease. They are Group I - 0–3 years, Group II - 3–10 years, Group III - 10–20 years, and Group IV - >20 years. Lepromatous Leprosy and Tuberculoid Leprosy are more common in Group IV and Group III patients. Oral manifestations recorded are pinkish discoloration of teeth, circumferential hypoplasia, shortened roots, depapillation of the dorsal aspect of the tongue, fissured tongue, and fibrosis of the soft palate and uvula. These oral manifestations are more common with the Lepromatous type when compared with the Tuberculoid type.[16]

Pereira et al., 2013 evaluated the oral health status of leprosy patients as low with high DMFT and plaque levels.[15]

Diagnosis and investigations

Diagnosis is initiated with the history of being in contact with infected patients with Leprosy and clinical findings of hypochromic patches and thickened nerve sheath. A skin smear can be done to have a note of the bacterial count.[21] Lepromatous leprosy has a high bacterial load when seen through light microscopy. The severity of infection can be assessed through the bacterial load. The advanced methods are the Polymerase Chain Reaction and serological test.[22] Polymerase Chain Reaction detects the M. leprae in Lepromatous leprosy patients. Serological tests showed positive antibody levels to detect Lepromatous Leprosy. The skin smear, polymerase chain reaction, and serological test are highly specific and cannot be used for the diagnostic confirmation of all forms of Leprosy. Skin biopsy is indicated for the confirmation of different forms of Leprosy and histopathological findings must be correlated with clinical findings.[22]

Histopathology of oral leprosy lesions

The Histopathology of Oral Leprosy lesions may show various features including the presence of granulomas and acid-alcohol-resistant bacilli, perivascular lymphomononuclear, and lymphoplasmacytic inflammatory infiltrate.[23] The clinical lesions of leprosy with papules, nodules, and ulcers generally show the histopathology of inflammatory infiltrates and acid-alcohol-resistant bacilli.[12],[23] Other histopathological features include epithelial atrophy, intense infiltration of macrophages, absence of Grenz zone separating the epidermis and the infiltrate, lymphocytes, and plasma cells, hyperkeratosis, vascular congestion, and fibrosis.[5],[12]


The treatment of Leprosy is multiple drug therapy which includes dapsone, rifampicin, and clofazimine.[22] The single drug is not advised for leprosy treatment due to the resistance of the drug to M. leprae.

World Health Organization 2018 advised the treatment of multibacillary leprosy patients with a combination of 600 mg of rifampin once per month, 300 mg of clofazimine once per month, and daily doses of clofazimine (50 mg) and dapsone (100 mg) for a period of 1 year.[24] The treatment of paucibacillary leprosy patients is a 600 mg dose of rifampin once per month and daily 100 mg doses of dapsone for 6 months.[24]

Treatment of Oral manifestations of Leprosy patients starts with multiple drug therapy and symptomatic relief could be given. In the initial stages of the disease, treatment should be given to.

Leprosy patients so that the disease should not get progressed to an advanced stage. Appropriate antimicrobial treatment may prevent the oral manifestations of the disease. Patients with Leprosy should be advised to maintain oral hygiene to decrease the progression of the disease. Treatment of dental infectious is required to reduce the recurrence and spread of Leprosy disease. Necessary precautions should include masks, gloves, and proper sterilization to prevent Leprosy disease. The oral lesions of Leprosy patients are generally reversible but must be discussed with the Leprologist in order to decrease the spread of Leprosy disease.

Reactions of leprosy

Leprosy reactions occur during the disease, especially after the start of treatment. These reactions are complications of treatment and can occur during the disease. Leprosy reactions are types of Type 1 reaction (Reversal reaction) and Type II reaction (Erythema nodosum leprosum).[25]

Type 1 reaction

These reactions have increased cellular immune response due to which CD4+ T cells of Th1 pattern are predominant. These lesions have increased the proliferation of IL-1, TNF-α, IL-2, and IFN-γ.[26] They are mostly associated with Borderline Leprosy.[27] Treating these patients will result in a decrease in the bacterial count, and they show the clinical features of tuberculoid leprosy. The untreated patients will have an increase in the bacterial count, and they show the clinical features of lepromatous leprosy.[1] The clinical feature includes erythematous plaques on the face, trunk with well-defined edges, hypochromic macules, edema of the face, nasal and labial mucosa extremities, thickening of the nerve sheath, neuritis, and associated pain.[28]

Treatment of Type I reaction

Corticosteroids are the first line of treatment for Type I reactions.[1] They help in the reduction of edema, decreasing the cellular immune response which decreases the inflammatory changes in the skin and nerves. Corticosteroids can be given in borderline leprosy patients for about 6 months and the most preferred drug is prednisolone.[29] Immunosuppressants can be combined with corticosteroids for the improvement of Type I reactions.[30] Immunosuppressants included for the treatment of Type I reactions include azathioprine and cyclosporine A.[30]

Type II reaction

These reactions occur mostly in patients with lepromatous leprosy.[27] These are immune-mediated diseases that are associated with skin lesions as well as systemic illnesses. The immune-mediated inflammatory reaction will result in an increase in IL-6, TNF-α IL-8, transforming growth factor-β, and IL-10.[15] CD8+ T cells of Th2 patterns are predominant in these reactions. Symmetrical inflammatory subcutaneous nodules are seen with systemic involvement in fever, malaise, lymph node enlargement, edema, and arthralgia.[1] The skin lesions can get ulcerated and necrotic in these reactions. Other areas that can be involved are the eyes, nerves, and joints.

Treatment of Type II reaction

Mild cases of erythema nodosum leprosum are treated with non-steroidal anti-inflammatory drugs. Moderate-to-severe cases of erythema nodosum leprosum is treated with prednisolone and thalidomide.[31] Other drugs which showed positive results include clofazimine, methotrexate, and azathioprine.


Early detection and treatment will help in decreasing the spread of leprosy. Oral and nasal routes are the route of transmission of M. leprae. Oral medicine specialists and dermatologists should be aware of the oral manifestations of leprosy so that the oral lesions could be managed at the early stage. Leprosy patients reporting to dermatologists should be asked for the oral lesions and should be referred for an examination of the oral cavity by an oral medicine specialist. The diagnosed cases of leprosy patients should be made aware of the oral manifestations of this disease so that appropriate dental intervention can be provided to them.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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