Year : 2006 | Volume
: 17 | Issue : 1 | Page : 41--44
Primary oral tuberculosis : Report of two cases
Jagadish Ebenezer1, Rekha Samuel2, George C Mathew1, Santosh Koshy1, Rabin K Chacko1, Mary V Jesudason3,
1 Dept of Dental and Oral Surgery, Christian Medical College, Vellore, Tamilnadu, India
2 Dept of General Pathology, Christian Medical College, Vellore, Tamilnadu, India
3 Dept of Microbiology, Christian Medical College, Vellore, Tamilnadu, India
Dept of Dental and Oral Surgery, Christian Medical College, Vellore, Tamilnadu
Oral lesions of tuberculosis though uncommon, are seen in both the primary and secondary stages of the disease. In secondary tuberculosis, the oral manifestations may be accompanied by lesions in the lungs, lymph nodes, or in any other part of the body and can be detected by a systemic examination. Primary oral tuberculosis may present as a diagnostic challenge for the clinician. Here we report two patients with primary tuberculosis in the oral cavity who presented to the dental department, were diagnosed and referred for medical management.
|How to cite this article:|
Ebenezer J, Samuel R, Mathew GC, Koshy S, Chacko RK, Jesudason MV. Primary oral tuberculosis : Report of two cases.Indian J Dent Res 2006;17:41-44
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Ebenezer J, Samuel R, Mathew GC, Koshy S, Chacko RK, Jesudason MV. Primary oral tuberculosis : Report of two cases. Indian J Dent Res [serial online] 2006 [cited 2021 Nov 29 ];17:41-44
Available from: https://www.ijdr.in/text.asp?2006/17/1/41/29893
Tuberculosis is a chronic granulornatous disease that can affect various systems of the body. In humans the disease is caused by Mycobacterium tuberculosis, Mycobacterium bovis and atypical Mycobacteria.
Pulmonary tuberculosis is the most common form of the disease. However, tuberculosis can also occur in the lymph nodes, meninges, kidneys, bone, skin and in the oral cavity . Most people make their first contact with the disease by inhalation of the bacilli through dust or droplets.. This initial infection often causes small parenchymatous lesions in the lungs, draining lymphatics and in the lymph nodes. These three components together form the primary complex of tuberculosis . The primary lesions in the lungs may heal by fibrosis and calcification or if the immune response is poor, may spread through the lymphatics or blood vessels to cause disseminated, miliary tuberculosis which may become life threatening. Sometimes the primary infection can heal as a result of treatment or due to the development of spontaneous resistance. However, even after clinical healing, the bacilli can remain dormant for several years and reactivate at an opportune moment. Primary infection can also affect the pharynx, cervical lymph nodes, intestine or oral mucosa.
The other type of this disease is known as secondary tuberculosis which occurs from a healed primary focus or due to endogenous spread ofthe infection. Secondary tuberculosis is usually chronic in nature and can cause considerable destruction of the involved tissue with caseation, cavity formation and/or fibrosis.
Both primary and secondary types of tuberculosis can cause lesions in the oral cavity. In secondary tuberculosis, lesions of the oral cavity may accompany lesions in the pharynx, lungs, lymph nodes or skin. When oral lesions of tuberculosis are the sole manifestations of the disease, the clinician may face a diagnostic challenge. This paper reports two patients with primary oral tuberculosis, who after diagnosis, were referred for the appropriate medical management.
CASE REPORT: 1
A 40 year old man presented to the department of dental and oral surgery complaining of an ulcer in the mouth which had been present for the last two months and was gradually increasing in size [Figure 1]. He did not have any systemic complaints, was not on any medications and had no history of any allergy. He was a chronic smoker and was unable to give up the habit. Physical examination did not reveal any extra oral abnormality. His left submandibular lymph nodes were enlarged, mobile and non tender to palpation.
Intraorally, his oral hygiene was graded as poor with generalized mobility of all teeth and moderate deposits of stains present throughout the dentition. Almost all of his teeth had some degree of attrition and some of his teeth were clinically missing. Soft tissue examination revealed a single discrete ulcer of less than 1 cm in diameter present on the left buccal mucosa. The ulcer was bordered by well defined margins around which were several small nodular swellings. On palpation, the ulcer was tender with indurated margins. The other mucosal surfaces in the mouth were normal. Panoramic radiographs did not reveal any abnormality in the maxillofacial region.
A complete general examination revealed no other contributory abnormalities. Correlating these features of a chronic ulcer of two months duration with an associated history of smoking and involvement of the sub mandibular lymph nodes, a differential diagnosis of malignant neoplasm, tuberculosis and mycoticulcer was arrived at.
The diagnostic workup included serum analysis for human immunodeficiency virus which turned out to be non reactive. Cultures for acid fast bacilli and fungi were negative. An incisional biopsy of the oral ulcer was done and the specimen was sent for histopathological examination. The histopathology showed multiple confluent and discrete granulomas composed of epithelioid histiocytes and Langhans giant cells with central caseous necrosis [Figure 2] confirming the diagnosis of tuberculosis. Following the biopsy report, a chest radiograph and a routine medical consultation were requested both of which turned out negative results. AFB tissue culture and smear were positive for M. tuberculosis [Figure 3]. The patient was then referred to the Department of Internal Medicine where he was started on anti tuberculosis therapy.
Six months later at follow up, the oral ulcer had healed.
CASE REPORT: 2
A 7 year old girl was referred to the Department of Dental and Oral Surgery for evaluation of a chronic painful ulcer in the mouth. History obtained from the parent revealed that the oral ulcer was present in the left lower gingiva since the last one month. The child had difficulty in eating and brushing her teeth. Her family history disclosed that one of her maternal aunts had been diagnosed with pulmonary tuberculosis and was on treatment.
On extra oral examination, multiple cervical lymph nodes and the left submandibula group of lymph nodes were enlarged and tender. Intra orally, her oral hygiene was fair and she was in the mixed dentition stage. A large irregular ulcer was present in the lower left gingiva involving the labial and the lingual aspects in relation to 31,72 and 73. The ulcer had extended to the labial vestibule, had a granular surface and was tender. The margins were well defined [Figure 4]. There was no other abnormality elsewhere within the oral cavity. Intra oral radiographs revealed unerupted 32 and 33. There was no radiographic evidence of involvement of the underlying bone. A complete general examination did not yield any significant findings. The differential diagnosis included tuberculosis and autoimmune disorder.
Laboratory investigations which included evaluation of immunoglobulins were found to be within normal limits. Serno analysis for HIV was negative. The ESR was 92mm at 1 hr. A chest radiograph showed increased vascular markings with no infiltrates or mediastinal adenopathy. An incisional biopsy of the ulcer was then done under general anaesthesia along with excision of the left submandibular lymph node and the specimens were sent for histopathological analysis.
Tissue samples were also sent for AFB culture and smear and returned positive for M.tuberculosis.The histopathology of the oral mucosal biopsy showed epithelioid granulomas (x 200)-[Figure 5]. Biopsy of the submandibular lymph node showed multiple confluent and discrete necrotizing granulomas (x 200)-[Figure 6]. The reports were confirmatory for tuberculosis.
The child was then referred back to the Department of Child Health where she was started on anti tuberculosis therapy.
Although tuberculosis has a definite affinity for the lungs, it can affect any part ofthe body including the mouth. Oral manifestations of tuberculosis are usually seen secondary to infection in some other part of the body. Studies of Farber et al  indicated that less than 0.1% of tuberculosis patients whom they examined exhibited oral lesions. According to Tiecke , the prevalence of oral manifestations in patients with pulmonary tuberculosis ranges from 0.8% -3.5%. Occasionally the recognition of an oral tuberculous lesion precedes the detection of pulmonary tuberculosis.
Compared with tuberculous involvement of other parts of the body, the primary occurrence of this disease in the oral cavity and jaw bones is relatively rare. Oral lesions of tuberculosis are non specific in their clinical presentation and are often overlooked by the clinician. Although the pathogenesis of oral involvement is not definitely established, it appears most likely that the organisms gain entry into the mucosal tissue through a break in the surface The probable importance of an intact mucosal epithelium in providing protection against the infection has support from the observation of Abbot et al  who were able to isolate the tubercle bacilli from mouth washings of 44.9 % of the patients with active pulmonary lesions. When the primary lesions of tuberculosis occur in the mouth, the most frequent sites of involvement are gingiva, tooth extraction sockets and the buccal folds.
The systemic factors that favour the chances of oral infection in tuberculosis includes lowered host resistance  and increased virulence of the organisms. The local predisposing factors may be poor oral hygiene , local trauma , the presence of existing lesions like leucoplakia , periapical granulomas, dental cysts, dental abscess, jaw fractures and periodontitis.
The common manifestation of oral tuberculosis is an ulcerative lesion of the mucosa. The lesion may be preceded by an opalescent vesicle or nodule which may break down as a result of caseation necrosis to form an ulcer. The typical tuberculous ulcer is an irregular lesion with ragged undermined edges, minimal induration and often with a yellowish granular base. Tiny single or multiple nodules called 'sentinel tubercles' may also be seen surrounding the ulcer. On the tongue, the common sites for atuberculous ulcer are the lateral border, tip, anterior dorsum and the ventral surface. The tongue lesions are usually painful, greyish-yellow, firm and well demarcated. The palatal lesions of tuberculosis may be seen as granulomas  or ulcerations  and are usually more common in the hard palate than in the soft palate. The gingival lesions may present as exuberant and granulating or as mucosal erosions. Sometimes these lesions may be seen simultaneously with marginal periodontitis .
Involvement of the maxilla and mandible usually results in tuberculous osteomyelitis. Tuberculosis of the jaw bones may be secondary or primary and occurs as a result of either deep extension of the gingival lesion, from an infected post-extraction socket or through hematogenous spread of the infection. The mandible shows a greater predisposition to the infection than the maxilla In a study conducted by Chapotel, fifty cases of tuberculous osteomyelitis involved the lower j aw bone.
Tuberculous lesions of the oral cavity can assume a non specific clinical appearance. If the mucosais involved, the lesions may present as ulcerations, nodules, fissures, plaques, granulomas and vemicous proliferations. When the jaw bones are involved, the disease presents features of chronic osteomyelitis. Primary lesions of tuberculosis manifest in the oral cavity as non healing chronic ulcers. When diagnosing such lesions with non healing tendency, tuberculosis should be considered in the differential diagnosis. In this assessment, a complete physical examination should also be included, with diagnostic tests such as chest radiographs, biopsy specimens for histological studies and culture of the organism. An early diagnosis with prompt treatment will usually result in a complete cure.
Note: The authors would like to thank Dr. Don K. Abraham for his technical expertise.
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