A 23-year-old girl reported to the department of oral medicine and radiology with progressive, nonpainful swelling of the gingiva on the labial aspect of the upper and lower anterior teeth with 6 months' duration. There was a history of evening rise in temperature and weakness over the last 3 months. The patient also had a loss of appetite over the last 4 months and a weight loss of about 4.5 kg during the last 8 months. There were no systemic problems, no cough with expectoration and no history of dental trauma or surgery in the affected area. Extraoral examination revealed no cervical lymphadenopathy. Intraoral examination revealed diffuse enlargement of the upper and lower gingiva on the labial surface of anterior maxillary and mandibular teeth []. On palpation, the swelling was slightly tender and firm. The rest of the OC was normal except for the few deep carious teeth. Differential diagnoses were enlargement due to drugs, infection and hematologic malignancy. The possibility of drug-induced enlargement was ruled out based on medical history. The biochemical tests were within normal limits, except for a marginal rise in leukocyte count (13 × 10 9/L) and an elevated ESR of 56 mm/h (Westergren method), which ruled out leukemia-associated enlargement and raised the possibility of one of the common causes of high ESR, TB. An incisional biopsy was carried out under LA in relation to the gingiva of the mandibular right central incisor, in collaboration with the department of periodontics and implantology. Histopathological examination was carried out that revealed clusters of epithelioid cells surrounded by a chronic inflammatory type of infiltrate. There was no evidence of caseating necrosis, but numerous Langhans giant cells were visible in the clusters of epithelioid cells suggestive of a “hard tubercle” [Figure and ]. To eliminate the possibility of localized granulomatous changes superimposed on an area of gingival enlargement, incisional biopsy was repeated in the remaining three quadrants. Histopathology showed similar granulomatous changes in all tissue specimens examined. The tuberculin (Mantoux) test was positive, suggesting tubercular infection. Chest radiography (posteroanterior view) revealed no abnormalities []. A computed tomography scan of the head and neck region was also performed to determine the status of the underlying maxilla and mandible. The scan did not reveal any bone abnormalities. A culture of the sputum, obtained by forceful coughing, was negative for M. tuberculosis. Special staining of formalin-fixed, paraffin-embedded tissue specimens for Mycobacteria, i.e., Ziehl–Neelsen and auramine–rhodamine stain, was negative. An immunologic test to detect antibodies against Mycobacterium in the patient's serum (ELISA) was positive. Polymerase chain reaction (PCR) assay was also carried out using six 5-μm sections of paraffin-embedded tissue to identify specific sequences of M. tuberculosis complex, with adequate controls. The DNA was used as an amplifying target for the sequence IS-6110, which is specific for M. tuberculosis. Positive PCR results confirmed the presence of M. tuberculosis in the tissue samples. In view of these findings, a final diagnosis of primary tuberculous gingival enlargement was made. In consultation with the patients' physicians, antitubercular therapy (ATT) was initiated. During this period, the patient was instructed not to undergo any ultrasonic scaling and polishing or surgical procedure within the OC and was warned about the chance of transmitting the disease to others via aerosol and salivary contamination. After completion of a 6-month regimen of basic periodontal therapy, which included scaling and root planning, oral hygiene instructions were instituted under CDC-issued guidelines. This resulted in significant regression of the enlarged gingivae in both the arches. Gingivectomy and gingivoplasty were performed to shape and contour the residual enlargement under universal aseptic conditions []. No recurrence of lesion occurred during 1-year follow-up [].
This 47-year-old male presented with a non-healing tongue ulcer of 3 months’ duration and associated pain for 2 months. He had initially noticed the asymptomatic ulcer on the ventral surface of tongue which had been increasing in size for the last 1 month. He had smoked beedis for the last 20 years and had consumed alcohol daily for past 15 years. On examination, ulcers were noticed in the tongue and buccal mucosa. A solitary ulcer (3 cm × 4 cm) with undermined edges and minimal induration was seen on right ventral surface of the tongue extending from the midline past the lateral border, up to the dorsal area of the anterior two-thirds of the tongue []. The area adjacent to the tongue ulcer appeared to be lobulated. Another ulcer (0.5 cm × 0.5 cm), also with an undermined edge was seen on the dorsal surface of tongue. In the left buccal mucosa, a single ulcer (1 × 1 cm2) covered with pseudomembrane was present, extending 3 cm from the angle of the mouth and 5 mm below the occlusal plane []. The patient was not aware of this ulcer. A single firm, non-tender (<1 cm) sub-mandibular lymph node was present on the right side.\nProvisional diagnoses of squamous cell carcinoma and lichen planus were given for the lesions of the tongue and buccal mucosa, respectively. Incisional biopsy from the edge of tongue ulcer revealed proliferating epithelium with the underlying connective tissue exhibiting chronic inflammatory cell infiltrate without evidence of epithelial dysplasia or malignant invasion. Biopsy was repeated from a different area of the tongue ulcer for further review. On examining serial sections, giant cells with peripherally arranged nucleus resembling Langerhans cells were appreciated along with caseous necrosis []. Chest radiography revealed bilateral upper lobe infiltrates [], and sputum was positive for acid-fast bacilli. HIV was negative. With anti-tuberculous therapy the lesions began to heal on a follow-up visit a month later. He was referred to local primary health care center for continuation of therapy.