ABSTRACT
Jaw actinomycosis is a quite rare invasive facultative bacterial infection caused by Actinomyces, Gram-positive filamentous bacilli found in human commensal. A break in continuity of epithelium due to surgery, trauma or previous infection can lead to deeper invasion of bacteria causing infection. The risk factors for actinomycosis are trauma, caries, debilitation, and poorly controlled diabetes mellitus. Clinical presentation can mimic other pathologies, such as fungal infection tuberculosis, granulomatous diseases, so the diagnosis of actinomycosis is delayed or misdiagnosed. For the definitive diagnosis of jaw actinomycosis, medical history, dental history histopathological examinations and microbiological culture are important parameters. Actinomycotic bacteria are sensitive to antibacterial agents hence chemotherapeutic agents are used for treatment. This report presents case series of jaw actinomycosis involving mandible and maxilla. The final diagnosis was supported by histopathology.
ABSTRACT
Basal cell adenoma (BCA) is a rare basaloid tumor, with only 20% of cases occurring in minor salivary glands. Histologically, BCA is characterized by the presence of basaloid cells and may frequently be mistaken with canalicular adenoma, basal cell adenocarcinoma, adenoid cystic carcinoma and basaloid squamous cell carcinoma. Immunohistochemistry may aid in arriving at a final diagnosis as in the present case. Reported here is a case of locally aggressive BCA. Histologically, the lesion mimicked ameloblastoma and other entities which posed a diagnostic challenge. There are no reports of BCA presenting as an aggressive lesion available in English literature so far; moreover, merely a single case of BCA of maxillary sinus has been previously reported to the best of our cognition. This case report highlights the rarity of this tumor with regards to its site of origin, clinical behavior and histopathological mimics.
ABSTRACT
Oral lichen planus (OLP) is a T cell-mediated chronic inflammatory disease with a varied clinical presentation. The present clinical study was carried out to clarify the demographic and clinical profile of 108 patients with OLP. The patients were identified based on the diagnostic criteria proposed by van der Meij et al. (2003) modified from the WHO (1978) clinical and histopathologic definition of OLP. Information such as age, gender, clinical presentation and type of OLP, site of involvement, symptoms, extraoral involvement, history of systemic disease, familial occurrence and risk factors like chewing and smoking tobacco, chewing betel quid, alcohol consumption were obtained. Mean age of OLP patients was 45.4 years, and among the identified patients, 70.4% were females. The most frequent clinical type was the reticular form (80.6%). The OLP lesions were symptomatic in 77.8% of the patients. The buccal mucosa was the most affected site (87.9%) and multiple oral lesions were observed in 41.7% of the patients. Among the OLP patients, 36.1% and 4.7% reported chewing tobacco and smoking tobacco, respectively. Histopathologically, epithelial dysplasia was seen in two cases. The chronic nature of OLP warrants patient education, psychological support and long-term follow up. (J Oral Sci 58, 43-47, 2016).
Subject(s)
Lichen Planus, Oral/pathology , Adolescent , Adult , Female , Humans , Male , Middle Aged , Young AdultABSTRACT
INTRODUCTION: Cleidocranial dysplasia (CCD) is characterized by aplasia or hypoplasia of the clavicles, characteristic craniofacial malformations, and the presence of numerous supernumerary and unerupted teeth. It affects bones derived from both intra-membranous and endochondral ossification. Incidence has been reported as 1 in 10,00,000. It is caused by mutation in the gene encoding transcription factor Core Binding Factor Subunit Alpha l (CBFAl) or Runt related transcription factor 2 (RUNX2). CASE REPORT: This presentation discusses the clinical and radiographic features of a familial case of cleidocranial dysplasia occurring in a father and a child. All the clinical and radiographic features, except that of the chest x-ray, were more prominent in the child than the father. This supports the fact that CCD is transmitted by an autosomal-dominant mode of inheritance with high penetrance and variable expressivity. It is sporadic in about 40% of cases. Each child of an individual with CCD has a 50% chance of in heriting the mutation. CONCLUSION: Diagnosis is mostly made on the basis of clinical and radiographic features. Molecular genetic testing such as sequence analysis or deletion analysis can be used in cleidocranial dysplasia. Some cases are diagnosed through incidental findings by physicians, treating patients for unrelated conditions. Treatment of these patients requires a multidisciplinary approach which includes orthopaedic and dental corrections along with management of any complications of cleidocranial dysplasia.
