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Aim To present a brief overview of etiopathogenesis, nomenclature, and treatment modality for a case of nonsyndromic bilateral cysts in the mandible. Background Odontogenic cysts, though comprise a distinct group of lesions have on and off posed challenges in etiopathogenesis and nomenclature. The prima facia role of development/inflammation in the buildup of fluid between the reduced enamel epithelium attached at the cementoenamel junction and the enamel in the pathogenesis of dentigerous cysts has long been discussed. Along with this, the spread of inflammatory exudate from an overlying primary tooth could also be the source of an inflammatory dentigerous cyst. Case description Bilateral swellings in a 12-year-old patient presented with a chief complaint of pain in the lower jaw for 4 months. The radiographic picture exhibited unilocular, well-circumscribed radiolucent areas extending from 34 to 37 on the left side and from 44 to 47 on the right side of the mandible and involving retained mandibular second premolars on both sides. Conclusion Mere expansion of a follicle due to inflammation from an overlying infected/necrosed/treated primary tooth in which the reduced enamel epithelium does not appear to be attached at the cementoenamel junction should be aptly referred to as an "inflammatory follicular cyst". Clinical significance The present article attempts to illuminate the notable differences between dentigerous cysts and inflammatory follicular cysts of jaws which requires an adequate distinction in pediatric cases for diagnostic and management considerations. How to cite this article Sethi A, Shetty DC, Tandon A, et al. Bilateral Nonsyndromic Cystic Lesions Involving Impacted Teeth: Nomenclature and Diagnostic Protocol. Int J Clin Pediatr Dent 2020;13(4):429-432.

Background The present study determines to correlate eosinophil, mast cell and microvessel densities with the histopathological grades and clinical staging of Oral Squamous Cell Carcinoma (OSCC) cases, as the potential role of inflammatory mediators within tumor stroma remains debatable. Methods The study sample comprised 60 cases consisting of 40 cases of Well to moderately differentiated OSCC (group 1) and 20 cases of poorly differentiated OSCC (group 2). Immunohistochemistry with anti-CD15 antibody and antifactor VIII antibody; and toluidine blue special stain were employed for the detection of eosinophils, microvessels, and mast cells, respectively. Results The mean numbers of eosinophils, mast cells, and microvessels per high power field in group 1 and group 2 were 15.37±11.86 and 12.62±14.30, 6.00±4.84 and 4.51±4.51, 13.96±6.25 and 6.62±2.05, respectively. Eosinophil density had a positive correlation with both mast cell and microvessel density. Also, the correlation of primary tumor size (T status) with microvessel density was found to be statistically significant (P≤0.05). Conclusions The cohesive interpretation of the aforementioned mediators in OSCC suggested that while these variables correlate well with the differentiation of tumor, the quantification did not correlate with the clinical staging of the disease.

Head and neck connective tissue lesions may have diverse calcifications within the fibrous connective tissue stroma. The perplexity involved in the identification and determination of the nature or degree of calcification through routine hematoxylin and eosin (HE) stains necessitates the usage of a specific, simple, and cost- and time-effective differential staining techniques. The aim of the present study was to develop criteria to distinguish bone formation from bone resorption using methylene blue-acid fuchsin (MB/AF) stain and the role of collagen fibers in the identification of stromal calcifications using polarizing microscopy with picrosirius red stain. Twenty cases with pathological diagnoses for various stromal calcifications in maxillofacial lesions were retrieved from the departmental archives. Decalcified formalin fixed paraffin embedded tissue sections were stained with hematoxylin and eosin, Masson's trichrome (MT), methylene blue-acid fuchsin (MB/AF), and picrosirius red. The stained sections were assessed to identify the calcifications found in the surrounding connective tissue stroma. It was observed that most cases showed maximum staining intensity with MB/AF stain as compared to the other staining methods. Moreover, the results suggested that contrast between calcification and stromal soft tissue was best distinguished with the MB/AF stain except in the case of dystrophic calcifications. Along with this, polarizing microscopy with picrosirius red enables better characterization of stromal components. Although the HE stain and a connective tissue stain i.e. Masson's trichrome, are employed routinely in histopathology; the use of special stains such as MB-AF and picrosirius red facilitates the identification of calcifications from the stromal tissues.

Aim The aim of the present study was to correlate the immunoexpression of alpha-smooth muscle actin (α-SMA) for myofibroblasts with the serum levels of transforming growth factor-β1 (TGF-β1) in oral submucous fibrosis (OSMF). Methods A total of 100 cases of histopathologically confirmed OSMF were assessed for α-SMA expression. Clinical data, such as age, sex, mouth opening, and habit history, were obtained for each case. Serum TGF-β1 levels were recorded in 73 patients with the help of enzymelinked immunosorbent assay technique. Results The staining index of α-SMA increased concomitantly with higher myofibroblast count in the increasing histopathological grades of OSMF (P ≤ .05). Serum TGF-β1 levels were highest in the intermediate grades of OSMF. Clinical parameters, such as mouth opening, cheek flexibility, and tongue protrusion, showed a direct correlation with increasing clinical grades of OSMF. Conclusions The progressive increase in myofibroblasts from early to advanced stages suggests their potential use as markers for evaluating the severity of OSMF. Additionally, as myofibroblasts are responsible for producing a variety of factors that are involved in the fibrotic processes; they could be the key link in the pathogenesis of OSMF. Interruption of their development, recruitment, or activation could provide a unique therapeutic target for future treatment options in patients with OSMF.