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Background: Ameloblastoma among benign tumors holds a unique position by its locally destructive and invasive nature. Tumors that originate from the odontogenic apparatus or its remnants in the jaws show diverse clinical presentations, behavior and histologic patterns. The differed biological behavior behind follicular and plexiform ameloblastomas has never attained completeness because of the lack of rhythmic correlation regarding the exact mechanism. Nuclear factor-kappa B (NF-κB) pathways play a crucial role in survival, death and differentiation during physiologic and pathologic conditions. With this background, the study has been aimed to investigate the expression of NF-κB in follicular and plexiform ameloblastomas. Objective: The objective of this study was to analyze the immunohistochemical expression pattern of NF-κB in ameloblastoma and to compare the immunohistochemical expression pattern of NF-κB among the histological types of ameloblastoma, follicular and plexiform patterns. Methodology: Total 20 ameloblastomas (10 follicular, 10 plexiform) were immunostained with antihuman NF-κB p65 mouse IgG monoclonal antibody, and the pattern of staining is statistically analyzed using Chi-square test with the level of significance (P < 0.05). Results: Twelve (3 follicular, 9 plexiform) out of 20 ameloblastomas showed immunoreactivity to NF-κB p65. In ameloblastoma, only the peripheral preameloblast-like tall columnar cells showed reactivity, whereas the stellate reticulum-like cells are immunonegative. The staining pattern was membranous in the immunoreactive cells. The results were studied with the associated and inducing pathways from the literature, and a possible mechanism has been proposed. Conclusion: The expression pattern of NF-κB was found to be higher in plexiform ameloblastoma than follicular ameloblastoma.

Background: Ameloblastoma is the second most common odontogenic tumor that holds a unique position among benign tumors due to its locally destructive and invasive nature. The differed tumor biology behind follicular and plexiform ameloblastoma is always an enigma. Nerve growth factor (NGF), a neurotrophin that plays a major role during odontogenesis, could also possibly play a role in the pathogenesis of odontogenic tumors such as ameloblastoma. With this background, the study was aimed to investigate the expression of NGF in follicular and plexiform ameloblastoma. Objectives: The objectives of this study were to analyze the immunohistochemical expression pattern of NGF in ameloblastoma and to compare the immunohistochemical expression pattern of NGF among the follicular and plexiform histological types of ameloblastoma. Materials and Methods: Forty histological sections of ameloblastomas (20 follicular and 20 plexiform) were stained immunohistochemically with anti-human NGF mouse IgG monoclonal antibody and the staining was analyzed statistically. Results: Almost all the 40 ameloblastoma samples (20 follicular and 20 plexiform) showed positive immunoreactivity to NGF. Both peripheral pre-ameloblast-like tall columnar cells and central stellate-reticulum-like cells showed positive reactivity. The pattern of staining was membranous in the immunoreactive cells. The χ2 value for the immunoexpression between follicular and plexiform ameloblastoma was statistically significant with a P value

Cells of the human biological system emerge from various concerted processes of cell growth, differentiation, repair, and regeneration to a degree. Neurotrophins (NTs) and Neurotrophin Receptors (NTRs) have robust effects on proliferation, differentiation, migration, survival, and synapse formation through physiologic regulatory signals. Dysregulation of such neurotrophic factors not only results in various age-related degenerative conditions but also paves the way to oncogenesis in neuronal and non-neuronal tissues. This review aims to highlight the emerging role of neurotrophins (NTs) and Neurotrophin Receptors (NTRs) in Oral Health and Disease and its molecular signaling pathway in physiologic and pathologic conditions. The electronic databases PubMed, MEDLINE, Scopus, and Google Scholar were searched for available data in the present review. A database search yielded more than 100 articles out of which 45 were included based on the core data. The role of NTs and NTRs in dental diseases is less explored and this was the very first attempt to collect the literature data of NTs and NTRs pertaining to head and neck tumors. The results and subsequent conclusions were extracted and reviewed. Expression of NTs and NTRs in neuronal and non-neuronal tissue is a spatial and time-bound event like odontogenesis. Recently NTs and NTRs expressions were detected in a few head and neck tumors. Unraveling the molecular signaling pathway of NTs and NTRs in head and neck tumors will help in elucidating the molecular pathogenesis and the prognosis, therefore, paving a path to expand our knowledge to understand and develop therapies for many pathologic conditions.

Objectives: The objective is to analyze the immunohistochemical expression pattern of tyrosine kinase receptor (TrK) in ameloblastoma and to compare the immunohistochemical expression pattern of TrK among the histological types of ameloblastoma, follicular and plexiform patterns. Materials and Methods: Forty ameloblastomas (20 follicular and 20 plexiform) were immunostained with anti-human TrK mouse IgG monoclonal antibody, and the pattern of staining is statistically analyzed. Results: Total 20 (4 follicular and 16 plexiform) out of 40 ameloblastomas showed immunoreactivity to TrK. Only the peripheral preameloblast like tall columnar cells showed reactivity, whereas the stellate reticulum like cells is immunonegative. The staining pattern was membranous in the immunoreactive cells. The Chi-square value for the immunoexpression between follicular and plexiform ameloblastoma was statistically significant with a P < 0.005. The results were studied with the downstream pathways from the literature, and a possible mechanism has been proposed. Conclusion: The expression pattern of TrK is found to be more in plexiform ameloblastoma than follicular ameloblastoma.