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Year : 2022  |  Volume : 16  |  Issue : 1  |  Page : 12-18

Analysis of cell cycle activity by expression of p-53 protein in different gingival overgrowths: An immunohistochemistry-based pilot study

Department of Periodontology, Army Dental Centre, Research and Referral, New Delhi, India

Correspondence Address:
Sunny Bhatia
Department of Periodontology, Army Dental Centre, Research and Referral, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jodd.jodd_3_21

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Context: It is a crucial protein expressed in cells to prevent tumor formation. Hence, the study of expression of p-53 protein is of high importance in gingival cells in various conditions such as drug-induced gingival enlargement and nondrug-induced gingival enlargements. Aims: This study aimed to analyze the cell cycle activity for the p-53 protein expression in the cells of drug-induced and nondrug-induced gingival overgrowths as compared to healthy subjects. Settings and Design: This was a single-blinded observational pilot study. Subjects and Methods: Patients were included on the basis of various inclusion and exclusion criteria and divided into three groups. Inclusion Criteria:
  1. Group A (patients with drug-induced gingival overgrowth)
    • Patients on drugs such as anticonvulsant, immunosuppressants, and calcium channel blockers ≥6 months.
  2. 2. Group B (patients with nondrug induced gingival overgrowth)
    • Patients not on drugs such as anticonvulsants, immunosuppressants, and calcium channel blockers ≥1 year.
  3. Group C (healthy subjects)
Exclusion Criteria: Patients on antibiotics and edentulous patients. Protocol:
  • Gingival samples were collected after obtaining consent from patients and were stored in 10% formalin
  • The samples were blinded and the assay for the expression of p-53 was done by immunohistochemistry along with histopathological examination.
Statistical Analysis Used: Statistical analysis was conducted by using SYSTAT-13 software. Results: Expression of p-53 protein in each group was analyzed after preparing slides for immunohistochemistry examination. A total of 10 samples were analyzed in each group to check for the expression of p-53 protein in basal as well as suprabasal cell layers. Each sample was then correlated with the corresponding slides for histopathological examination of each sample for each group. Conclusions: The p-53 protein expression in the hyperplastic gingival epithelia noted in our present study suggests that gingival hyperplasia induced by drugs or by inflammation has possible implications for pathogenesis accompanied with impaired DNA. On the other hand, our study also suggests that the growth arrest takes place in the representative rete pegs deeply elongated into lamina propria of hyperplastic gingival tissues, which contributes to the inhibition of DNA damaged cell expansion within gingival tissues followed by promoting the tumorigenic aberrations of gingival hyperplasia.

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