Abstract
Background: Although periodontal bacteria are the causative agents of periodontitis, subsequent progression and disease severity are thought to be determined by a host's immune responses. HSPs may be expressed during periodontal diseases.
 Objective: To compare the HSP 70 expression within layers of epithelium and connective tissue and correlate the expression of HSP 70 with the severity of periodontal disease.
 Materials & Methods: The study population comprised of 25 patients with periodontitis, and 23 patients with gingivitis and 21 controls with healthy gingival; tissue samples collected from the Department of Periodontology /Oral and Maxillofacial Surgery respectively. An immunohistochemical analysis was done for HSP 70 expression.
 Results: One way ANOVA results indicate a statistically significant expression in basal layer for mild inflammation (mean=2.36) and intensity in stratum spinosum for mild (mean=2.27) and minimum (mean=2.39) inflammation. An overall greater HSP 70 expression is noticed in periodontitis group (total IRIDI = 25.41) however not statistically significant
 Conclusion: We elucidated that there was significant HSP 70 expression in stratum basale and spinosum for mild inflammation that did not increase with severity of inflammation. The overall expression of HSP70 is insignificantly elevated in periodontitis compared to health & gingivitis.
 Statistical analysis used: One way Analysis of Variance (ANOVA), Mann Whitney U test and Kruskal Wallis Test.
 Keywords: Heat shock protein 70 (HSP 70), Immunohistochemistry (IHC), Porphyromonas gingivalis.
Highlights
Periodontitis is defined as “an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both[1]
Materials & Methods: The study population comprised of 25 patients with periodontitis, and 23 patients with gingivitis and 21 controls with healthy gingival; tissue samples collected from the Department of Periodontology /Oral and Maxillofacial Surgery respectively
An overall greater heat-shock proteins (HSPs) 70 expression is noticed in periodontitis group not statistically significant Conclusion: We elucidated that there was significant Heat shock protein 70 (HSP 70) expression in stratum basale and spinosum for mild inflammation that did not increase with severity of inflammation
Summary
Periodontitis is defined as “an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both[1]. Heat shock proteins (Hsp) are highly conserved proteins found in all prokaryotes and eukaryotes. Of all heat shock proteins, the Hsp[70] family constitutes the most conserved and best-studied class. HSPs may be expressed during periodontal diseases. Objective: To compare the HSP 70 expression within layers of epithelium and connective tissue and correlate the expression of HSP 70 with the severity of periodontal disease. Results: One way ANOVA results indicate a statistically significant expression in basal layer for mild inflammation (mean=2.36) and intensity in stratum spinosum for mild (mean=2.27) and minimum (mean=2.39) inflammation. An overall greater HSP 70 expression is noticed in periodontitis group (total IRIDI = 25.41) not statistically significant Conclusion: We elucidated that there was significant HSP 70 expression in stratum basale and spinosum for mild inflammation that did not increase with severity of inflammation. Statistical analysis used: One way Analysis of Variance (ANOVA), Mann Whitney U test and Kruskal Wallis Test
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
