Comparative Analysis of Periodontal and Biochemical Parameters in Chronic Generalized Periodontitis Patients with and Without Hyperlipidemia – A Retrospective Clinicobiochemical Study

Abstract Background: Chronic generalized periodontitis (CGP) and hyperlipidemia are two prevalent inflammatory conditions that share common pathogenic pathways, including cytokine mediated tissue destruction and altered lipid metabolism. Periodontal pathogens such as Porphyromonas gingivalis release lipopolysaccharides that trigger systemic inflammation, dyslipidemia further amplifies this response by increasing circulating pro‐inflammatory cytokines. Despite mounting evidence of a bidirectional relationship between periodontitis and lipid abnormalities, comprehensive analyses comparing periodontal indices and complete lipid profiles within the same cohort remain limited. Materials and Methods: A total of 100 patients with CGP were divided into two categories: Group I consisted of 50 normolipidemic participants with triglyceride (TG) levels <150 mg/dL, low-density lipoprotein (LDL) <130 mg/dL and high-density lipoprotein (HDL) ≥40 mg/dL; Group II included 51 hyperlipidemic participants featuring TG ≥150 mg/dL, and/or LDL ≥130 mg/dL, and/or HDL <40 mg/dL. Initial assessments of periodontal health involved measuring the full-mouth bleeding score (FMBS), plaque index (PI), probing pocket depth (PPD) and clinical attachment level (CAL) at six locations around each tooth. Laboratory tests measured blood levels of TC, TG, LDL and HDL. Differences between the groups were analyzed via Student's t-test, where a p-value less than 0.05 indicated statistical significance. Results: Lipid Profile: Group II exhibited significantly elevated TG (220.17 ± 140.50 mg/dL) and LDL (133.55 ± 28.86 mg/dL) compared to Group I (TG 114.00 ± 18.97 mg/dL; LDL 116.13 ± 25.76 mg/dL; p < 0.001). HDL was lower in Group II (35.16 ± 8.68 mg/dL) than in Group I (41.70 ± 7.11 mg/dL; p < 0.001). Periodontal Parameters: Mean PPD and CAL were significantly greater in hyperlipidemic patients (PPD 5.31 ± 2.31 mm; CAL 4.89 ± 1.05 mm) than in normolipidemic controls (PPD 4.12 ± 2.31 mm; CAL 4.08 ± 1.08 mm; p < 0.001). FMBS was also higher in Group II (54.21 ± 17.66%) versus Group I (47.04 ± 22.50%; p >0.05), indicating increased gingival inflammation. No significant intergroup difference was observed for PI suggesting comparable plaque levels. Conclusion: Hyperlipidemia in patients with CGP is associated with significantly worse periodontal outcomes deeper pockets, greater attachment loss, and heightened gingival bleeding—despite similar plaque accumulation. Notably, low HDL levels emerged as a key factor in amplifying gingival inflammation, while elevated TG and LDL exacerbate tissue breakdown. These findings reinforce the concept of a bidirectional link between systemic lipid metabolism and periodontal health and highlight the importance of multidisciplinary management of Periodontitis. Early screening for dyslipidemia in patients with periodontitis and integrated therapeutic approaches may improve both oral and cardiovascular outcomes.