Background: The aim of this study was to comprehensively investigate the potential degenerative effects of periodontitis severity on retinal and choroidal structures in patients with different types of diabetic retinopathy (DR). Materials and Methods: The study’s Clinical Trials Registration Number is NCT07137013. A total of 100 participants (56 females and 44 males), each group consisting of 20 individuals, were allocated into five groups: systemically healthy controls (G1), diabetic patients without DR (G2: DM+ DR−), non-proliferative DR without diabetic macular edema (G3: NPDR DME−), non-proliferative DR with diabetic macular edema (G4: NPDR DME+), and proliferative DR (G5: PDR). Ocular examinations were performed using optical coherence tomography (OCT) and OCT angiography (OCTA). Retinal layer thicknesses, choroid-sclera interface (CSI), ganglion cell layer (GCL), retinal nerve fiber layer (RNFL), and peripapillary CSI were assessed by OCT, whereas superficial and deep retinal vessel densities and the foveal avascular zone (FAZ) were evaluated by OCTA. Clinical periodontal status was assessed using plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment loss (CAL). Results: In the G3 and G5 groups, the presence of stage III–IV periodontitis was associated with a marked increase in retinal layer thickness. GCL + Inner Plexiform Layer (GCL+) thickness was significantly reduced in individuals with stage III–IV periodontitis in almost all regions of the G5 group, except for the 3 mm nasal and inferior areas. Peripapillary CSI values showed a significant decrease with increasing periodontitis severity. RNFL thickness was significantly reduced in individuals with stage III–IV periodontitis, particularly in the G5 group. OCTA analyses demonstrated significant reductions in superficial and deep retinal vessel densities in several regions in the presence of stage III–IV periodontitis. Moreover, FAZ areas were significantly enlarged in individuals with stage III–IV periodontitis in the G2 and G5 groups. Conclusions: Periodontal inflammation, particularly in advanced periodontitis (stage III–IV), induces degenerative changes in the retinal microvasculature and neural tissues. Increasing periodontitis severity may represent a potential provoking factor in the pathogenesis of DR.

Background/Objectives: Periodontitis is a chronic inflammatory disease in which host response and oxidative stress contribute to periodontal tissue destruction. Apelin isoforms may be involved in inflammatory regulation, tissue remodeling, and oxidative balance. This study evaluated changes in gingival crevicular fluid (GCF) apelin-13, apelin-36, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) following non-surgical periodontal therapy (NSPT) in systemically healthy individuals with stage I–II or stage III–IV periodontitis. Methods: A total of 61 systemically healthy individuals with periodontitis were included and divided into two groups: stage I–II periodontitis (n = 31) and stage III–IV periodontitis (n = 30). Clinical periodontal parameters and GCF samples were obtained at baseline and at 1, 3, and 6 months after NSPT. Apelin-13 and apelin-36 levels were measured by enzyme-linked immunosorbent assay, while TAS and TOS levels were determined using commercial assay kits. OSI was calculated as the percentage ratio of TOS to TAS. The study was retrospectively registered at ClinicalTrials.gov (NCT06850987). Results: Baseline apelin-13 levels were significantly higher in stage III–IV periodontitis and decreased in both groups after NSPT, whereas apelin-36 increased over time and was higher in stage I–II periodontitis at baseline. Apelin-13 was positively associated with clinical periodontal parameters, while apelin-36 showed negative associations. TAS remained higher in stage I–II periodontitis, whereas OSI was consistently higher in stage III–IV periodontitis. Conclusions: These findings suggest that the combined assessment of GCF apelin isoforms and oxidative stress markers may provide useful biomarker information for distinguishing periodontitis severity and monitoring biochemical responses to NSPT.