Detection of periodontal bone loss patterns and furcation defects from panoramic radiographs using deep learning algorithm: a retrospective study.

BACKGROUND: This retrospective study aimed to develop a deep learning algorithm for the interpretation of panoramic radiographs and to examine the performance of this algorithm in the detection of periodontal bone losses and bone loss patterns. METHODS: A total of 1121 panoramic radiographs were used in this study. Bone losses in the maxilla and mandibula (total alveolar bone loss) (n = 2251), interdental bone losses (n = 25303), and furcation defects (n = 2815) were labeled using the segmentation method. In addition, interdental bone losses were divided into horizontal (n = 21839) and vertical (n = 3464) bone losses according to the defect patterns. A Convolutional Neural Network (CNN)-based artificial intelligence (AI) system was developed using U-Net architecture. The performance of the deep learning algorithm was statistically evaluated by the confusion matrix and ROC curve analysis. RESULTS: The system showed the highest diagnostic performance in the detection of total alveolar bone losses (AUC = 0.951) and the lowest in the detection of vertical bone losses (AUC = 0.733). The sensitivity, precision, F1 score, accuracy, and AUC values were found as 1, 0.995, 0.997, 0.994, 0.951 for total alveolar bone loss; found as 0.947, 0.939, 0.943, 0.892, 0.910 for horizontal bone losses; found as 0.558, 0.846, 0.673, 0.506, 0.733 for vertical bone losses and found as 0.892, 0.933, 0.912, 0.837, 0.868 for furcation defects (respectively). CONCLUSIONS: AI systems offer promising results in determining periodontal bone loss patterns and furcation defects from dental radiographs. This suggests that CNN algorithms can also be used to provide more detailed information such as automatic determination of periodontal disease severity and treatment planning in various dental radiographs.

Preventive effects of melatonin on periodontal tissue destruction due to psychological stress in rats with experimentally induced periodontitis.

OBJECTIVE AND BACKGROUND: Psychological stress is a potential modifiable environmental risk factor causally related to the exacerbation of periodontitis and other chronic inflammatory diseases. This animal study aimed to investigate comprehensively the preventive efficacy of systemic melatonin administration on the possible effects of restraint stress on the periodontal structures of rats with periodontitis. METHODS: Forty-eight male Sprague Dawley rats were randomly divided into six groups: control, restraint stress (S), S-melatonin (S-Mel), experimental periodontitis (Ep), S-Ep, and S-Ep-Mel. Periodontitis was induced by placing a 3.0 silk suture in a sub-paramarginal position around the cervix of the right and left lower first molars of the rats and keeping the suture in place for 5 weeks. Restraint stress was applied simultaneously by ligation. Melatonin and carriers were administered to the control, S, Ep, and S-Ep groups intraperitoneally (10 mg/body weight/day, 14 days) starting on day 21 following ligation and subjection to restraint stress. An open field test was performed on all groups on day 35 of the study. Periodontal bone loss was measured via histological sections. Histomorphometric and immunohistochemical (RANKL and OPG) evaluations were performed on right mandibular tissue samples and biochemical (TOS (total oxidant status), TAS (total antioxidant status), OSI (oxidative stress index), IL-1ß, IL-10, and IL-1ß/IL-10) evaluations were performed on left mandibular tissue samples. RESULTS: Melatonin significantly limited serum corticosterone elevation related to restraint stress (p < .05). Restraint stress aggravated alveolar bone loss in rats with periodontitis, while systemic melatonin administration significantly reduced stress-related periodontal bone loss. According to the biochemical analyses, melatonin significantly lowered IL-1ß/IL-10, OSI (TOS/TAS), and RANKL/OPG rates, which were significantly elevated in the S-Ep group. CONCLUSION: Melatonin can significantly prevent the limited destructive effects of stress on periodontal tissues by suppressing RANKL-related osteoclastogenesis and oxidative stress.

Melatonin supports nonsurgical periodontal treatment in patients with Type 2 diabetes mellitus and periodontitis: A randomized clinical trial.

BACKGROUND: Diabetes mellitus (DM)-associated hyperinflammatory host response significantly provokes periodontal tissue destruction. In this context, the support of nonsurgical periodontal therapy in diabetics with host modulation agents is a current field of study. This clinical study aims to investigate the clinical efficacy of melatonin supplementation and discuss its possible biological mechanisms in nonsurgical periodontal treatment in patients with DM and periodontitis through some fundamental markers. METHODS: In this randomized controlled and single-blind study, 27 of 55 diabetic patients with periodontitis (stage III/IV and grade C) underwent full-mouth scaling and root planing (fmSRP) alone and 28 patients underwent melatonin administration (6 mg daily, 30 days) in addition to fmSRP (full-mouth scaling and root planing plus melatonin, fmSRP-mel). The potential therapeutic contribution of melatonin was evaluated clinically and biochemically (gingival crevicular fluid RANKL, OPG, MMP-8, and serum IL-1ß levels) at 3rd and 6th months. RESULTS: Melatonin (tablet, 6 mg daily, 30 days) did not cause any local or systemic side effects. fmSRP alone resulted in significant reduction in serum IL-1ß levels, pocket depths, gingival inflammation, and gingival crevicular fluid RANKL and MMP-8 levels (p < 0.05). Moreover, melatonin supplementation resulted in a more significant decrease in bleeding and pocket depth scores at probing, especially at 3 months (p < 0.05). Furthermore, RANKL and MMP-8 levels were significantly lower at 3 months and IL-1ß levels at 6 months compared to the control group (p < 0.05). However, OPG levels were not affected significantly by the treatments (p > 0.05). CONCLUSION: Melatonin, as a host modulation agent, significantly increases the clinical efficacy of fmSRP. The reduction in periodontal inflammation and pocket depths may be a result of marked suppression of RANKL-associated osteoclastogenesis and extracellular matrix damage by melatonin.

Detection of tooth numbering, frenulum attachment, gingival overgrowth, and gingival inflammation signs on dental photographs using convolutional neural network algorithms: a retrospective study.

OBJECTIVES: This study aimed to develop an artificial intelligence (AI) model that can determine automatic tooth numbering, frenulum attachments, gingival overgrowth areas, and gingival inflammation signs on intraoral photographs and to evaluate the performance of this model. METHOD AND MATERIALS: A total of 654 intraoral photographs were used in the study (n = 654). All photographs were reviewed by three periodontists, and all teeth, frenulum attachment, gingival overgrowth areas, and gingival inflammation signs on photographs were labeled using the segmentation method in a web-based labeling software. In addition, tooth numbering was carried out according to the FDI system. An AI model was developed with the help of YOLOv5x architecture with labels of 16,795 teeth, 2,493 frenulum attachments, 1,211 gingival overgrowth areas, and 2,956 gingival inflammation signs. The confusion matrix system and ROC (receiver operator characteristic) analysis were used to statistically evaluate the success of the developed model. RESULTS: The sensitivity, precision, F1 score, and AUC (area under the curve) for tooth numbering were 0.990, 0.784, 0.875, and 0.989; for frenulum attachment these were 0.894, 0.775, 0.830, and 0.827; for gingival overgrowth area these were 0.757, 0.675, 0.714, and 0.774; and for gingival inflammation sign 0.737, 0.823, 0.777, and 0.802, respectively. CONCLUSION: The results of the present study show that AI systems can be successfully used to interpret intraoral photographs. These systems have the potential to accelerate the digital transformation in the clinical and academic functioning of dentistry with the automatic determination of anatomical structures and dental conditions from intraoral photographs.

Influences of periodontitis on hippocampal inflammation, oxidative stress, and apoptosis in rats.

BACKGROUND AND AIM: The hippocampus, which has a central role in cognitive and behavioral activities, is one of the most sensitive parts of the brain to systemic inflammatory diseases. This animal study aims to comprehensively investigate the possible inflammatory, oxidative, and apoptotic effects of periodontitis on the hippocampus. METHODS: Sixteen male Sprague-Dawley rats were randomly assigned to two groups: control and experimental periodontitis (Ep). In the Ep group, periodontitis was induced by placing 3.0 sutures sub-paramarginally around the necks of right and left mandibular first molars and maintaining the ligatures in place for 5 weeks. Following the euthanasia, mandibula and hippocampus samples were collected bilaterally. Alveolar bone loss was measured histomorphometrically and radiologically on the right and left mandibles. On the right hippocampal sections histological (Caspase-3, TNF-α, and 8-OHdG) and the left hippocampal sections, biochemical (IL-1ß, Aß1-42 , MDA, GSH, and TAS levels) evaluations were performed. RESULTS: Histopathological changes associated with periodontitis were limited (p > .05). A slight increase in caspase-3 positive neuron density in EP rats showed that apoptotic changes were also limited (p > .05). 8-OHdG activity, on the other hand, was significantly higher compared to controls (p < .05). In biochemical analysis, there was a significant increase in IL-1ß levels and oxidative membrane damage (MDA) (p < .05) whereas Aß1-42 and antioxidant marker (GSH and TAS) levels were slightly increased (p > .05). CONCLUSION: Periodontitis causes marked increases in IL-1ß levels and oxidative stress in the hippocampus, but limited degenerative and apoptotic changes.

Periodontitis exacerbates the renal degenerative effects of obesity in rats.

BACKGROUND/OBJECTIVES: Obesity and periodontitis are systemic subclinical inflammatory diseases with established negative renal effects. The aim of this animal study was to thoroughly investigate the possible effects of these two diseases on renal structure and function. METHODS: Thirty-two male Sprague Dawley rats were divided into four groups: control (C), obesity (Ob), experimental periodontitis (Ep), and Ob + Ep. The first 16 weeks of the experiment were aimed for the induction of obesity and the last 5 weeks for the induction of periodontitis. Throughout the experimental period, the C and Ep groups were fed standard rat chow, while the Ob groups (Ob and Ob + Ep) were fed high-fat rat chow. Right after the establishment of obesity, periodontal tissue destruction was achieved by placing 3.0 silk sutures in sub-paramarginal position around the cervices of mandibular right-left first molar teeth and preserving them for 5 weeks. On the last day of the 22nd week, following blood collection, all rats were euthanized, and kidneys and mandibles were collected. Alveolar bone loss was measured on microcomputed tomographic slices. Histopathological evaluations (light microscopy, semi-quantitative analysis of renal corpuscle area, and immunohistochemical analysis of caspase-3 activity) were done on right kidneys and biochemical evaluations (malonyl-aldehyde [MDA], glutathione [GSH], total oxidant status [TOS], total antioxidant status [TAS], oxidative stress [OSI], tumor necrosis factor-α [TNF-α], interleukin-1ß [IL-1ß], matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D [CtD] levels) were done on left kidneys. Renal functional status was evaluated with levels of serum creatinine, urea, and cystatin C. RESULTS: Periodontal bone loss was significantly higher in the Ep and Ob + Ep groups, compared with the C and Ob groups (p < .05). All parameters except TAS and GSH were highest in the Ob + Ep group, and the differences were statistically significant compared with the control group (p < .05). Although the mean TAS and GSH levels were lower in the Ob + Ep group than the other groups, the differences were not statistically significant (p > .05). While the atypical glomeruli score was significantly higher in the Ob + Ep group than in all other groups (p < .05), the acute tubular necrosis and histopathological scores were significantly different only compared with the control group (p < .05). CONCLUSION: This experimental study showed that the negative effects of the co-existence of periodontitis and obesity on inflammatory stress and apoptotic changes in the kidneys together with the functional parameters were significantly more severe, compared with the presence of one of these diseases alone. TNF-α could have a central role in the periodontitis and obesity-related structural and functional renal changes.

Melatonin improves periodontitis-induced kidney damage by decreasing inflammatory stress and apoptosis in rats.

BACKGROUND: Two main aims of this animal study were to inspect the possible effects of periodontitis on the structure and functions of the kidneys and the therapeutic effectiveness of melatonin. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep-melatonin (Ep-Mel). Periodontitis was induced by placing 3.0-silk sutures sub-paramarginally around the cervix of right-left mandibular first molars and maintaining the sutures for 5 weeks. Then melatonin (10 mg/kg body weight/day, 14 days), and the vehicle was administered intraperitonally. Mandibular and kidney tissue samples were obtained following the euthanasia. Periodontal bone loss was measured via histological and microcomputed tomographic slices. On right kidney histopathological and immunohistochemical, and on the left kidney biochemical (malonyl-aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]-α, interleukin [IL]-1ß, matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D levels) evaluations were performed. Renal functional status was analyzed by levels of serum creatinine, urea, cystatin-C, and urea creatinine. RESULTS: Melatonin significantly restricted ligature-induced periodontal bone loss (P <0 .01) and suppressed the levels of proinflammatory cytokines (TNF-α and IL-1ß), oxidative stress (MDA and OSI), and proteases (MMP-8, MMP-9, and CtD) that was significantly higher in the kidneys of the rats with periodontitis (P <0.05). In addition, periodontitis-related histological damages and apoptotic activity were also significantly lower in the Ep-Mel group (P <0.05). However, the markers of renal function of the Ep group were detected slightly impaired in comparison with the control group (P >0.05); and the therapeutic activity of melatonin was limited (P >0.05). CONCLUSION: Melatonin restricts the periodontitis-induced inflammatory stress, apoptosis, and structural but not functional impairments.

Melatonin ameliorates periodontitis-related inflammatory stress at cardiac left ventricular tissues in rats.

BACKGROUND: The aim of this experimental rat study was to investigate the potential inflammatory effects of periodontitis on cardiac left ventricular tissue and the therapeutic activity of melatonin on these effects. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep-melatonin (Ep-Mel). Experimental periodontitis was induced by placing and maintaining 3.0 silk ligatures at a peri marginal position on the left and right mandibular first molars for 5 weeks. Afterward, following the removal of ligatures, melatonin (10 mg/body weight) to Ep-Mel group, and vehicle (saline) to Ep and control groups were administered intraperitoneally for 14 days. On the first day of the eighth week, mandibular and cardiac left ventricular tissue samples were obtained following the euthanasia of the rats in all groups. Alveolar bone loss measurements were made on histological and microcomputed tomographic slices. Cardiac tissue levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix metalloproteinase-9 (MMP-9), and cardiac Troponin-T (cTnT) were evaluated by appropriate biochemical methods. RESULTS: Measurements made on the histological and microcomputed tomographic slices showed that melatonin significantly limits the ligature-induced periodontal tissue destruction (P <0.01). In addition, melatonin was detected to cause a significant decrease of MDA, MMP-9, and cTnT levels which were found to be significantly higher on rats with Ep (P <0.05) while having no significant effect on antioxidant levels (GSH, SOD, and CAT) (P >0.05). CONCLUSION: Melatonin might be regarded as an important supportive therapeutic agent to reduce the early degenerative changes and possible hypertrophic remodeling at cardiac left ventricular tissues provoked by periodontitis-related bacteria and/or periodontal inflammation.

The effect of leukocyte-platelet-rich fibrin on bone morphogenetic protein-2 and insulin-like growth factor-1 levels in patients with chronic periodontitis: a randomized split mouth clinical trail.

The present study evaluates the effects of leukocyte-platelet-rich fibrin (L-PRF) combined with open flap debridement (OFD) on clinical parameters and growth factors levels (GFL) in chronic periodontitis (CP) patients. This trial was registered at clinicaltrials.gov as NCT02594605. 16 patients (32 sites) with chronic periodontitis who had at least two areas of horizontal bone loss, were treated with OFD alone or L-PRF with OFD (OFD + L-PRF). GFL in gingival crevicular fluid (GCF) were analyzed at baseline, 1 week, 2 weeks and 4 weeks after operation. Probing depth (PD) and clinical attachment level (CAL) were measured at baseline and 6 months postoperatively. PD reduction and CAL gain were significantly higher in the OFD + L-PRF sites than in OFD sites. OFD + L-PRF group showed significantly increased bone morphogenetic protein-2 and insulin-like growth factor-1 at 2 weeks compared with baseline. L-PRF combined with OFD significantly increases GFL and thus, it enhances the periodontal healing on CP patients.

Advantages of Autologous Platelet-Rich Fibrin Membrane on Gingival Crevicular Fluid Growth Factor Levels and Periodontal Healing: A Randomized Split-Mouth Clinical Study.

BACKGROUND: This study evaluates contributions of platelet-rich fibrin (PRF) combined with conventional flap surgery on growth factor levels in gingival crevicular fluid (GCF) and periodontal healing. METHODS: Twenty-six patients (52 sites) with chronic periodontitis were treated either with autologous PRF with open flap debridement (OFD+PRF) or OFD alone. Growth factor levels in GCF at baseline and 2, 4, and 6 weeks after surgery were analyzed, and clinical parameters such as probing depth (PD), relative clinical attachment level (rCAL), and gingival margin level (GML) at baseline and 9 months after surgery were measured. RESULTS: Mean PD reduction and rCAL gain were significantly greater in OFD+PRF sites than in OFD sites. Mean GML change was -0.38 + 0.10 mm in OFD sites and 0.11 + 0.08 mm in the test group; difference between the two groups was statistically significant (P <0.05). Both groups demonstrated increased expression levels of fibroblast growth factor-2, transforming growth factor-ß1, and platelet-derived growth factor-BB at 2 weeks compared with baseline, followed by reductions at 4 and 6 weeks. The OFD+PRF group showed significantly higher growth factor levels compared with the OFD group at 2 and 4 weeks. CONCLUSION: PRF membrane combined with OFD provides significantly higher GCF concentrations of angiogenic biomarkers for ≈2 to 4 weeks and better periodontal healing in terms of conventional flap sites.

Influences of Fucoxanthin on Alveolar Bone Resorption in Induced Periodontitis in Rat Molars.

The aim of this study was to evaluate the effects of systemic fucoxanthin treatment on alveolar bone resorption in rats with periodontitis. Thirty rats were divided into control, experimental periodontitis (EP), and experimental periodontitis-fucoxanthin (EP-FUCO) groups. Periodontitis was induced by ligature for four weeks. After removal of the ligature, the rats in the EP-FUCO group were treated with a single dose of fucoxanthin (200 mg/kg bw) per day for 28 consecutive days. At the end of the study, all of the rats were euthanized and intracardiac blood and mandible tissue samples were obtained for biochemical, immunohistochemical, and histometric analyses. Fucoxanthin treatment resulted in a slight decrease in tumor necrosis factor-α, interleukin-1ß, and interleukin-6 levels and a significant decrease in oxidative stress index. It was observed that fucoxanthin caused a significant reduction in receptor activator of nuclear factor kappa-ß ligand (RANKL) levels and a statistically non-significant elevation in osteoprotegerin and bone-alkaline phosphatase levels. There were no significant differences in alveolar bone loss levels between the EP and EP-FUCO groups. This experimental study revealed that fucoxanthin provides a limited reduction in alveolar bone resorption in rats with periodontitis. One of the mechanisms underlying the mentioned limited effect might be related to the ability of fucoxanthin to inhibit oxidative stress-related RANKL-mediated osteoclastogenesis.

Effects of Melatonin on Oxidative Stress Index and Alveolar Bone Loss in Diabetic Rats With Periodontitis.

BACKGROUND: The aim of this study is to evaluate the effects of systemic melatonin treatment on serum oxidative stress index (OSI) and alveolar bone loss (ABL) in rats with diabetes mellitus (DM) and periodontitis. METHODS: Seventy Sprague Dawley rats were divided into control, experimentally induced periodontitis (EP), DM, EP-DM, EP and melatonin treatment (EP-MEL), DM and melatonin treatment (DMMEL), and EP-DM-MEL groups. DM was induced by alloxan, after which periodontitis was induced by ligature for 4 weeks. After removal of the ligature, the rats in the melatonin groups (EP-MEL, DM-MEL, and EP-DM-MEL) were treated with a single dose of melatonin (10 mg/body weight) every day for 14 consecutive days. At the end of the study, all of the rats were euthanized, and intracardiac blood samples and mandible tissues were obtained for biochemical and histologic analyses. Serum levels of total oxidant status/total antioxidant status and OSI were measured. In addition, neutrophil and osteoclast densities and myeloperoxidase activities were determined in gingival tissue homogenates, and ABL was evaluated with histometric measurements. RESULTS: Melatonin treatment significantly reduced fasting plasma glucose levels in the rats with DM. In addition, reduced OSI and ABL levels were detected in the EP-MEL and DM-MEL groups; the reductions in the EP-DM-MEL group were found to be more prominent. Melatonin also significantly decreased the increased myeloperoxidase activities and osteoclast and neutrophil densities in the EP, DM, and EP-DM groups. CONCLUSION: It is revealed in this experimental study that melatonin significantly inhibited hyperglycemia-induced oxidative stress and ABL through antiDM and antioxidant effects in rats with DM and periodontitis.

Therapeutic Effects of Melatonin on Alveolar Bone Resorption After Experimental Periodontitis in Rats: A Biochemical and Immunohistochemical Study.

BACKGROUND: The present study aims to investigate the effects of systemic melatonin administration on alveolar bone resorption in experimental periodontitis in rats. METHODS: Twenty-four male Sprague-Dawley rats were divided into three groups (control, experimental periodontitis [Ped], and experimental periodontitis treated with melatonin [Mel-Ped]). For periodontitis induction, first molars were ligatured submarginally for 4 weeks. After ligature removal, rats in the Mel-Ped group were treated with a daily single dose of 10 mg/kg body weight melatonin for 15 consecutive days. At the end of the study, intracardiac blood samples and mandible tissues were obtained for histologic, biochemical, and radiographic analysis. Serum markers related to bone turnover, calcium, phosphorus, bone alkaline phosphatase (b-ALP), and terminal C telopeptide of collagen Type I (CTX) were analyzed. Myeloperoxidase levels were determined in gingival tissue homogenates, and receptor activator of nuclear factor-kappa B ligand (RANKL) activation was analyzed in the mandible samples stereologically. Alveolar bone loss was also evaluated radiographically in the mandible samples of each group. RESULTS: Melatonin treatment decreased serum CTX levels and increased b-ALP levels. Serum calcium and phosphorus levels were not statistically different among groups (P >0.05). Alveolar bone resorption and myeloperoxidase activity were statistically higher in the Ped group compared to the Mel-Ped group (P <0.05). Immunohistochemical staining of RANKL and osteoclast activity were significantly lower in the Mel-Ped group compared to the Ped group (P <0.05). CONCLUSION: This study reveals that melatonin treatment significantly inhibits regional alveolar bone resorption and contributes to periodontal healing in an experimental periodontitis rat model.