Modelling time-varying risk factors of tooth loss: Results from joint model compared with extended Cox regression model.

AIM: To illustrate the use of joint models (JMs) for longitudinal and survival data in estimating risk factors of tooth loss as a function of time-varying endogenous periodontal biomarkers (probing pocket depth [PPD], alveolar bone loss [ABL] and mobility [MOB]). MATERIALS AND METHODS: We used data from the Veterans Affairs Dental Longitudinal Study, a longitudinal cohort study of over 30 years of follow-up. We compared the results from the JM with those from the extended Cox regression model which assumes that the time-varying covariates are exogenous. RESULTS: Our results showed that PPD is an important risk factor of tooth loss, but each model produced different estimates of the hazard. In the tooth-level analysis, based on the JM, the hazard of tooth loss increased by 4.57 (95% confidence interval [CI]: 2.13-8.50) times for a 1-mm increase in maximum PPD, whereas based on the extended Cox model, the hazard of tooth loss increased by 1.60 (95% CI: 1.37-1.87) times. CONCLUSIONS: JMs can incorporate time-varying periodontal biomarkers to estimate the hazard of tooth loss. As JMs are not commonly used in oral health research, we provide a comprehensive set of R codes and an example dataset to implement the method.

Periodontitis is associated with an increased hazard of mortality in a longitudinal cohort study over 50 years.

AIM: To evaluate the association between periodontal disease and all-cause mortality in a longitudinal cohort study over 50 years. MATERIALS AND METHODS: Participants (N = 1156) in the Veterans Affairs Dental Longitudinal Study, aged 25-85 years at enrollment in 1968, received comprehensive medical and oral exams approximately every 3 years through 2007. Periodontal status was defined using person-level, mean whole-mouth radiographic alveolar bone loss (ABL) scores using a five-point Schei ruler, each unit representing 20% increments of ABL. Time-varying Cox regression models estimated hazard ratios (HRs) for the association between continuous and categorical ABL and mortality, adjusting for covariates. RESULTS: Each one-unit increase in mean ABL score was associated with a 14% increase in the hazard of mortality (adjusted HR = 1.14, 95% confidence interval [CI] 1.02, 1.27). When assessed categorically, HRs for average scores of 2 to <3 and 3 to ≤5 showed increasing associations with hazard of mortality, relative to 0 to <1 (adjusted HR = 1.17, 95% CI 0.94, 1.46; and HR = 1.65, 95% CI 0.94, 2.85, respectively). By contrast, we observed null associations for average scores of 1 to <2 relative to 0 to <1 (adjusted HR = 1.00, 95% CI 0.86, 1.17). CONCLUSIONS: Time-varying periodontal status assessed using radiographic ABL was positively associated with all-cause mortality even after confounder adjustment.

Effect of artesunate on cardiovascular complications in periodontitis in a type I diabetes rat model and related mechanisms.

PURPOSE: Both cardiovascular disease and periodontitis are complications of diabetes that have a great impact on human life and health. Our previous research found that artesunate can effectively improve cardiovascular disease in diabetes and has an inhibitory effect on periodontal disease. Therefore, the present study aimed to explore the potential therapeutic possibility of artesunate in the protection against cardiovascular complications in periodontitis with type I diabetes rats and to elucidate the possible underlying mechanisms. METHODS: Sprague‒Dawley rats were randomly divided into the healthy, diabetic, periodontitis, diabetic with periodontitis, and artesunate treatment groups (10, 30, and 60 mg/kg, i.g.). After artesunate treatment, oral swabs were collected and used to determine changes in the oral flora. Micro-CT was performed to observe changes in alveolar bone. Blood samples were processed to measure various parameters, while cardiovascular tissues were evaluated by haematoxylin-eosin, Masson, Sirius red, and TUNEL staining to observe fibrosis and apoptosis. The protein and mRNA expression levels in the alveolar bone and cardiovascular tissues were detected using immunohistochemistry and RT‒PCR. RESULTS: Diabetic rats with periodontitis and cardiovascular complications maintained heart and body weight but exhibited reduced blood glucose levels, and they were able to regulate blood lipid indicators at normal levels after artesunate treatment. The staining assays suggested that treatment with 60 mg/kg artesunate has a significant therapeutic effect on myocardial apoptotic fibrosis. The high expression of NF-κB, TLR4, VEGF, ICAM-1, p38 MAPK, TGF-ß, Smad2, and MMP9 in the alveolar bone and cardiovascular tissue in the type I diabetes and type I diabetes with periodontitis rat models was reduced after treatment with artesunate in a concentration-dependent manner. Micro-CT showed that treatment with 60 mg/kg artesunate effectively alleviated alveolar bone resorption and density reduction. The sequencing results suggested that each model group of rats had vascular and oral flora dysbiosis, but artesunate treatment could correct the dysbacteriosis. CONCLUSIONS: Periodontitis-related pathogenic bacteria cause dysbiosis of the oral and intravascular flora in type I diabetes and aggravate cardiovascular complications. The mechanism by which periodontitis aggravates cardiovascular complications involves the NF-κB pathway, which induces myocardial apoptosis, fibrosis, and vascular inflammation.

Infrared laser therapy decreases systemic oxidative stress and inflammation in hypercholesterolemic mice with periodontitis.

BACKGROUND: Near-infrared irradiation photobiomodulation (NIR-PBM) has been successfully used in periodontal treatment as an adjuvant tool to locally improve cell function and regeneration. Although the relationship between periodontitis and systemic disease constitutes an important aspect of periodontal clinical research, the systemic effects of NIR-PBM in periodontitis are not well known. In this study, we aimed to investigate the effects of NIR-PBM on systemic oxidative stress and inflammation in an apolipoprotein E (ApoE) knockout mouse model of periodontal disease (PD). METHODS: We evaluated alveolar bone loss by measuring the distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC), reactive oxygen species (ROS) production in blood cells, inflammatory activity, plasma cholesterol levels, and lipid peroxidation levels in three experimental groups: (1) ApoEC, control group without intervention; (2) ApoEP, first molar ligation-induced periodontitis for 4 weeks; and (3) ApoEP + PBM, exposed to 808 nm continuous wave, ø ~ 3 mm2, 100 mW, 60 s of NIR-PBM for 7 consecutive days after 4 weeks of periodontitis. At the end of the experimental protocols, ApoEP mice presented significantly increased alveolar bone loss, ROS production, inflammatory activity, plasma cholesterol, and lipid peroxidation levels compared to the ApoEC group (P < 0.05). NIR-PBM for 7 days in the ApoEP + PBM mice significantly decreased systemic ROS production, inflammatory response, plasma cholesterol, and lipid peroxidation levels, similar to those found in the ApoEC group (P > 0.05). However, it was not capable of preventing alveolar bone loss (P > 0.05 compared to ApoEP mice). CONCLUSION: A 7-day treatment with NIR-PBM effectively reduces systemic oxidative stress and inflammatory parameters in hypercholesterolemic mice with PD. However, more studies with longer evaluation times are needed to confirm the systemic effects of locally applied NIR-PBM on PD associated with hypercholesterolemia.

Risk indicators of long-term outcome of implant therapy in patients with a history of severe periodontitis or no history of periodontitis: A retrospective cohort study.

OBJECTIVE: The aim of this retrospective cohort study was to assess factors associated with peri-implant disease in partially edentulous patients with a history of severe periodontitis or no history of periodontitis. METHODS: Partially edentulous patients with a history of severe periodontitis/without history of periodontitis who received implant surgery within the past 6 to 8 years were recalled. Clinical and radiographic examinations were recorded. Periodontal probing depth, marginal bone loss (MBL) and peri-implantitis were considered as the primary outcome and peri-implant bleeding on probing (BOP) was considered as the secondary outcome. The following criteria were considered as the predictors, as well: history of severe periodontitis, gender, age, smoking, brushing frequency, recall interval, full-mouth plaque score, full-mouth bleeding score, splinted prosthesis, open/tight interproximal contact, width of keratinized mucosa, mucosal thickness, implants placed in the grafted bone and implant type. Univariate and multivariate regression analyses were utilized. RESULTS: A total of 88 patients (186 implants) fulfilled the study. Forty-seven patients (108 implants) had a history of severe periodontitis and 41 patients (78 implants) had no history of periodontitis. There was a higher chance of peri-implantitis in patients with a history of severe periodontitis (OR = 11.13; p = 0.045), implants with lack of peri-implant KM (<2 mm) and implants placed in the grafted bone (OR = 14.94, p < 0.001; OR = 4.93, p = 0.047). The risk of peri-implant MBL ≥3 mm was higher in patients with greater FMBS (OR = 1.20; p < 0.001). The chance of peri-implant BOP was independently higher in patients who brushed their teeth at most once per day (OR = 3.20; p = 0.04), higher FMBS (OR = 1.16; p < 0.001) and irregular recall visits (OR = 15.34; p = 0.001). CONCLUSIONS: Partially edentulous patients with the history of severe periodontitis, lack of peri-implant KM and implants placed in bone-grafted sites expressed higher probability of peri-implantitis. In addition, inadequate frequency of brushing (at most once daily) and irregular recall visits were associated with greater chance of peri-implant BOP.

Osteoporosis and periodontal diseases - An update on their association and mechanistic links.

Periodontitis and osteoporosis are prevalent inflammation-associated skeletal disorders that pose significant public health challenges to our aging population. Both periodontitis and osteoporosis are bone disorders closely associated with inflammation and aging. There has been consistent intrigue on whether a systemic skeletal disease such as osteoporosis will amplify the alveolar bone loss in periodontitis. A survey of the literature published in the past 25 years indicates that systemic low bone mineral density (BMD) is associated with alveolar bone loss, while recent evidence also suggests a correlation between clinical attachment loss and other parameters of periodontitis. Inflammation and its influence on bone remodeling play critical roles in the pathogenesis of both osteoporosis and periodontitis and could serve as the central mechanistic link between these disorders. Enhanced cytokine production and elevated inflammatory response exacerbate osteoclastic bone resorption while inhibiting osteoblastic bone formation, resulting in a net bone loss. With aging, accumulation of oxidative stress and cellular senescence drive the progression of osteoporosis and exacerbation of periodontitis. Vitamin D deficiency and smoking are shared risk factors and may mediate the connection between osteoporosis and periodontitis, through increasing oxidative stress and impairing host response to inflammation. With the connection between systemic and localized bone loss in mind, routine dental exams and intraoral radiographs may serve as a low-cost screening tool for low systemic BMD and increased fracture risk. Conversely, patients with fracture risk beyond the intervention threshold are at greater risk for developing severe periodontitis and undergo tooth loss. Various Food and Drug Administration-approved therapies for osteoporosis have shown promising results for treating periodontitis. Understanding the molecular mechanisms underlying their connection sheds light on potential therapeutic strategies that may facilitate co-management of systemic and localized bone loss.

Distribution of neutrophil and monocyte/macrophage populations induced by the CXCR4 inhibitor AMD3100 in blood and periodontal tissue early after periodontitis induction.

CXCR4, a CXCL12 receptor, is expressed on epithelial cells, fibroblasts, and inflammatory cells. The CXCR4-CXCL12 interaction is related to the migration of neutrophils and monocytes/macrophages. Periodontitis, an inflammatory disease mainly caused by gram-negative bacteria, is characterized by infiltration of circulating inflammatory cells and alveolar bone (AB) loss. To investigate whether CXCR4 is involved in the distribution of neutrophils and monocytes/macrophages early after periodontitis induction, we examined the effects of AMD3100 (AMD), a CXCR4 antagonist, in ligature-induced periodontitis mice and LPS-injected air pouch mice. The periodontitis study was accomplished in control (C), periodontitis (P), and P + AMD groups. Periodontitis was induced by ligation of the mandibular first molar. AMD was intraperitoneally administered daily beginning the day before ligation until sacrifice on the third day after ligation. The air pouch study was accomplished in C, lipopolysaccharide (LPS), and LPS + AMD groups. Air pouches on mice backs were formed by subcutaneous injection of sterilized air. AMD was administered and then LPS was injected into the air pouch. For the detection of neutrophils and monocytes/macrophages in blood and air pouch exudates, flow cytometry was performed with anti-Ly6G/anti-CD11b antibodies (Abs) and anti-CD115 Ab, respectively. In periodontal tissue, Ly6G+ cells and CD115+ cells were counted by immunohistological analysis. AB loss was estimated by the periodontal ligament area in the furcation. In the periodontitis study, the P group showed higher numbers of Ly6G+ cells and CD115+ cells in blood and periodontal tissue than the C group. The P + AMD group showed a greater number of Ly6G+ cells and CD115+ cells in blood, but not in periodontal tissue compared to the P group. There was no difference in AB loss between the P and P + AMD groups. In the air pouch study, the LPS group had higher levels of Ly6G+ CD11b+ cells and CD115+ cells in both blood and exudates than the C group. The number of these cells in the LPS + AMD group was higher in blood than in the LPS group, but not in the exudates. The CXCR4 antagonist further increased neutrophil and monocyte/macrophage populations in the blood, but did not alter the levels in the periodontal tissue and exudates in mice with periodontitis and LPS-injected air pouches. These results suggest that during inflammatory conditions such as periodontitis, CXCR4 is involved in the distribution of neutrophils and monocytes/macrophages in the blood, but not in inflamed peripheral tissues.

Unloading of occlusal force aggravates alveolar bone loss in periodontitis.

BACKGROUND AND OBJECTIVE: Periodontitis (PD), a chronic infectious inflammatory disease initiated by bacteria, is associated with several local contributing factors including occlusal trauma. Previous studies have found that the traumatic occlusal force could aggravate alveolar bone loss during PD. However, the effect of reduced occlusal force during PD remains unclear. This study aimed to explore the effect of occlusal force unloading on PD onset and progression and its underlying mechanism as an effort to provide restoration suggestions for PD patients with dentition defect in clinic. This study might also propose occlusal force unloading could be a new local contributing factor for PD. MATERIALS AND METHODS: C57BL/6 mice were used to establish a PD model by the ligation of 5-0 silk around the mandibular left first molar (PD group) and an unloading experiment model by the extraction of their left maxillary first molar (EX group). The THP-1-derived macrophages were used to verify in vivo results. RESULTS: Micro-CT scanning and H&E staining results consistently showed that PD + EX group experienced the most severe alveolar bone resorption as compared to PD group and control group. Further RNA-sequencing analysis suggested that occlusal force unloading significantly enhanced osteoclastic resorption, inhibited osteoblastic activity, and promotes M1 and M2 macrophages polarization. Immunofluorescence staining (IF) results showed that compared with the PD group, PD + EX group significantly increased the ratio of M1/M2 polarization. Similar results were observed by RT-qPCR and IF in vitro: removal of compressive force led to an increased ratio of M1/M2 polarization in LPS-stimulated THP-1-derived macrophages. CONCLUSIONS: Our study demonstrated that occlusal force unloading aggravates bone resorption by increasing the ratio of M1/M2 macrophages polarization during PD, suggesting a previously unknown local contributing factor for PD, and providing a novel insight for dentists to restore missing teeth as an effort to maintain remaining dentition.

Study on the role of pyroptosis in bone resorption induced by occlusal trauma with or without periodontitis.

BACKGROUND AND OBJECTIVE: Occlusal trauma is considered to be a contributing factor to bone loss associated with inflammatory periodontal disease. We hypothesized that pyroptosis, a recently discovered inflammation-induced programmed cell death pathway, plays a role in occlusal trauma. MATERIALS AND METHODS: The occlusal trauma model was established using a cemented 1-mm elevated computer-aided design and manufacturing (CAD/CAM) metal crown. The periodontitis model was established by periodontal wire ligation with lipopolysaccharide (LPS) injection. The rats were sacrificed at 1, 2, 3, and 4 weeks. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze the expression of pyroptosis-, inflammation-, and osteoclast-related markers. Micro-computed tomography (micro-CT) was used to determine bone morphology parameters. Tissue morphology was evaluated using hematoxylin and eosin staining (H&E). Osteoclasts were identified using tartrate-resistant acid phosphatase (TRAP) staining. The expression and distribution of factors related to pyroptosis and inflammation were evaluated by immunohistochemistry (IHC). The colocalization of dead cells and cysteinyl aspartate-specific proteinase-1 (caspase-1)-positive cells was analyzed by immunofluorescence. RESULTS: Quantitative real-time polymerase chain reaction and IHC results showed that occlusal trauma induced the expression of pyroptotic factors during the early stages, while occlusal trauma with periodontitis upregulated the expression of pyroptotic factors at the later stages. The results of qRT-PCR, TRAP staining, and micro-CT showed that occlusal trauma with periodontitis increased the production of proinflammatory cytokines, leading to severe bone loss. Glyburide, an NOD-like receptor pyrin domain containing protein 3 (NLRP3)inhibitor, reduced the expression of pyroptosis markers induced by occlusal trauma with periodontitis and reversed bone resorption. CONCLUSIONS: Pyroptosis was involved in bone loss induced by occlusal trauma with or without periodontitis, while glyburide reversed inflammation and bone resorption.

Acid sphingomyelinase deficiency exacerbates LPS-induced experimental periodontitis.

BACKGROUND: Mutation of the gene for acid sphingomyelinase (ASMase) causes Niemann-Pick disease. However, the effect of ASMase deficiency on periodontal health is unknown. Periodontal disease is a disease resulting from infection and inflammation of periodontal tissue and alveolar bone that support the teeth. The goal of this study was to determine the role of ASMase deficiency in periodontal inflammation and alveolar bone loss. METHODS: We induced periodontitis in wild-type and ASMase-deficient (ASMase-/- ) mice with periodontal lipopolysaccharide (LPS) injection and compared the alveolar bone loss and periodontal inflammation between these mice. RESULTS: Results showed that ASMase deficiency did not significantly change metabolic parameters, but exacerbated LPS-induced alveolar bone loss, osteoclastogenesis, and periodontal tissue inflammation. To understand the mechanisms by which ASMase deficiency aggravates LPS-induced periodontitis, we analyzed sphingolipids in periodontal tissues. Results showed that ASMase deficiency led to increases in not only sphingomyelin, but also ceramide (CER), a bioactive sphingolipid known to promote inflammation. Results further showed that ASMase deficiency increased CER de novo synthesis. CONCLUSION: ASMase deficiency exacerbated LPS-induced alveolar bone loss and periodontal inflammation. ASMase deficiency leads to an unexpected CER increase by stimulating de novo synthesis CER, which is likely to be involved in the ASMase deficiency-exacerbated periodontitis.

Blood Oxidative Stress Modulates Alveolar Bone Loss in Chronically Stressed Rats.

We aimed to investigate the effects of chronic stress (CS) on experimental periodontitis (EP) in rats. For this, 28 Wistar rats were divided into four groups: control, ligature-induced experimental periodontitis (EP), chronic stress (CS; by physical restraint model) and CS+EP (association of chronic stress and ligature-induced periodontitis). The experimental period lasted 30 days, including exposure to CS every day and ligature was performed on the 15th experimental day. After 30 days, the animals were submitted to the behavioral test of the elevated plus maze (EPM). Next, rats were euthanized for blood and mandible collection in order to evaluate the oxidative biochemistry (by nitric oxide (NO), reduced-glutathione activity (GSH), and thiobarbituric acid reactive substance levels (TBARS)) and alveolar bone characterization (by morphometric, micro-CT, and immunohistochemistry), respectively. The behavioral parameters evaluated in EPM indicated higher anxiogenic activity in the CS and CS+EP, groups, which is a behavioral reflex of CS. The results showed that CS was able to change the blood oxidative biochemistry in CS and CS+EP groups, decrease GSH activity in the blood, and increase the NO and TBARS concentrations. Thus, CS induces oxidative blood imbalance, which can potentialize or generate morphological, structural, and metabolic damages to the alveolar bone.

Crestal Bone Loss Around Submerged and Non-Submerged Dental Implants in Individuals with Type-2 Diabetes Mellitus: A 7-Year Prospective Clinical Study.

OBJECTIVE: In establishing an evidence-based rationale for the optimal use of implant therapy in patients with type 2 diabetes mellitus (T2DM), it is essential to first understand the impact of glycemic control on early healing and the success of dental implants. The objective of this study was to evaluate crestal bone loss (CBL) and stability around submerged and non-submerged dental implants in Saudi patients with well- and poorly controlled T2DM. SUBJECT AND METHODS: Thirty-five patients with well-controlled T2DM (24 males and 11 females) and 32 poorly controlled T2DM patients (19 males and 13 females) were included. CBL was measured on digital radiographs; resonance frequency analysis (RFA) measurements were made for each implant at the time of fixture placement and at 3 months in both the groups. A p value less than 0.05 was considered statistically significant. RESULTS: A total of 124 dental implants were placed. Mean RFA values between baseline and 3 months in poorly controlled T2DM patients was statistically significant (p = 0.048). CBL at first year (p = 0.047), second year (p = 0.041), third year (p = 0.046), and seventh year (p = 0.035) was significantly worse in poorly controlled T2DM. CBL around non-submerged dental implants showed statistically significant differences at all time-intervals (p < 0.05). CONCLUSION: Poorly controlled T2DM patients present worse peri-implant bone outcomes as compared to patients with well-controlled T2DM. We suggest that the predictability of successful dental implant therapy outcomes depends on the maintenance of optimal haemoglobin A1c levels.

Oral Rehabilitation with Implant-Retained Overdenture in a Patient with Down Syndrome.

Down syndrome, known as trisomy 21, is the most common chromosomal disorder. The disorder affects mental and systemic development as well as oral structure, including dental anomalies, high susceptibility of periodontal disease, and poor quality of alveolar bone. This report presents a case of dental rehabilitation by means of dental implants of a patient with Down syndrome. Two titanium dental implants were placed in the maxilla, and three titanium dental implants were installed in the mandible. One implant was lost during the osseointegration period. The prosthetic rehabilitation was performed with implant-retained maxillary and mandibular overdentures with the Locator attachment system. After a 2-year follow-up period, the patient was doing well, and all implants were clinically stable with no signs of bone loss or inflammation. The present study emphasizes that implant-retained overdentures with Locator attachment system could be a therapeutic option even for patients with Down syndrome. This therapy prevents crestal bone loss around the implants, improves functional and esthetic outcomes, and provides optimum oral hygiene for patients with mild mental impairment. Careful patient selection and education of patients and caregivers are essential considerations for a successful and safe treatment with dental implants in Down syndrome patients.

Simvastatin attenuates tibial bone loss in rats with type 1 diabetes and periodontitis.

BACKGROUND: Diabetes induces long bone loss and aggravation of periodontitis-induced alveolar bone loss. Simvastatin (SIM), which is a lipid-lowering agent is known to have an anabolic effect on bone. Therefore, we investigated effect of SIM on tibial and alveolar bone loss in type 1 diabetic rats with periodontitis. METHODS: Rats were divided into control (C), diabetes with periodontitis (DP), and diabetes with periodontitis treated with SIM (DPS) groups. DP and DPS groups were intravenously injected with streptozotocin (50 mg/kg), and C group was injected with citrate buffer. Seven days later (day 0), periodontitis was induced by ligatures of mandibular first molars. DP and DPS groups were orally administered vehicle or SIM (30 mg/kg) from day 0 to days 3, 10, or 20. Alveolar and tibial bone loss was measured using histological and m-CT analysis alone or in combination. Osteoclast number and sclerostin-positive osteocytes in tibiae were evaluated by tartrate-resistant acid phosphatase and immunohistochemical staining, respectively. Glucose, triglyceride (TG), cholesterol (CHO), and low-density lipoprotein (LDL) were evaluated. RESULTS: Consistent with diabetes induction, the DP group showed higher glucose and TG levels at all timepoints and higher CHO levels on day 20 than C group. Compared to the DP group, the DPS group exhibited reduced levels of glucose (day 3), TG (days 10 and 20), CHO, and LDL levels (day 20). Bone loss analysis revealed that the DP group had lower bone volume fraction, bone mineral density, bone surface density, and trabecular number in tibiae than C group at all timepoints. Interestingly, the DPS group exhibited elevation of these indices at early stages compared to the DP group. The DPS group showed reduction of osteoclasts (day 3) and sclerostin-positive osteocytes (days 3 and 20) compared with the DP group. There was no difference in alveolar bone loss between DP and DPS groups. CONCLUSIONS: These results suggest that SIM attenuates tibial, but not alveolar bone loss in type 1 diabetic rats with periodontitis. Moreover, attenuation of tibial bone loss by SIM may be related to inhibition of osteoclast formation and reduction of sclerostin expression.

Oral rehabilitation of the cancer patient: A formidable challenge.

Rehabilitation of oral functions following surgery on the jaws is a goal that is often difficult to achieve. Removable dentures supported by remaining teeth or gum are often unstable and seldom satisfactory. On the other hand, endosseous (dental) implants offer a mechanism to provide stability to the dentures. This review, discusses factors related to the tumor, patient, treatment, and physicians which impact upon the feasibility and success of dental implants in patients with oral cancer.

Clinical and Radiographic Peri-Implant Parameters and Whole Salivary Interleukin-1ß and Interleukin-6 Levels among Type-2 Diabetic and Nondiabetic Patients with and without Peri-Implantitis.

OBJECTIVE: The aim was to assess the peri-implant clinical and radiographic parameters and whole salivary levels of interleukin (IL)-1ß and IL-6 among type 2 diabetic and nondiabetic patients with and without peri-implantitis. MATERIAL AND METHODS: Ninety-one implants were placed in patients without type 2 diabetes mellitus (39 patients with and 52 patients without peri-implantitis; group 1). Eighty implants were placed in patients with diabetes (35 patients with and 45 patients without peri-implantitis; group 2). Peri-implant plaque index, bleeding on probing, probing depth, and marginal bone loss were measured. Unstimulated whole saliva samples were collected and IL-1ß and IL-6 levels were measured using standard techniques. p < 0.05 was considered statistically significant. RESULTS: In group 1, plaque index (p < 0.001), bleeding on probing (p < 0.001), probing depth (p < 0.001), and whole salivary IL-1ß (p < 0.001) and IL-6 (p < 0.001) levels were significantly higher in patients with peri-implantitis than in those without peri-implantitis. Plaque index, bleeding on probing, probing depth, and marginal bone loss were comparable among all of the patients in group 2. Among patients with peri-implantitis, plaque index (p < 0.001), bleeding on probing (p < 0.001), probing depth (p < 0.001), marginal bone loss (p < 0.001), and whole salivary IL-1ß (p < 0.001) and IL-6 (p < 0.001) levels were significantly higher in those with diabetes than in those without diabetes. CONCLUSION: Among individuals without diabetes, peri-implant plaque index, bleeding on probing, probing depth, marginal bone loss, and whole salivary IL-1 ß and IL-6 levels were higher among patients with peri-implantitis compared to patients without peri-implantitis. Among patients with diabetes, the severity of the measured parameters appears to be influenced by the glycemic status rather than by peri-implantitis.

Relation between periodontal disease and arterial stiffness.

BACKGROUND AND OBJECTIVE: Periodontal disease has been described as playing a role in the atherosclerosis process, and its relation with intimal thickness and vascular endothelial function (EF) has been investigated. The present study sought to determine whether there are differences in parameters of arterial stiffness and EF between patients with and without severe periodontal disease (SPD). MATERIAL AND METHODS: Patients referred to the School of Dentistry University of Buenos Aires, were assessed. Demographic characteristics, atherogenic risk factors and concomitant pathologies were recorded. Patients with known cardiovascular pathology were excluded. Using carotid Doppler ultrasound an operator assessed arterial stiffness parameters: compliance, elastic modulus (EM), ß stiffness index (ßSI) and vascular EF by brachial artery flow-mediated dilatation. The patients were divided into two groups: with and without SPD. RESULTS: Forty patients were included; 60% were women; 15 were in the SPD group and 25 in the group without SPD. Respective results of the studied variables were: age 56.53 ± 17.58 vs. 51.12 ± 12.97 years (NS); probing depth 2.53 ± 1.30 (95% CI 1.81-3.25) vs. 1.25 ± 0.51 (95% CI 1.31-1.73) p = 0.02; clinical attachment level 4.80 ± 2.00 (95% CI 3.69-5.91) vs. 1.72 ± 0.93 (95% CI 1.33-2.11) p = 0.001; intimal thickness 0.10 ± 0.17 (95% CI 0.095-0.11) vs. 0.82 ± 0.18 (95% CI 0.074-0.98) (NS); EM 48.33 ± 12.53 vs. 38.86 ± 7.69 (p = 0.005); ßSI 4.21 ± 1.03 vs. 3.64 ± 1.02 (p = 0.004); EF 16.13 ± 5.02 vs. 22.76 ± 4.50 (p = 0.0003). Correlation between: EM and clinical attachment level r = 0.58 (p < 0.001), ßSI and clinical attachment level r = 0.66 (p < 0.001), EF and clinical attachment level 0.59 (p < 0.001). CONCLUSIONS: Parameters of arterial stiffness and EF were worse in patients with SPD and correlated moderately with clinical attachment level. Correlation with compliance and EF was negative.

Tooth loss in generalized aggressive periodontitis: Prognostic factors after 17 years of supportive periodontal treatment.

AIM: This retrospective longitudinal study assessed the risk of and prognostic factors for tooth loss in patients with generalized aggressive periodontitis (GAgP) after periodontal treatment in a university setting. METHODS: Fifty-seven patients (1,505 teeth) were examined before (T0) and after active periodontal therapy (APT, T1) as well as after 17.4 ± 4.8 [range: 9-28] years of supportive periodontal therapy (SPT, T2). Descriptive statistics and a Cox-proportional-hazards shared-frailty model were applied. RESULTS: Overall, 98 and 134 teeth were lost during APT and SPT, respectively, with 0.14 ± 0.18 teeth being lost per patient and year. During SPT, three patients (5%) lost ≥10 teeth, 14 (25%) lost 4-9 teeth, 40 lost 0-3 (70%) teeth, respectively. One-third (n = 19) of all patients lost no teeth. Mean PPD of the teeth surviving SPT was stable from T1 (3.5 ± 1.1 mm) to T2 (3.4 ± 1.1 mm). Nearly, 84% of all survived teeth showed stable or improved bone level at T2. Risk of tooth loss was significantly increased in active smokers (HR[95% CI]: 4.94[1.91/12.75]), the upper dental arch (1.94[1,16/3.25]), with each mm of residual PPD (1.41[1.29/1.53]), teeth with furcation involvement (FI) (HR 4.00-4.44 for different degrees) and mobility (5.39 [2.06/14.1] for degree III). CONCLUSION: Within the provided conservative treatment regimen, GAgP patients lost only few teeth.

A principal components analysis: how pneumatization and edentulism contribute to maxillary atrophy.

OBJECTIVE: The aim of this retrospective cohort study was to investigate the role of sinus pneumatization and residual ridge resorption in maxillary bone loss in 400 computed tomography (CT) scans. MATERIALS AND METHODS: In 200 dentate and 200 edentulous patients, both sinuses were analysed using CT scans. The image analysis sequence consisted of manual placement of 24 reference points, followed by automated segmentation and final manual refinement. Finally, a principal components analysis was performed. RESULTS: A total of 788 sinuses were included into the analysis. The edentulous group (98 female: 67.77 ± 11.28 years, 99 male: 65.22 ± 9.87) was significantly older than the group with teeth (99 female: 46.89 ± 16.77 years, 96 male: 49.74 ± 16.2). Female and male patients did not differ regarding age. The alveolar height differed significantly between the groups (edentulous: 7.1 ± 4.3 mm, with teeth: 9.7 ± 4.1 mm), but not between gender (female: 8.3 ± 4.4 mm, male: 8.5 ± 4.4 mm). Principal components analysis was able to explain 90% of the variation in sinus morphology. CONCLUSIONS: Prolonged edentulism in the maxillary molar region leads to centripetal and to minor degrees centrifugal ridge resorption. Minor pneumatization occurs in the sinus walls, but the sinus depth underlies the anatomical variation independent of dentition.

Failure of Osseointegrated Dental Implant After Alveolar Nerve Transposition: A Report of an Unusual Complication and Surgical Management.

PURPOSE: To describe an unusual case of mandibular fracture after osseointegrated dental implant removal placed after inferior alveolar nerve transposition. REPORT OF CASE: The patient underwent inferior nerve transposition for implant placement due to lack of interarch space. Two months after metal-ceramic crowns installation, the patient began to complain of pain in the region of the implant. In an attempt to remove the implant, there was a fracture of the implant, and only two third of it was removed, leaving only the apical portion of the implant in the mandible. The patient opted for the total removal of implant. At 15 days of follow-up, the patient returned with mandibular fracture, which was treated through an internal fixation with a titanium reconstruction plate of 2.0-mm thickness with locking screws. CONCLUSION: The inferior alveolar nerve transposition may represent the only rehabilitation option, especially in cases where there is insufficient bone remaining for installation of short implants with reduced interarch space.