Alveolar bone healing after upper incisor extraction in rats is a classical model of preclinical studies. The underlying morphometric, cellular and molecular mechanism, however, remains imprecise in a unique study.

Recent evidence suggests an association between hypertension and periodontitis, although the pathways and implications underlying both chronic conditions are still poorly understood. Therefore, the aim of this study was to evaluate the relationship between hypertension and periodontitis through an observational clinical study using periodontal, physical, and biochemical analyses in hypertensive and non-hypertensive individuals with periodontitis. A total of one hundred patients were divided into two groups. The first group was hypertensive patients with periodontitis. The second group was non-hypertensive patients with periodontitis. Periodontal parameters of probing depth, bleeding on probing, and clinical attachment level were evaluated. The systolic, diastolic, mean, and differential blood pressure were measured in the physical examination. In addition, body mass index and waist–hip ratio were verified. Biochemical tests for glycated hemoglobin, fasting blood glucose, estimated blood glucose, total cholesterol, high-density lipoprotein, creatinine, glutamate pyruvate transaminase, glutamic oxaloacetic transaminase, and C-reactive protein were evaluated. The data were submitted for statistical analysis (α = 0.05%). The results of this study demonstrated that patients with cardiovascular disease did not present with worse periodontal clinical parameters in the conditions studied. However, it is important to bear in mind that this cross-sectional study has some inherent limitations to its design; therefore, to study the relationship between hypertension and periodontitis further, an interventional randomized clinical trial should be conducted.

The aim of this study was to analyze the stages of the alveolar bone repair in type 2 diabetic rats evaluating the mechanism of mineralization and bone remodeling processes after dental extraction. Forty-eight rats were divided into normoglycemic (NG) and type 2 diabetes (T2D) groups. The upper right incisor was extracted and after 3, 7, 14 and 42 days the animals were euthanized. The following analyses were performed: immunolabeling against antibodies TNFα, TGFβ, IL6, WNT, OCN and TRAP, collagen fibers maturation, microtomography and confocal microscopy. Data were submitted to statistical analysis. The immunolabeling analysis showed that the T2D presented a more pronounced alveolar inflammation than NG. Labeling of proteins responsible for bone formation and mineralization was higher in NG than T2D, which presented greater resorptive activity characterized by TRAP labeling. Also, T2D group showed a decrease in the amount of collagen fibers. Micro-CT analysis showed that T2D causes a decrease in bone volume percentage due to deficient trabecular parameters and higher porosity. The T2D bone dynamics show a loss in bone remodeling process. T2D prolongs the local inflammatory process, which impairs the organization and maturation of collagen fibers, delaying bone formation that generates impact on mineralization and bone turnover.

(1) Background: Evaluate the osteoconduction capability of a biphasic calcium phosphate (BCP) ceramic composed of hydroxyapatite and β-tricalcium phosphate 60%/40% in a rat model. (2) Methods: In the calvarial bone of 54 adult male rats, 7-mm diameter critical size defects were performed. The animals were randomly allocated to three experimental groups according to the type of material: blood clot (BCG), blood clot covered with a bovine-derived collagen membrane (MBCG), and BCP ceramic covered with a bovine-derived collagen membrane (BCPG). In each group, 6 animals were euthanatized at post-operative days 7, 30, and 60 for histological and histometric analysis. (3) Results: The qualitative analysis revealed the persistence of the collagen membrane at seven days, with no relevant newly bone formation in all groups. At 30 days, centripetal bone formation was observed residual particles of the biomaterial surrounded by fibroblasts noted in the BCPG. At 60 days, while BCG and MBCG showed a partial maturation with the central part of the defect populated by a fibrous connective tissue, in the BCPG the critical area was entirely occupied by newly formed bone. In the intra groups analysis was noted a significant increase in new bone formation during the experimental period (p < 0.05). At 60 days, BCPG showed a higher percentage area of new bone formation (p < 0.05). (4) Conclusion: BCP promoted a new bone formation by osteoconduction and might be considered a valid alternative in bone regeneration procedures.

Hypertension and estrogen deficiency can affect bone metabolism and therefore increase the risk of osseointegration. Antihypertensive drugs such as losartan not only control blood pressure but also enhance bone healing. In addition, alendronate sodium is widely used to treat postmenopausal osteoporosis. Hence, we evaluated the effect of systemic antihypertensive and local alendronate coted on implants on osseointegration under hypertensive and estrogen-deficiency conditions. A total of 64 spontaneously hypertensive rats (SHRs) treated with losartan were randomly divided according to the estrogen-deficiency induction by ovariectomy (OVX) or not (SHAM), and whether the implant surface was coated with sodium alendronate (ALE) or not, resulting in four groups: SHR SHAM, SHR SHAM ALE, SHR OVX, and SHR OVX ALE. The removal torque, microcomputed tomography, and epifluorescence microscopy were the adopted analyses. The hypertensive and estrogen-deficiency animals presented a lower removal torque even when treated with alendronate on implant surface. The microcomputed tomography revealed a higher bone volume and bone-to-implant contact in the SHRs than the SHR OVX rats. Epifluorescence showed a decreased mineral apposition ratio in the SHR OVX ALE group. The data presented indicate that estrogen deficiency impairs osseointegration in hypertensive rats; in addition, alendronate coated on the implant surface does not fully reverse this impaired condition caused by estrogen deficiency.