Type 1 diabetes and periodontitis: prevalence and periodontal destruction-a systematic review.

AIMS: Data about the association between periodontal disease or periodontitis (PD), diabetes and hyperglycemia have been reported mostly in patients with type 2 diabetes. Conversely, information about PD in type 1 diabetes (T1DM) is relatively scarce. The aim of this meta-analysis is therefore: (1) to assess the prevalence and severity of PD in patients affected by T1DM in comparison with the general population and (2) to verify the association between severity of PD and glycemic control in type 1 diabetics. METHODS: An electronic search was performed on MEDLINE, Cochrane Central Register of Trials and EMBASE, up to October 31, 2019. Estimates of prevalence of PD in T1DM were calculated together with Mantel-Haenszel odds ratios (MH-OR) of the risk of PD associated with T1DM; weighed mean difference in CAL between T1DM and control and weighed mean difference in CAL in patients with T1DM and unsatisfactory glycemic control as compared with those in good glycemic control were also evaluated.. RESULTS: The prevalence of PD in type 1 diabetes was 18.5 [8.0; 37.1] %; the MH-OR for PD is 2.51 (1.32;4.76) in T1DM patients versus general population (p = 0.005). The weighed mean difference in CAL depth between T1DM patients and controls is 0.506 [0.181; 0.832] mm (p < 0.005), and in T1DM patients with good glycemic control CAL depth is - 0.71 [- 1.00; - 0.42] mm less deep than in subjects with HbA1c > 7%. CONCLUSIONS: The present data confirm that T1DM is a relevant risk factor for the development of PD. The proportion of patients affected by PD is more than doubled in subjects with T1DM in comparison with non-diabetic individual, and among patients with T1DM, PD seems to be more severe and the differences appear very wide between subjects in optimal and suboptimal glycemic control.

Digital and Orthodontically Driven Implant Planning: A Multidisciplinary Case History Report.

Patients presenting both severe maxillary atrophy and dental malposition require a multidisciplinary treatment approach to achieve optimal esthetic and functional results. This case history report demonstrates how digital treatment planning and teeth set-up can serve as a reference for surgical, orthodontic, and prosthodontic procedures, leading to an all-ceramic full-arch implant-supported fixed prosthesis.

Occlusal hypofunction causes periodontal atrophy and VEGF/VEGFR inhibition in tooth movement.

OBJECTIVE: To examine changes in microvasculature and the expression of vascular endothelial growth factor A (VEGF-A) and VEGF receptor 2 (VEGFR-2) in rat hypofunctional periodontal ligament (PDL) during experimental tooth movement. MATERIALS AND METHODS: Twelve-week-old male Sprague-Dawley rats were divided into normal occlusion and occlusal hypofunction groups. After a 2-week bite-raising period, rat first molar was moved mesially using a 10-gf titanium-nickel alloy closed coil spring in both groups. On days 0, 1, 2, 3, and 7 after tooth movement, histologic changes were examined by micro-computed tomography and immunohistochemistry using CD31, VEGF-A, VEGFR-2, and the terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method. RESULTS: Hypofunctional molars inclined more than normal molars and did not move notably after day 1 of tooth movement. Blood vessels increased on the tension side of the PDL in normal teeth. Immunoreactivities for VEGF-A and VEGFR-2 in normal teeth were greater than those in hypofunctional teeth during tooth movement. Compressive force rapidly caused apoptosis of the PDL and vascular endothelial cells in hypofunctional teeth, but not in normal teeth. CONCLUSIONS: Occlusal hypofunction induces vascular constriction through a decrease in the expression of VEGF-A and VEGFR-2, and apoptosis of the PDL and vascular cells occurs during tooth movement.

A misadventure with an elastic band, 38 years later.

This case report is of maxillary central incisors still in place 38 years after periodontal surgery to correct the damage to supporting tooth structure caused by an orthodontic elastic band.

Occlusal hypofunction induces atrophic changes in rat gingiva.

OBJECTIVE: To clarify the influence of occlusal hypofunction on the integrity of gingival tissue and gingival extracellular matrix biosynthesis. MATERIALS AND METHODS: Thirteen-week-old male Wistar rats were divided into two groups. To eliminate occlusal forces, all the right maxillary molars were extracted in the hypofunctional group. The control group was anesthetized but not subjected to surgery. The rats were killed at 2 and 4 weeks after the procedure, and the lower right second molars were prepared for histological analysis. To investigate the effect of occlusal hypofunction on collagen biosynthesis, the expression of connective tissue growth factor (CTGF) and lysyl oxidase (LOX) was determined by immunohistochemistry as well as histological examination by hematoxylin and eosin staining. RESULTS: Disorientation of the collagen fibers, proliferation of the connective tissue fibroblasts, and enlargement of epithelial intercellular gaps were observed in gingival tissue of rat molars with experimental occlusal hypofunction. Immunohistochemically, the expression of CTGF and LOX was increased significantly (P < .05) in the hypofunctional group. CONCLUSION: These results suggest that occlusal hypofunction can affect the structural integrity and the expression of CTGF and LOX in gingival tissue.