ABSTRACT
Reports on the association of periodontal disease (PD) with systemic lupus erythematosus (SLE) have regularly been published. PD is a set of chronic inflammatory conditions linked to a dysbiotic microbial biofilm, which affects the periodontal tissues, resulting eventually in their destruction and contributing to systemic inflammation. SLE is a multi-system chronic inflammatory autoimmune disease that has a wide range of clinical presentations, touching multiple organ systems. Many epidemiological studies have investigated the two-way relationship between PD and SLE, though their results are heterogeneous. SLE and PD are multifactorial conditions and many biological-based hypotheses suggest common physiopathological pathways between the two diseases, including genetics, microbiology, immunity, and environmental common risk factors. By focusing on recent clinical and translational research, this review aimed to discuss and give an overview of the relationship of SLE with PD, as well as looking at the similarities in the immune-pathological aspects and the possible mechanisms connecting the development and progression of both diseases.
ABSTRACT
Periodontitis is based on a complex inflammatory over-response combined with possible genetic predisposition factors. The RANKL/RANK/OPG signaling pathway is implicated in bone resorption through its key function in osteoclast differentiation and activation, as well as in the inflammatory response. This central element of osteo-immunology has been suggested to be perturbed in several diseases, including periodontitis, as it is a predisposing factor for this disease. The aim of the present study was to validate this hypothesis using a transgenic mouse line, which over-expresses RANK (RTg) and develops a periodontitis-like phenotype at 5 months of age. RTg mice exhibited severe alveolar bone loss, an increased number of TRAP positive cells, and disorganization of periodontal ligaments. This phenotype was more pronounced in females. We also observed dental root resorption lacunas. Hyperplasia of the gingival epithelium, including Malassez epithelial rests, was visible as early as 25 days, preceding any other symptoms. These results demonstrate that perturbations of the RANKL/RANK/OPG system constitute a core element of periodontitis, and more globally, osteo-immune diseases.
ABSTRACT
Introduction. To evaluate outcomes of wide-diameter (6 mm) implants immediately provisionalized with cement-retained single crowns in posterior molar sites. Materials and Methods. Forty-eight consecutive patients received a total of 53 moderately rough-surface, 6 mm diameter implants in healed sites. All implants were immediately provisionalized with a cement-retained provisional crown. Final prosthesis with cement-retained porcelain fused to metal crowns was delivered 3-6 months later. Patients were followed up for 1 year. Outcome measures were implant failures and success rate, complications, marginal bone levels, bone level changes, papilla index, bleeding on probing, and inflammation. Results. One patient was lost to follow-up. At one year, the implant survival and success rate were 98.1%. The mean marginal bone loss after 1 year was -0.17 ± 1.84 mm. Ideal papilla score was recorded at 83.8% of the sites. More than 95.6% of the sites showed no bleeding or inflammation. No procedure-related or device-related adverse events were reported. Conclusion. Wide-diameter (6 mm) implants can safely and successfully replace single posterior molars. Longer follow-up studies are necessary to evaluate the long-term success of these implants.