Vitamin D plays an essential role in calcium and bone metabolism, immune regulation and possesses profound anti‐inflammatory effects. Evidence suggests that low serum vitamin D is associated with increased severity of periodontitis, a chronic inflammatory condition characterised by destruction of the supporting tissues surrounding the tooth, which has several shared risk factors with other chronic non‐communicable diseases. The biological functions of vitamin D are mediated by its strong anti‐microbial, anti‐inflammatory, and host modulatory properties. Experimental periodontitis models involving targeted deletion of 1α‐hydroxylase, the enzyme responsible for the conversion of inactive substrate to active 1,25(OH)₂D₃ (calcitriol), showed augmented alveolar bone loss and gingival inflammation. Vitamin D receptor (VDR) gene polymorphisms have also been associated with increased severity of periodontitis. Thus, the involvement of vitamin D in the pathogenesis of periodontitis is biological plausible. Clinical studies have consistently demonstrated an inverse relationship between serum 25OHD₃ and periodontal disease inflammation. However, due to the paucity of well‐designed longitudinal studies, there is less support for the impact of vitamin D status on periodontal disease progression and tooth loss. The evidence emphasises the importance of maintaining vitamin D sufficiency in supporting periodontal health. This review aims to first examine the biological mechanisms by which vitamin D might influence the pathogenesis of periodontal disease and second, discuss the clinical evidence which implicate the role of vitamin D in periodontal disease.

Vitamin D has important anti-inflammatory, anti-microbial properties and plays a central role in the host immune response. Due to the crucial role of the kidneys in the metabolism of vitamin D, patients with chronic kidney disease (CKD) are prone to vitamin D deficiency. The resultant reduction in the production of calcitriol, the activated form of vitamin D, in patients with CKD is responsible for exacerbating the existing renal impairment and periodontal inflammation. Recent evidence suggests a bidirectional, causal relationship between periodontitis and renal functional status. Both conditions have shared pathophysiological mechanisms including oxidative stress, increases in the systemic inflammatory burden and impaired host response. This review explores the association between vitamin D, CKD and periodontitis. The review summarises the current evidence base for the classical and non-classical vitamin D metabolic pathways, the biological mechanisms linking vitamin D deficiency, CKD and periodontitis, as well as the bidirectional relationship between the two chronic inflammatory conditions. Finally, the paper explores the impact of vitamin D deficiency on CKD, periodontitis, and related co-morbidities.

Clinical studies have shown favorable outcomes following use of platelet rich fibrin (PRF), either alone or in conjunction with biomaterials for alveolar ridge reconstruction (ARR) or guided bone regeneration (GBR) . While PRF application accelerates wound healing and reduces postoperative discomfort, its effects on the alveolar bone gain, as part of ARR or GBR is less clear. Therefore, this study aims to investigate the clinical effectiveness of PRF when used in ARR or GBR, as well as postoperative discomfort following these procedures. A systematic search using the Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) method was performed to include database searches from MEDLINE (OVID interface, 1946 onwards), EMBASE (OVID interface, 1974 onwards) and Global Health (OVID interface, 1973 onwards). Of the 74 studies initially identified, 7 studies were included for the systematic review, including 6 randomized controlled trials (RCTs) and 1 cohort study. The meta-analysis showed that the incorporation of PRF as part of ARR or GBR resulted in an increase in horizontal ridge width, a reduction in the rate of resorption increase, while postoperative discomfort was the same or slightly improved. The risk of bias quality was low for only 1 out of the 6 RCTs and the Newcastle Ottawa scale assessment showed that cohort study was of high quality. PRF application in ARR or GBR is associated with increased horizonal alveolar ridge width and reduce rate of graft resorption. However, the findings related to both outcome measures were based on a limited number of studies. PRF application can be effectively used as part of ARR or GBR to increase the horizontal ridge width and reduce the rate of graft resorption.

Objectives: To investigate the underlying molecular mechanisms by which gingival and periodontal ligament (PDL) fibroblasts regulate epithelial phenotype.Background: Fibroblast populations regulate the epithelial phenotype through epithelial‐mesenchymal interactions (EMI). Previous studies have proposed that maintenance of the junctional epithelium (JE) is dependent on the differential effects from gingival and PDL tissues. However, these cell populations are undefined and the signalling mechanisms which may regulate JE are unknown.Methods: Immunohistochemical analyses were performed on formalin‐fixed paraffin‐embedded sections of dentogingival tissues to identify phenotypic differences in fibroblast populations. The effect of distinct fibroblasts on epithelial phenotype was studied via 3D organotypic cultures, consisting of an H400 epithelium supported by human gingival fibroblasts (HGF) or human periodontal ligament fibroblasts (HPDLF), embedded in collagen gel. To investigate the involvement of Wnt signalling in EMI, the Wnt antagonist rhDKK1 was added to HGF constructs. The gene expression of Wnt antagonists and agonists was tested via RNA extraction and qPCR. Specific gene silencing using RNA interference was performed on HPDLF/HGF constructs.Results: Gingival fibroblasts were characterized by Sca1 expression, and PDL fibroblasts, characterized by Periostin and Asporin expression. Through the construction of 3D organotypic cultures, we showed that HGF supported epithelial multilayering, whilst HPDLF failed to support epithelial cell growth. Furthermore, HGF constructs treated with rhDKK1 resulted in a profound reduction in epithelial thickness. We identified SFRP4 to be highly specifically expressed in HPDLF, at both the mRNA and protein levels. A knockdown of SFRP4 in HPDLF constructs led to an increase in epithelial growth.Conclusion: The study demonstrates the presence of phenotypically distinct fibroblast populations within dentogingival tissues and that these specific populations have different influences on the epithelium. Our data suggest that a downregulation of Wnt signalling within PDL may be important in maintaining the integrity and anatomical position of the JE.

Aim: To assess the potential benefits of minimally invasive non‐surgical therapy (MINST) in teeth with intrabony defects and to explore factors associated with the outcomes.Materials and Methods: A multi‐centre trial was conducted in 100 intrabony defects in periodontitis patients in private practice. Steps 1 and 2 periodontal therapy including MINST were provided. Clinical and radiographic data were analysed at baseline and 12 months after treatment, with the primary aim being change in radiographic defect depth at 12 months.Results: Eighty‐four patients completed the 12‐month follow up. The mean total radiographic defect depth reduced by 1.42 mm and the defect angle increased by 3° (both p < .05). Statistically significant improvements in probing pocket depth (PPD) and clinical attachment level (CAL) were seen at 12 months compared to baseline (p < .001). Fifty‐six defects (66.7%) achieved pocket closure (PPD ≤ 4 mm) and 49 defects (58.3%) achieved the composite outcome (PPD ≤ 4 mm and CAL gain ≥3 mm). Deeper and narrower angled defects were positively correlated with radiographic and clinical improvements, respectively.Conclusions: Improvements in clinical and radiographic outcomes were seen after MINST. This study highlights the generalizability and wide applicability of this approach, further supporting its effectiveness in the treatment of intrabony defects. Clinical trial registration: NCT03741374. https://clinicaltrials.gov/study/NCT03741374?cond=minimally%20invasive%20non%20surgical%20therapy&locStr=UK&country=United%20Kingdom&distance=50&rank=2.

To study human neutrophil (polymorphonuclear leukocyte (PMN)) migration and killing of bacteria in an environment similar to that found in inflamed tissues in vivo, we have used fibrin gels. Fibrin gels (1500 μm thick) containing Staphylococcus epidermidis were formed in Boyden-type chemotaxis chambers. PMN migrated <300 μm into these gels in 6 h and did not kill S. epidermidis when the gels contained heat-inactivated serum, C5-deficient serum, a streptococcal peptidase specific for a fragment of cleaved C5 (C5a), or anti-C5aR IgG. In contrast, in gels containing normal human serum, PMN migrated ∼1000 μm into the gels in 4 h and into the full thickness of the gels in 6 h, and killed 90% of S. epidermidis in 6 h. fMLP reduced PMN migration into fibrin gels and allowed S. epidermidis to increase by ∼300% in 4 h, whereas leukotriene B₄ stimulated PMN to migrate the full thickness of the gels and to kill 80% of S. epidermidis in 4 h. We conclude that both complement opsonization and C5a-stimulated chemotaxis are required for PMN bacterial killing in fibrin gels, and that fMLP inhibits PMN bactericidal activity in fibrin gels. The latter finding is surprising and suggests that in the presence of fibrin fMLP promotes bacterial virulence.