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Aim To evaluate the long-term (≥2 years) stability of root coverage procedures for single gingival recessions. Materials and methods A complete literature search was performed up to July 2018. Randomized controlled trials (RCTs) following ≥2 years were selected. Primary outcomes were complete root coverage (CRC) and mean root coverage (MRC). Secondary outcomes were width of keratinized tissue (KTW) and patient-centred parameters. Meta-analysis was conducted when possible. Results A total of fifteen RCTs were included. The results demonstrated significantly higher MRC in short-term than long-term after coronally advanced flap (CAF; 7.29%, p = 0.006). When CAF combined with connective tissue graft (CTG), no significant difference was observed in CRC or MRC for short-term versus long-term (1.00, p = 0.97; 2.35%, p = 0.09), and it resulted in better long-term efficacy than CAF alone in terms of CRC (0.69, p = 0.0006) and KTW (-0.63 mm, p = 0.04). For CAF plus enamel matrix derivative, the meta-analysis showed no significant difference between the short-term and long-term results of CRC (1.26, p = 0.21). Conclusions CAF alone could result in decreased postoperative percentage of root coverage with time. CAF + CTG could maintain long-term stability and result in better root coverage outcomes than CAF.

Objective and background Recently, decellularized matrix (DCM) is considered as a new biomaterial for tissue regeneration. To explore the possible application of DCM in periodontal regeneration, the effect of DCM from three different cells on the proliferation and differentiation of human periodontal ligament stem cells (PDLSCs) was investigated. Methods DCM derived from human periodontal ligament cells (PDLCs), dental pulp cells (DPCs), and gingival fibroblasts (GFs) were fabricated using Triton X-100/NH4 OH combined with DNase I. Allogeneic PDLSCs were cultured on PDLC-DCM, DPC-DCM, and GF-DCM, respectively. The proliferative capacity of PDLSCs was evaluated by PicoGreen assay kit. The expression of alkaline phosphatase (ALP), runt-related transcription factor-2 (RUNX2), osteocalcin (OCN), collagen I (COL1), periostin (POSTN), and cementum protein 1 (CEMP1) were detected by qRT-PCR and western blotting. Results PDLC-DCM, DPC-DCM, and GF-DCM had similar and integrated networks of extracellular matrix, as well as significantly decreased DNA content. Compared with control group in which PDLSCs were directly seeded in culture plates, PDLC-DCM, DPC-DCM, and GF-DCM promoted the proliferation of re-seeded PDLSCs. Additionally, PDLSCs on DCM exhibited higher mRNA and protein expression levels of ALP, RUNX2, OCN, and COL1. The expression of POSTN in PDLC-DCM group was significantly higher than control group at both mRNA and protein levels. Conclusions PDLC-DCM, DPC-DCM, and GF-DCM could enhance the proliferation of PDLSCs. PDLC-DCM facilitated osteogenic differentiation and periodontal ligament differentiation of PDLSCs, while DPC-DCM and GF-DCM promoted osteogenic differentiation.

Periodontal disease (PD), as an age-related disease, prevalent in middle-aged and elderly population, is characterized as inflammatory periodontal tissue loss, including gingival inflammation and alveolar bone resorption. However, the definite mechanism of aging-related inflammation in PD pathology needs further investigation. Our study is aimed at exploring the effect of inflamm-aging-related cytokines of interleukin-17 (IL-17) and interferon-γ (IFN-γ) on osteoclastogenesis in vitro and periodontal destruction in vivo. For receptor activator of nuclear factor-κB ligand- (RANKL-) primed bone marrow macrophages (BMMs), IL-17 and IFN-γ enhanced osteoclastogenesis, with the expression of osteoclastogenic mRNA (TRAP, c-Fos, MMP-9, Ctsk, and NFATc1) and protein (c-Fos and MMP-9) upregulated. Ligament-induced rat models were established to investigate the role of IL-17 and IFN-γ on experimental periodontitis. Both IL-17 and IFN-γ could enhance the local inflammation in gingival tissues. Although there might be an antagonistic interaction between IL-17 and IFN-γ, IL-17 and IFN-γ could facilitate alveolar bone loss and osteoclast differentiation.

Additional file 1: Table S1. Characteristics of included patients.

Objective Interleukin-17 (IL-17) and interferon-gamma (IFN-γ) are all pro-inflammatory cytokines produced by specific subsets of T-cells and are also considered crucial regulators in bone remodeling, but their effects on osteogenesis have not been carefully studied. So, this study aimed to investigate the effects of secreting cytokines IL-17 and IFN-γ on the osteogenesis of primary osteoblasts and to clarify the potential roles of the related Janus activated kinase 2 (JAK2) and downstream signal transducer and activator of transcription 3 (STAT3) signaling pathway in bone remodeling. Methods The proliferation of osteoblasts was evaluated by MTT assay. Osteogenic activity was tested by alkaline phosphatase (ALP) activity assay and alizarin red staining. The mRNA levels of ALP, osteocalcin, osteoprotegerin (OPG), Runt-related transcription factor 2 (Runx2) and receptor activator of nuclear factor-kappa B ligand (RANKL) were also measured by real-time quantitative PCR. The JAK2-STAT3 pathway was evaluated by Western blot. Results Osteoblasts showed no obvious proliferation when treated with IL-17 and/or IFN-γ, but higher ALP activities were observed in primary osteoblasts treated with IL-17 or IL-17 + IFN-γ in induction medium. We also found that IL-17 could promote the gene expression of Alp , Runx2 , Osteocalcin , Opg , and Rankl , while IFN-γ might attenuate this effect. Nevertheless, IL-17 and IFN-γ exhibited an inhibitory effect on the calcification of p rimary osteoblasts. We also found that IL-17 could directly facilitate RANKL expressions by JAK2-STAT3 pathway. Conclusion The positive effects of IL-17 and IFN-γ on the early-stage differentiation and the negative effects on the calcification of murine calvarial osteoblasts contribute to our understanding of the role and interaction of inflammatory factors in the bone remodeling and as fundamental mechanisms involved in the destruction of alveolar bone.

Interleukin (IL)‑17A exhibits pleiotropic biological activities and serves a role in the progression of periodontitis. However, data describing the association between IL‑17 and osteogenesis are not conclusive. It was previously demonstrated that RAC‑β serine/threonine protein kinase (AKT2)‑specific knockdown in MC3T3‑E1 cells weakened osteogenic effects. The role of AKT2 in the regulation of IL‑17A for osteoblast differentiation and calcification remains unclear. The MTT method was adopted in the present study to assess cell proliferation; cell cycle distribution was analyzed by flow cytometry. Following osteogenic induction treatment, the involvement of phosphatidylinositol 3‑kinase (PI3K) and phosphorylated‑PI3K was evaluated by western blotting. The effects of IL‑17A on osteogenesis‑associated markers, including Runt‑related transcription factor 2 (Runx‑2), alkaline phosphatase (ALP) and osteocalcin (OCN) were evaluated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis. An ALP activity assay and Alizarin Red S staining were used to assess the differentiation and calcification functions. AKT2 knockdown inhibited MC3T3‑E1 cell proliferation, inducing significantly increased G0/G1 cell counts, and reduced S and G2/M cell numbers. IL‑17A exerted no significant effects. The protein levels of p‑PI3K, gene expression levels of IL‑17A, Runx‑2, ALP and OCN, and relative ALP activity and calcification areas were increased in the induction group, and these effects were markedly promoted by treatment with IL‑17A. AKT2 knockdown in MC3T3‑E1 cells resulted in reduced IL‑17A‑induced differentiation and calcification, although it was not completely inhibited. The results of the present study suggested that AKT2 signaling was required for MC3T3‑E1 cell proliferation. IL‑17A promoted osteoblast differentiation and calcification in a partly AKT2‑dependent manner in MC3T3‑E1 cells in vitro, possibly reflecting compensation by other signaling pathways. The results of the present study may offer novel perspectives to guide the clinical strategy for the prevention and treatment of periodontitis.

Background: 15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), one of the major metabolites from prostaglandin D2 in arachidonic acid metabolic pathway, has potential anti-inflammatory properties. The objective of this study was to explore the effects of 15d-PGJ2-loaded poly(D,L-lactide-co-glycolide) nanocapsules (15d-PGJ2-NC) on inflammatory responses and bone regeneration in local bone defect. Methods: The study was conducted on 96 Wistar rats from June 2014 to March 2016. Saline, unloaded nanoparticles, free 15d-PGJ2 or 15d-PGJ2-NC, were delivered through a collagen vehicle inside surgically created transcortical defects in rat femurs. Interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) levels in the surrounding soft tissue were analyzed by Western blot and in the defect by quantitative real-time polymerase chain reaction over 14 days. Simultaneously, bone morphogenetic protein-6 (BMP-6) and platelet-derived growth factor-B (PDGF-B) messenger RNA (mRNA) in the defect were examined. New bone formation and EphrinB2 and osteoprotegerin (OPG) protein expression in the cortical defect were observed by Masson’s Trichrome staining and immunohistochemistry over 28 days. Data were analyzed by one-way analysis of variance. Least-significant difference and Dunnett’s T3 methods were used with a bilateral P < 0.05. Results: Application of l5d-PGJ2-NC (100 μg/ml) in the local bone defect significantly decreased IL-6, IL-1β, and TNF-α mRNA and protein, compared with saline-treated controls (P < 0.05). l5d-PGJ2-NC upregulated BMP-6 and PDGF-B mRNA (P < 0.05). New bone formation was observed in the cortical defect in l5d-PGJ2-NC-treated animals from 7th day onward (P < 0.001). Expression of EphrinB2 and OPG presented early on day 3 and persisted through day 28 in 15d-PGJ2-NC group (P < 0.05). Conclusion: Stable l5d-PGJ2-NC complexes were prepared that could attenuate IL-6, IL-1β, and TNF-α expression, while increasing new bone formation and growth factors related to bone regeneration. Key words: 15-Deoxy-Δ 12,14-prostaglandin J2; Interleukin-1 Beta; Interleukin-6; Nanocapsules; Osteogenesis

Background Dentine hypersensitivity (DH) could occur or intensify after non-surgical periodontal therapy because of the exposure of dentine tubules, but currently no gold standard exists to treat DH. It has been demonstrated that nano-sized particles presented potential for dentine tubules blocking and remineralization. This randomized controlled trial aimed to investigate the efficacy of dentifrice containing nano-carbonate apatite (n-CAP) in reducing dentine hypersensitivity (DH) after non-surgical periodontal therapy. Methods 48 periodontitis patients with DH were included in this clinical trial. After non-surgical periodontal therapy, patients included were randomized to test and control group and the respective dentifrices were applied at chairside, after which they were instructed to brush teeth with the allocated dentifrices twice a day at home. Periodontal parameters were recorded at baseline and the last follow-up. DH was measured by air-blast test and recorded by visual analogue scale (VAS) and Schiff sensitivity scale at baseline, after polishing (0 week) and 2/4/6 weeks. Results 45 participants completed the follow-up. Periodontal parameters were improved and comparable between groups. Significant reduction in DH was observed in both groups at all time-points compared to baseline in terms of VAS and Schiff score. The test group achieved significantly greater relief from hypersensitivity compared with the control group after 4-week at-home use (for change of VAS, test group: 2.27 ± 2.47 versus control group: 1.68 ± 2.24, p = 0.036; for change of Schiff, test group: 0.94 ± 0.92 versus control group: 0.61 ± 0.83, p p = 0.027) and no significance in terms of change of VAS (p = 0.256). Conclusions Home-use of n-CAP based dentifrice had some benefit on alleviation of DH following non-surgical periodontal therapy after 4 weeks compared to the control product. Trial registration Chinese Clinical Trials Registry (No. ChiCTR-IPR-17011678, http://www.chictr.org.cn/, registered 16 June, 2017).

Interleukin 17A (IL-17A) exerts pleiotropic effects on periodontitis, partially through enhancement of alveolar bone loss. Osteoclasts are the main culprits that absorb alveolar bone. However, studies describing the correlation between IL-17A and osteoclasts are not conclusive. Previously, autophagy was revealed to be involved in osteoclast differentiation and bone resorption. However, the role of autophagy in IL-17A-mediated osteoclast formation is yet to be clarified. In the present study, bone marrow macrophages (BMMs) were treated with or without IL-17A. 3-Methyladenine (3-MA) was applied to inhibit autophagy. Osteoclast formation was detected by tartrate-resistant acid phosphatase (TRAP) staining, immunofluorescence, and scanning electron microscope. The effects of IL-17A on osteoclast-specific genes and autophagy-related genes during osteoclast differentiation were examined by real-time quantitative polymerase chain reaction and western blot analysis. Autophagosomes were observed by transmission electron microscope. Hematoxylin and eosin (H&E), and TRAP staining was adopted to assess alveolar bone destruction and the number of osteoclasts, respectively in a rat periodontitis model. Consequently, IL-17A stimulated osteoclast differentiation and bone resorption of BMMs accompanied by an increase in the mRNA expression of osteoclast-specific genes. Furthermore, IL-17A increased the levels of autophagy-related genes and proteins, and inhibition of autophagy with 3-MA attenuated the IL-17A-mediated osteoclastogenesis. In addition, there was an increase in the number of osteoclasts and alveolar bone resorption with IL-17A treatment in the periodontitis rat model. Collectively, these findings indicated that IL-17A facilitated osteoclast differentiation and bone resorption in vitro and in vivo, which may contribute to the understanding of the molecular basis of IL-17A in alveolar bone destruction and provide insight on the clinical therapeutic targets for periodontitis.

Objectives This review aims to evaluate the efficacy of xenogeneic collagen matrix (XCM) for the treatment of single or multiple gingival recessions in terms of clinical parameters and patient-related outcomes. Materials and methods Various electronic databases (The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, etc.) from 1966 to April 2018 and hand literatures were searched. Quality of the included studies was assessed through the Cochrane Collaboration's Risk of Bias tool. A meta-analysis was performed to calculate risk ratios and mean differences. Results Nine randomized controlled trials were included. The results revealed a higher percentage of mean root coverage (MRC) and a greater recession reduction (RecRed) for single recessions for the combination of coronally advanced flap (CAF) with XCM compared to CAF alone (n = 3; MD = 10.00%; 95%CI [3.56%; 16.43%]; p = 0.002) (n = 3; MD = 0.35 mm; 95%CI [0.10 mm; 0.60 mm]; p = 0.005). Comparing XCM with connective tissue graft (CTG), no significant differences were detected in MRC or RecRed for single and multiple recessions. Conclusions The addition of XCM under CAF could improve MRC and RecRed at single tooth recessions. Initial data suggest that XCM shows promising results to improve the clinical efficacy of CAF for multiple recessions. In addition, XCM could be a valid alternative to CTG in terms of MRC and RecRed at both single and multiple recessions. Based on limited evidence, XCM may decrease postoperative morbidity and operation time compared to CTG.

Lipopolysaccharide (LPS)-binding protein (LBP) as an acute-phase protein plays a crucial role in innate host response to bacterial challenge. Our previous study shows that LBP expression in human gingiva is associated with periodontal status. Porphyromonas gingivalis is a keystone periodontopathogen, and its LPS with lipid A structural heterogeneity critically accounts for periodontal pathogenesis. This study investigated the effects of LBP and its interactions with two featured isoforms of P. gingivalis LPS (tetra-acylated LPS1435/1449 and penta-acylated LPS1690) on the expression of pro-inflammatory cytokines in human oral keratinocytes (HOKs), and the involvement of Toll-like receptor (TLR) signaling. HOKs were pre-incubated with recombinant human LBP (rhLBP) at 10ng/ml, 100ng/ml and 1μg/ml for 1 h, followed by the treatment of P. gingivalis LPS1690 or LPS1435/1449 for 3h or 24h respectively. The expression of IL-6 and IL-8, and involvements of TLR2 and TLR4 were analyzed. The genes associated with TLR signaling were assessed by PCR array. Interestingly, rhLBP per se significantly up-regulated the expression of IL-6 and IL-8 in HOKs (p

LPS-binding protein (LBP) functions as a crucial molecule in innate immune responses to bacterial challenge. Our study has shown the expression of LBP in human gingiva and its significant association with periodontal health and disease. Porphyromonas gingivalis is a key pathogen of periodontal disease. P. gingivalis LPS as a main virulence factor is strongly involved in periodontal pathogenesis and it displays a significant lipid A structural heterogeneity. Currently, it remains unknown whether, and to what extent, the lipid A structural heterogeneity of P. gingivalis LPS affects LBP expression. The present study investigated the expression profile of LBP in human oral keratinocytes (HOKs) stimulated by two isoforms of P. gingivalis LPS [tetra- (LPS1435/1449) and penta-acylated (LPS1690)] and Escherichia coli LPS, and the involvement of TLRs in LBP expression. The results showed that the expression of LBP mRNA and peptide was significantly up-regulated by P. gingivalis LPS1690 and E. coli LPS, while P. gingivalis LPS1435/1449 did not affect LBP expression. Blocking assay and siRNA gene silencing revealed that P. gingivalis LPS1690-induced LBP expression was through both TLR2 and TLR4. This in vitro study demonstrates that P. gingivalis LPS with a lipid A structural heterogeneity differentially modulates LBP expression in HOKs.

To investigate if Drynariae rhizoma (DR) and its main ingredient Naringin could reduce alveolar bone loss by stimulating the proliferation and differentiation of osteoblasts.The effect of DR water (DRWE), ethanolic extract (DREE), and Naringin on MC3T3-E1 cells was evaluated respectively by MTT method and by measuring the activity of alkaline phosphatase (ALP activity) as well as the level of osteocalcin in medium. Bone mineral density (BMD) detection, osteoclast counting by tartrate resistant acid phosphatase staining, and histopathological analysis were performed in an induced rat model of alveolar bone resorption after gastric perfusion with DR extracts or Naringin.DRWE and Naringin effectively increased the proliferation of MC3T3-E1 cells, whilst DREE and Naringin enhanced the differentiation of osteoblastic cells. The in vivo study indicated an elevated BMD value in the tooth-periodontal tissues from DRWE, DREE and Naringin treated groups after 10, 20 and 30 days of perfusion (P0.05). In DRWE treated group, the number of osteoclasts at days 10, 20 and 30 decreased remarkably as compared to the corresponding negative controls (P0.05), and no osteoclast could be found at day 30. New non-calcified bone-like matrix attached by osteoblasts at the root furcation was also shown.DR could be a supplementary medicine for periodontal therapy as it could reduce bone resorption in rat model of alveolar bone resorption and exert osteogenic effect on osteoblasts.