Effects of extraoral storage time on autologous gingival graft early healing: A split-mouth randomized study.

AIMS: Despite the established use of palatal tissue grafts for mucogingival procedures, there are no studies on the effect of extraoral storage time on graft outcomes. This prospective split-mouth randomized experimental clinical trial aimed to assess whether gingival graft extraoral storage time affects graft healing. METHODS: Standardized grafts were harvested from the palate and stored extraorally for 2 (Control) or 40 (Test) minutes before being placed at recipient beds. Intraoral scans, clinical photographs, and tissue blood perfusion were obtained preoperatively, postoperatively, and at follow-up visits (Days 2 (PO2), 3 (PO3), 7 (PO7), and 14 (PO14)). Healing Score Index (HSI) and wound fluid (WF) biomarkers (angiogenin, IL-6, IL-8 (CXCL8), IL-33, VEGF-A, and ENA-78 (CXCL5)) were also assessed. RESULTS: Twenty-three participants completed all study visits. Extraoral storage time was 2.3 ± 1.1 min and 42.8 ± 3.4 min for C and T grafts, respectively (p < .0001). Recipient beds remained open for 21.4 ± 1.7 min. No graft underwent necrosis or failed to heal by PO14. Minimal volumetric changes were observed, without significant intergroup differences (p ≥ .11). Graft perfusion initially decreased post-harvesting before peaking on PO7 for both C and T grafts, with no significant intergroup differences (p ≥ .14). HSI values progressively increased, with no significant intergroup differences (p ≥ .22). WF analysis revealed detectable levels for all biomarkers tested, without significant intergroup differences (p ≥ .23). CONCLUSION: Extraoral storage time of 40 min has neither statistically significant nor clinically discernible effects on autologous graft revascularization, early healing, or survival, as determined by physiological, wound healing, and molecular parameters.

The therapeutic effects of gingival mesenchymal stem cells and their exosomes in a chimeric model of rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis is a chronic systemic autoimmune disease that involves transformation of the lining of synovial joints into an invasive and destructive tissue. Synovial fibroblasts become transformed, invading and destroying the bone and cartilage of the affected joint(s). Due to the significant role these cells play in the progression of the disease process, developing a therapeutic strategy to target and inhibit their invasive destructive nature could help patients who are afflicted with this debilitating disease. Gingival-derived mesenchymal stem cells are known to possess immunomodulatory properties and have been studied extensively as potential cell-based therapeutics for several autoimmune disorders. METHODS: A chimeric human/mouse model of synovitis was created by surgically implanting SCID mice with a piece of human articular cartilage surrounded by RASF. Mice were injected once with either GMSC or GMSCExo at 5-7 days post-implantation. Histology and IHC were used to assess RASF invasion of the cartilage. Flow cytometry was used to understand the homing ability of GMSC in vivo and the incidence of apoptosis of RASF in vitro. RESULTS: We demonstrate that both GMSC and GMSCExo are potent inhibitors of the deleterious effects of RASF. Both treatments were effective in inhibiting the invasive destructive properties of RASF as well as the potential for these cells to migrate to secondary locations and attack the cartilage. GMSC home to the site of the implant and induce programmed cell death of the RASF. CONCLUSIONS: Our results indicate that both GMSC and GMSCExo can block the pathological effects of RASF in this chimeric model of RA. A single dose of either GMSC or GMSCExo can inhibit the deleterious effects of RASF. These treatments can also block the invasive migration of the RASF, suggesting that they can inhibit the spread of RA to other joints. Because the gingival tissue is harvested with little difficulty, relatively small amounts of tissue are required to expand the cells, the simple in vitro expansion process, and the increasing technological advances in the production of therapeutic exosomes, we believe that GMSCExo are excellent candidates as a potential therapeutic for RA.

Therapeutic Effects of Gingival Mesenchymal Stem Cells and Their Exosomes in a Chimeric Model of Rheumatoid Arthritis.

Background: Rheumatoid arthritis is a chronic systemic autoimmune disease that involves transformation of the lining of synovial joints into an invasive and destructive tissue. Synovial fibroblasts become transformed, invading and destroying bone and cartilage of the affected joint(s). Due to the significant role these cells play in the progression of the disease process, developing a therapeutic strategy to target and inhibit their invasive destructive nature could help patients who are affiicted with this debilitating disease. Gingival-derived mesenchymal stem cells are known to possess immunomodulatory properties and have been studied extensively as potential cell-based therapeutics for several autoimmune disorders. Methods: A chimeric human/mouse model of synovitis was created by surgically implanting SCID mice with a piece of human articular cartilage surrounded by RASF. Mice were injected once with either GMSC or GMSCExo at 5-7 days post-implantation. Histology and IHC were used to assess RASF invasion of the cartilage. Flow cytometry was used to understand the homing ability of GMSC in vivo and the incidence of apoptosis of RASF in vitro. Results: We demonstrate that both GMSC and GMSCExo are potent inhibitors of the deleterious effects of RASF. Both treatments were effective in inhibiting the invasive destructive properties of RASF as well as the potential of these cells to migrate to secondary locations and attack the cartilage. GMSC home to the site of the implant and induce programmed cell death of the RASF. Conclusions: Our results indicate that both GMSC and GMSCExo can block the pathological effects of RASF in this chimeric model of RA. A single dose of either GMSC or GMSCExo can inhibit the deleterious effects of RASF. These treatments can also block the invasive migration of the RASF, suggesting that they can inhibit the spread of RA to other joints. Because the gingival tissue is harvested with little difficulty, relatively small amounts of tissue are required to expand the cells, the simple in vitro expansion process, and the increasing technological advances in the production of therapeutic exosomes, we believe that GMSCExo are excellent candidates as a potential therapeutic for RA.

Complications following alveolar ridge augmentation procedures.

Oral rehabilitation through implant supported dental restorations often requires a ridge augmentation procedure (RAP) prior to implant fixture placement since tooth extraction/loss results in alveolar ridge deficiencies. Although RAP-related surgical techniques and biomaterials have been in practice for several decades, outcomes are not always predictable. Post-surgical complications experienced during the early or late wound healing phases may jeopardize the targeted ideal ridge dimensions, required for implant fixture placement, and may have other consequences, such as negatively impacting the patient's quality of life. This review describes reported post-surgical complications following RAP under the following subtitles: complications by tissue type, complications in function and aesthetics, complications by healing time, complications by biomaterial type, and complications by surgical protocol modalities. Specifically, RAP performed by using particulate bone graft substitutes and related complications are explored. Modalities developed to prevent/manage these complications are also discussed.

Titanium as a Possible Modifier of Inflammation Around Dental Implants.

PURPOSE: The exact etiopathogenesis of peri-implant diseases remains unclear. While significant information on molecular markers is available, studies on biomarkers related to possible biocorrosion are sparse. This study aimed to evaluate periimplant crevicular fluid (PICF) for possible titanium (Ti) contamination and explore associations between clinical findings, inflammatory mediators, and Ti levels. MATERIALS AND METHODS: Patients with implant-supported restoration (≥ 1 year in function) were recruited for this cross-sectional study. Demographics, systemic, and periodontal health history were recorded. Clinical evaluations were conducted to reach peri-implant/periodontal diagnoses and grade severity of peri-implant soft tissue inflammation. Crevicular fluid (CF) was collected from both implants and adjacent teeth (PICF, gingival crevicular fluid [GCF]) and analyzed for Ti (inductively coupled plasma mass spectrometry) and inflammatory mediators (V-plex assays). Multiple regression analysis with a linear mixed effect model was used to analyze possible associations between clinical diagnosis, PICF/GCF cytokine, and Ti concentrations. RESULTS: Seventy-seven patients (aged 62 ± 2 years; 39 male) with 117 implants (9 ± 1 years in function) were recruited. Diabetes, positive periodontitis history, and current/former smoking were reported by 8%, 39%, and 39% of subjects, respectively. Seventy-nine implant sites (63 patients) were included in CF cytokine analysis, and 45 of these sites (42 patients) were paired with Ti analysis. Statistically significant increases from health to disease were noted in log-transformed PICF concentrations of IL-1ß, IL-6, IL-10, and INF-γ (P ≤ .05). Also, statistically significant increases from health to severe clinical inflammation were detected in log-transformed PICF concentrations of IL-8, IL-13, and TNF-α (P ≤ .05). Ti was detected in the majority (82%) of PICF and GCF samples. There was no statistically significant difference in log-transformed Ti concentration based on disease status. However, log-transformed Ti concentration was positively correlated to IL-1ß, IL-2, IL-4, IL-8, IL-13, and INF-γ concentrations when data were adjusted for site-specific health (P ≤ .05). CONCLUSION: Ti was detectable in PICF and adjacent GCF, even in health. Specific inflammatory mediator concentrations were increased in peri-implant disease and significantly associated with Ti concentrations, even when data were adjusted for peri-implant health status. Increased GCF inflammatory mediator concentrations were also associated with increased Ti concentrations. Ti effects on peri-implant as well as periodontal tissues require additional longitudinal investigations.

3D engineered human gingiva fabricated with electrospun collagen scaffolds provides a platform for in vitro analysis of gingival seal to abutment materials.

In order to advance models of human oral mucosa towards routine use, these models must faithfully mimic the native tissue structure while also being scalable and cost efficient. The goal of this study was to develop a low-cost, keratinized human gingival model with high fidelity to human attached gingiva and demonstrate its utility for studying the implant-tissue interface. Primary human gingival fibroblasts (HGF) and keratinocytes (HGK) were isolated from clinically healthy gingival biopsies. Four matrices, electrospun collagen (ES), decellularized dermis (DD), type I collagen gels (Gel) and released type I collagen gels (Gel-R)) were tested to engineer lamina propria and gingiva. HGF viability was similar in all matrices except for Gel-R, which was significantly decreased. Cell penetration was largely limited to the top layers of all matrices. Histomorphometrically, engineered human gingiva was found to have similar appearance to the native normal human gingiva except absence of rete pegs. Immunohistochemical staining for cell phenotype, differentiation and extracellular matrix composition and organization within 3D engineered gingiva made with electrospun collagen was mostly in agreement with normal gingival tissue staining. Additionally, five types of dental material posts (5-mm diameter x 3-mm height) with different surface characteristics were used [machined titanium, SLA (sandblasted-acid etched) titanium, TiN-coated (titanium nitride-coated) titanium, ceramic, and PEEK (Polyetheretherketone) to investigate peri-implant soft tissue attachment studied by histology and SEM. Engineered epithelial and stromal tissue migration to the implant-gingival tissue interface was observed in machined, SLA, ceramic, and PEEK groups, while TiN was lacking attachment. Taken together, the results suggest that electrospun collagen scaffolds provide a scalable, reproducible and cost-effective lamina propria and 3D engineered gingiva that can be used to explore biomaterial-soft tissue interface.

Bone grafting history affects soft tissue healing following implant placement.

BACKGROUND: This study aimed to determine and compare soft tissue healing outcomes following implant placement in grafted (GG) and non-grafted bone (NGG). METHODS: Patients receiving single implant in a tooth-bound maxillary non-molar site were recruited. Clinical healing was documented. Volume and content of wound fluid (WF; at 3, 6, and 9 days) were compared with adjacent gingival crevicular fluid (GCF; at baseline, 1, and 4 months). Buccal flap blood perfusion recovery and changes in bone thickness were recorded. Linear mixed model regression analysis and generalized estimating equations with Bonferroni adjustments were conducted for repeated measures. RESULTS: Twenty-five patients (49 ± 4 years; 13 males; nine NGG) completed the study. Soft tissue closure was slower in GG (P < 0.01). Differential response in WF/GCF protein concentrations was detected for ACTH (increased in GG only) and insulin, leptin, osteocalcin (decreased in NGG only) at day 6 (P ≤0.04), with no inter-group differences at any time(P > 0.05). Blood perfusion rate decreased immediately postoperatively (P < 0.01, GG) followed by 3-day hyperemia (P > 0.05 both groups). The recovery to baseline values was almost complete for NGG whereas GG stayed ischemic even at 4 months (P = 0.05). Buccal bone thickness changes were significant in GG sites (P ≤ 0.05). CONCLUSION: History of bone grafting alters the clinical, physiological, and molecular healing response of overlying soft tissues after implant placement surgery.

Soft tissue healing around platform-switching and platform-matching single implants: A randomized clinical trial.

BACKGROUND: Implants with platform-switching (PS) design have been demonstrated to reduce marginal bone loss. However, the influence on peri-implant soft tissue healing is unclear. This study was designed to investigate its effect on peri-implant soft tissue healing after implant uncovery. METHODS: Non-smokers needing two implants in different quadrants were recruited in this study. For each individual, one PS and one platform-matching (PM) implants were placed using two-stage protocol. Following 2 to 8 months of healing, all implants were uncovered and connected to the corresponding healing abutments. Clinical measurements and peri-implant crevicular fluid (PICF) were taken at 1-, 2-, 4-, and 6-week after 2nd stage surgery. The cytokine concentrations in PICF were analyzed. Peri-implant mucosa (1 × 2 × 2 mm) was harvested around the healing abutment for the analysis of gene expression at uncovery and 6-week post-uncovery. RESULTS: Eighteen participants (nine males; 51.7 ± 14.9 years) were recruited. Compared to PM, PS showed significantly lower probing depth (PD) at 1- and 2-week as well as modified sulcus bleeding index (mSBI) at 1-, 4-, and 6-week (P < 0.05). Over time, a decrease in osteoprotegerin and interleukin-1ß concentrations in PICF along with an increase in receptor activator of unclear factor kappa-B ligand, periostin, and peroxidasin gene expressions in peri-implant mucosa were noted within both groups (P < 0.05) without significant intergroup differences. CONCLUSION: Within the limits, implants with PS design rendered significant benefits over PM design in PD and mSBI reduction during a 6-week healing. However, molecular changes within PICF and peri-implant mucosa as a response to PM and PS appear negligible.

Wound Fluid Cytokine Profile Following Bone Regeneration Procedures.

Clinical parameters available to evaluate early healing phases of bone regeneration procedures are limited. This study explores wound fluid (WF) content for molecular markers to differentiate wound healing responses in the early postoperative period after bone graft placement. Fifteen patients (50 ± 5 years old; 8 men) scheduled to receive tooth extraction and bone graft placement at maxillary nonmolar single-tooth sites were recruited. Primary wound closure was not intended at time of surgery. Gingival crevicular fluid from adjacent teeth or WF from surgical wound edges were collected (30 seconds) at baseline, at 3, 6, and 9 days, and at 1 and 4 months. Multiplex protein assay was used to determine concentration of various wound healing mediators. Immediately after surgery, 87% of surgical sites exhibited open wound. At day 9, mean wound exposure was 4.8 ± 0.4 mm. At 1 month, all wounds were clinically closed. The WF tripled in volume at day 3 and day 6 (P ≤ .05), compared with baseline gingival crevicular fluid, and gradually decreased as wounds closed. The WF concentrations of interleukin (IL)-6, placental growth factor, plasminogen activator inhibitor 1, insulin-like growth factor binding protein 1, and soluble cluster determinant 40 ligand were increased during early healing days, generally with peak concentration at day 6 (P ≤ .004). Conversely, WF concentrations of IL-18 and epidermal growth factor were decreased after surgery, generally not reaching baseline values until wound closure (P ≤ .008). In general, WF cytokine expression kinetics were concordant with wound closure dynamics (P ≤ .04). These results suggest that WF molecular markers such as IL-6, and to a lesser extent placental growth factor and IL-18, might help differentiate wound healing responses after bone regeneration procedures.

Ferutinin directs dental pulp-derived stem cells towards the osteogenic lineage by epigenetically regulating canonical Wnt signaling.

Osteoporosis is a silent systemic disease that causes bone deterioration, and affects over 10 million people in the US alone. This study was undertaken to develop a potential stem cell therapy for osteoporosis. We have isolated and expanded human dental pulp-derived stem cells (DPSCs), characterized them, and confirmed their multipotential differentiation abilities. Stem cells often remain quiescent and require activation to differentiate and function. Herein, we show that ferutinin activates DPSCs by modulating the Wnt/ß-catenin signaling pathway and key osteoblast-secreted proteins osteocalcin and collagen 1A1 both mRNA and protein levels. To confirm that ferutinin modulates the Wnt pathway, we inhibited glycogen synthase kinase 3 (GSK3) and found that protein expression patterns were similar to those found in ferutinin-treated DPSCs. To evaluate the role of ferutinin in epigenetic regulation of canonical Wnt signaling, the pathway molecules Wnt3a and Dvl3 were analyzed using chromatin immunoprecipitation (ChIP)-quantitative PCR approaches. We confirmed that active marks of both H3K9 acetylation and H3K4 trimethylation were significantly enhanced in the promoter sites of the WNT3A and DVL3 genes in DPSCs after addition of ferutinin. These data provide evidence that ferutinin activates and promotes osteogenic differentiation of DPSCs, and could be used as an inducer as a potentially effective stem cell therapy for osteoporosis.

Gingival Perfusion and Tissue Biomarkers During Early Healing of Postextraction Regenerative Procedures: A Prospective Case Series.

BACKGROUND: Postextraction alveolar bone loss, mostly affecting the buccal plate, occurs despite regenerative procedures. To better understand possible determinants, this prospective case series assesses gingival blood perfusion and tissue molecular responses in relation to postextraction regenerative outcomes. METHODS: Adults scheduled to receive bone grafting in maxillary, non-molar, single-tooth extraction sites were recruited. Clinical documentation included the following: 1) probing depth (PD); 2) keratinized tissue width (KT); 3) tissue biotype (TB); and 4) plaque level. Wound closure was clinically evaluated. Gingival blood perfusion was measured by laser Doppler flowmetry (LDF). Wound fluid (WF) and gingival biopsies were analyzed for protein levels and gene expression, respectively, of relevant molecular markers. Bone healing outcomes were determined radiographically (cone-beam computed tomography). Healing was followed for 4 months. RESULTS: Data from 15 patients are reported. Postoperatively, neither complications nor changes in PD, KT, or TB were observed. LDF revealed decreased perfusion followed by hyperemia that persisted for 1 month (P ≤0.05). WF levels of angiopoietin-2, interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-α), and vascular endothelial growth factor peaked on day 6 (P ≤0.05) and decreased thereafter. Only IL-8 and TNF-α exhibited increased gene expression. Linear bone changes were negligible. Volumetric bone changes were minimal but statistically significant, with more bone loss when membrane was used (P = 0.05). CONCLUSIONS: Gingival blood perfusion after postextraction bone regenerative procedures follows an ischemia-reperfusion model. Transient increases in angiogenic factor levels and prolonged hyperemia characterize the soft tissue response. These soft tissue responses do not determine radiographic bone changes.

The Effect of Platform Switching on Periimplant Crevicular Fluid Content During Early Wound Healing.

PURPOSE: The objective of this study was to investigate the soft tissue response and periimplant crevicular fluid (PICF) content around platform-switched (PS) and platform-matched (PM) implants during early healing. MATERIALS AND METHODS: Nonsmokers treatment planned to receive a single implant in 2 quadrants were recruited. Two-stage implant placement protocol with 1 PM and 1 PS implant was implemented. Periimplant probing depths (PDs), modified sulcus bleeding index, and plaque indices were recorded, and PICF was collected at 1, 2, 4, and 6 weeks after abutment connection. RESULTS: PD readings were higher at week 1 than at week 6 for both groups (P = 0.0005). PD was statistically deeper in PM than in PS at week 1 (P = 0.03). There was a time-dependent decrease in total PICF volume for both groups. This decrease was statistically significant for PS (P = 0.0005), with no differences between the 2 groups at any time (P > 0.05). The decrease observed in both PM and PS for PICF interleukin 6 and macrophage inflammatory protein-1ß, and in PS for tumor necrosis factor-α (TNF-α) was statistically significant (P ≤ 0.03). TNF-α was statistically higher in PS than in PM at week 1 (P = 0.005). CONCLUSION: Within the limits of this study, it seems that periimplant soft tissue response around PM and PS implants is mostly similar during the early healing period.

Smoking, pregnancy and the subgingival microbiome.

The periodontal microbiome is known to be altered during pregnancy as well as by smoking. However, despite the fact that 2.1 million women in the United States smoke during their pregnancy, the potentially synergistic effects of smoking and pregnancy on the subgingival microbiome have never been studied. Subgingival plaque was collected from 44 systemically and periodontally healthy non-pregnant nonsmokers (control), non-pregnant smokers, pregnant nonsmokers and pregnant smokers and sequenced using 16S-pyrotag sequencing. 331601 classifiable sequences were compared against HOMD. Community ordination methods and co-occurrence networks were used along with non-parametric tests to identify differences between groups. Linear Discriminant Analysis revealed significant clustering based on pregnancy and smoking status. Alpha diversity was similar between groups, however, pregnant women (smokers and nonsmokers) demonstrated higher levels of gram-positive and gram-negative facultatives, and lower levels of gram-negative anaerobes when compared to smokers. Each environmental perturbation induced distinctive co-occurrence patterns between species, with unique network anchors in each group. Our study thus suggests that the impact of each environmental perturbation on the periodontal microbiome is unique, and that when they are superimposed, the sum is greater than its parts. The persistence of these effects following cessation of the environmental disruption warrants further investigation.

Comparison of Azithromycin and Amoxicillin Before Dental Implant Placement: An Exploratory Study of Bioavailability and Resolution of Postoperative Inflammation.

BACKGROUND: Studies suggest that a single prophylactic dose of amoxicillin reduces early implant complications, but it is unclear whether other antibiotics are also effective. This study compared the local antimicrobial and anti-inflammatory effects resulting from a single dose of azithromycin or amoxicillin before surgical placement of one-stage dental implants. METHODS: Healthy adult patients requiring one-stage dental implant placement were allocated randomly to receive either 2 g amoxicillin (n = 7) or 500 mg azithromycin (n = 6) before surgery. Peri-implant crevicular fluid (PICF) samples from the new implant and gingival crevicular fluid (GCF) from adjacent teeth were sampled on postoperative days 6, 13, and 20. Inflammatory mediators in the samples were analyzed by immunoassay, and antibiotic levels were measured by bioassay. RESULTS: On day 6, azithromycin concentrations in GCF and PICF were 3.39 ± 0.73 and 2.77 ± 0.90 µg/mL, respectively, whereas amoxicillin was below the limit of detection. During early healing, patents in the azithromycin group exhibited a significantly greater decrease in GCF volume (P = 0.03, analysis of variance). At specific times during healing, the azithromycin group exhibited significantly lower levels of interleukin (IL)-6 and IL-8 in GCF than the amoxicillin group and exhibited significantly lower levels of granulocyte colony stimulating factor, IL-8, macrophage inflammatory protein-1ß, and interferon-gamma-inducible protein-10 in PICF. CONCLUSIONS: Azithromycin was available at the surgical site for a longer period of time than amoxicillin, and patients taking azithromycin exhibited lower levels of specific proinflammatory cytokines and chemokines in GCF and PICF. Thus, preoperative azithromycin may enhance resolution of postoperative inflammation to a greater extent than amoxicillin.

Poor Sleep Quality and Associated Inflammation Predict Preterm Birth: Heightened Risk among African Americans.

STUDY OBJECTIVES: Poor sleep promotes inflammation. In turn, inflammation is a causal mechanism in term as well as preterm parturition. In the United States, a persistent racial disparity in preterm birth exists, with African Americans showing ∼1.5 times greater risk. This study examined associations among sleep quality, serum proinflammatory cytokines, and length of gestation in a racially diverse sample of 138 pregnant women. DESIGN: Observational. MEASUREMENTS: Women completed the Pittsburgh Sleep Quality Index (PSQI) and other psychosocial and behavioral measures during midpregnancy. Serum levels of interleukin (IL)-6, IL-8, IL-1ß, and tumor necrosis factor (TNF)-α were determined by high-sensitivity assays. Birth outcomes were determined via medical record review. RESULTS: Among African American women (n = 79), shorter gestation was predicted by poorer overall sleep (rs = -0.35, P = 0.002) as well the following PSQI subscales: subjective sleep quality (rs = -0.34, P = 0.002), sleep latency (rs = -0.27, P = 0.02), and sleep efficiency (rs = -0.27, P = 0.02). African American women with poor sleep quality (PSQI > 5) had 10.2 times the odds of preterm birth compared to those with good sleep quality. In contrast, among European American women (n = 53), gestational length was not significantly predicted by sleep quality (Ps > 0.12). Bootstrapping analyses showed that, among African Americans, IL-8 significantly mediated the association between sleep quality and length of gestation (indirect effect estimate -0.029; 95% confidence interval -0.06, -0.002). CONCLUSIONS: The data provide novel evidence that African American women exhibit greater inflammation in response to sleep disturbance than European American women and these effects correspond with length of gestation. Racial differences in susceptibility to sleep induced immune dysregulation may contribute to marked racial disparities in preterm birth.

A Comparison of Zirconia and Titanium Abutments for Microleakage.

BACKGROUND: Microleakage through the interface has been documented in implant systems with titanium (Ti) abutments. There is a current increase in the use of zirconia (Zi) abutments especially in esthetic zone in where higher risk of visible metal color through the peri-implant tissues exists. PURPOSE: The aim of the present in vitro study is to evaluate the leakage at the implant fixture-abutment interface with two different screw-retained abutment systems at different torque values in a nonloading condition. MATERIALS AND METHODS: In vitro study design included four groups (Ti and Zi torqued at 25 and 15 Ncm [N = 8/group]). Microcomputed tomography (micro-CT) was chosen to detect microgap. Microleakage from the implant chamber to the external milieu was evaluated using limulus amebocyte lysate (LAL) test, while microleakage from external milieu to the implant chamber was evaluated using toluidine blue dye (TBD) and colorimeter. RESULTS: Micro-CT images did not reveal any microgap. LAL test showed that there is a time-, abutment-, and torque-dependent increase in microleakage (p = .001) with Zi torqued at 15 Ncm having higher leakage with time compared with Ti torqued at 15 Ncm (p = .002), as well as Zi torqued at 15 Ncm having higher leakage with time compared with Zi torqued at 25 Ncm (p = .01). TBD test showed a nonsignificant increase in microleakage with higher leakage related to titanium abutment groups (p > .05). Repeated torque/antitorque handling differentially affected microleakage (p = .01). CONCLUSIONS: Within the limits of this study, there is a statistically significant difference in bidirectional microleakage with time, abutment type, and torque values being major players for leakage from internal implant chamber to external milieu, while the abutment type and time but not the torque value being important factors for leakage from external milieu into implant chamber in nonloading condition. Future studies are needed to determine peri-implant health around Zi abutments.

Immediate effects of tooth extraction on ridge integrity and dimensions.

OBJECTIVES: This study aims to assess possible immediate post-extraction changes in ridge integrity and width. METHODS: Tooth extractions (53 teeth in 30 adults) were performed following atraumatic techniques. Root trunk and ridge width were measured at the crest level in buccolingual direction. Similarly, socket width and buccal plate thickness were also determined. Pre- and post-extraction buccal plate dehiscence, fenestration, or fracture was recorded. Diameter and length of extracted tooth root were also measured. Multinomial logistic regression was used to reveal relationships between ridge outcome (expanded, stable, or collapsed groups) and assessed tooth/site parameters. RESULTS: Post-extraction, buccal plate fracture developed in 5 (9%), dehiscence in 15 (28%), and complete buccal plate loss in 2 sites (4%). Following extraction, ridge width was expanded in 30 (57%), collapsed in 12 (23%), and remained unchanged in 11 (21%) sites. In most sites (72%), post-extraction socket size was wider than pre-extraction root trunk width (p < 0.0001). Socket size was a statistically significant predictor for ridge outcome (expansion or collapse compared to stable) (p < 0.01). CONCLUSION: Loss of ridge integrity is uncommon, while ridge width expansion is a common finding immediately following tooth extraction. The significance of such expansion compared to integrity of socket walls remains to be established. CLINICAL RELEVANCE: Tooth extraction approaches that preserve ridge integrity are accompanied by mainly ridge expansion in ridge width. The significance of such immediate changes for the long-term ridge outcomes (i.e., effect on bone remodeling especially in relation to buccal bone integrity) needs further investigation.

Mechanosignaling in bone health, trauma and inflammation.

SIGNIFICANCE: Mechanosignaling is vital for maintaining the structural integrity of bone under physiologic conditions. These signals activate and suppress multiple signaling cascades regulating bone formation and resorption. Understanding these pathways is of prime importance to exploit their therapeutic potential in disorders associated with bone loss due to disuse, trauma, or disruption of homeostatic mechanisms. RECENT ADVANCES: In the case of cells of the bone, an impressive amount of data has been generated that provides evidence of a complex mechanism by which mechanical signals can maintain or disrupt cellular homeostasis by driving transcriptional regulation of growth factors, matrix proteins and inflammatory mediators in health and inflammation. Mechanical signals act on cells in a magnitude dependent manner to induce bone deposition or resorption. During health, physiological levels of these signals are essential for maintaining bone strength and architecture, whereas during inflammation, similar signals can curb inflammation by suppressing the nuclear factor kappa B (NF-κB) signaling cascade, while upregulating matrix synthesis via mothers against decapentaplegic homolog and/or Wnt signaling cascades. Contrarily, excessive mechanical forces can induce inflammation via activation of the NF-κB signaling cascade. CRITICAL ISSUES: Given the osteogenic potential of mechanical signals, it is imperative to exploit their therapeutic efficacy for the treatment of bone disorders. Here we review select signaling pathways and mediators stimulated by mechanical signals to modulate the strength and integrity of the bone. FUTURE DIRECTIONS: Understanding the mechanisms of mechanotransduction and its effects on bone lay the groundwork for development of nonpharmacologic mechanostimulatory approaches for osteodegenerative diseases and optimal bone health.

Peri-implant versus periodontal wound healing.

AIM: Peri-implant gingival healing following one-stage implant placement was investigated and compared to periodontal healing. METHODS: Healing at surgical sites [implant (I) and adjacent teeth (T+)] was compared to non-operated tooth (T-) in non-smokers receiving one-stage implant. Periodontal Indices (PI, GI) were recorded at surgery and up to 12 weeks post-operatively. Peri-implant (PICF) and gingival crevicular fluids (GCF) were analysed for cytokines, collagenases and inhibitors. Data were analysed by linear mixed model regression analysis and repeated measures anova. RESULTS: Forty patients (22 females; 21-74 years old) completed the study. Surgical site GI, increased at week 1, decreased significantly during early healing (weeks 1-3; p = 0.0003) and continually decreased during late healing (weeks 6-12) for I (p < 0.01). PICF volume decreased threefold by week 12 (p = 0.0003). IL-6, IL-8, MIP-1ß and TIMP-1 levels significantly increased at surgical sites at week one, significantly decreasing thereafter (p < 0.016). Week one IL-6, IL-8 and MIP-1ß levels were ~threefold higher and TIMP-1 levels 63% higher, at I compared to T+ (p = 0.001). CONCLUSION: Peri-implant gingival healing, as determined by crevicular fluid molecular composition, differs from periodontal healing. The observed differences suggest that peri-implant tissues, compared to periodontal tissues, represent a higher pro-inflammatory state.