Influence of periodontal surgery on the subgingival microbiome-A systematic review and meta-analysis.

OBJECTIVE: The objective of this systematic review and meta-analysis was to evaluate the effect of periodontal surgery on the subgingival microbiome. BACKGROUND: Periodontitis is a chronic inflammation of the tooth supporting tissues caused by the dysbiosis of the subgingival biofilm. It is managed through different non-surgical and surgical treatment modalities. Recent EFP S3 guidelines recommended performing periodontal surgery as part of Step 3 periodontitis treatment after Step 1 and Step 2 periodontal therapy, with the aim to achieve pocket closure of persisting sites. Changes in the sub-gingival microbiome may explain the treatment outcomes observed at different time points. Various microbiological detection techniques for disease-associated pathogens have been evolved over time and have been described in the literature. However, the impact of different types of periodontal surgery on the subgingival microbiome remains unclear. METHODS: A systematic literature search was conducted in Medline, Embase, LILACS and Cochrane Library supplemented by manual search (23DEC2019, updated 21APR2022). RESULTS: From an initial search of 3046 studies, 28 were included according to our specific inclusion criteria. Seven microbiological detection techniques were used to analyse disease-associated species in subgingival plaque samples: optical microscope, culture, polymerase chain reaction (PCR), checkerboard, enzymatic reactions, immunofluorescence and 16S gene sequencing. The included studies exhibited differences in various aspects of their methodologies such as subgingival plaque sample collection or treatment modalities. Clinical data showed a significant decrease in probing pocket depths (PPD) and clinical attachment loss (CAL) after periodontal surgery. Microbiological findings were overall heterogeneous. Meta-analysis was performed on a sub-cohort of studies all using checkerboard as a microbiological detection technique. Random effect models for Treponema denticola (T. denticola), Porphyromonas gingivalis (P. gingivalis) and Tannerella forsythia (T. forsythia) did not show a significant effect on mean counts 3 months after periodontal surgery. Notably, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) showed a significant increase 3 months after periodontal surgery. 16S gene sequencing was used in one included study and reported a decrease in disease-associated species with an increase in health-associated species after periodontal surgery at 3 and 6 months. CONCLUSION: This systematic review has shown that the effect of periodontal surgery on the changes in subgingival microbiome is heterogeneous and may not always be associated with a decrease in disease-associated species. The variability could be attributed to the microbiological techniques employed for the analysis. Therefore, there is a need for well-designed and adequately powered studies to understand how periodontal surgery influences the subgingival microbiome and how the individual's microbiome affects treatment outcomes after periodontal surgery.

The effect of furcation involvement on tooth loss in a population without regular periodontal therapy.

AIM: We aimed to assess the association between furcation involvement (FI) and tooth loss for subjects not undergoing regular periodontal treatment. MATERIALS AND METHODS: Data from 2333 subjects participating in the baseline and 11-year follow-up of the Study of Health in Pomerania (SHIP) were used. All subjects had half-mouth periodontal examinations, including FI in one upper and one lower molar, at baseline. A total of 1897 subjects and 3267 molars were included in the final analysis. RESULTS: In total, 375 subjects (19.8%) lost molars during the follow-up period. Respectively, 5.6%, 12.7%, 34.0% and 55.6% of molars without FI, degree I FI, degree II FI and degree III FI were lost. Initial probing pocket depth (PPD) and clinical attachment level (CAL) were associated with molar loss (p < .001). Baseline degree I FI was associated with a 1.73 IRR (incidence rate ratio) (95% CI=1.34-2.23, p < .001) of tooth loss while degree II-III was associated with a 3.88 IRR (95% CI=2.94-5.11, p < .001) of tooth loss compared to molars without FI at baseline. CONCLUSION: This study provides evidence for an increased risk of molar loss affected by periodontal furcation involvement in a general population not undergoing regular periodontal care.

Minimum end-tidal sevoflurane concentration necessary to prevent movement during a constant rate infusion of morphine, or morphine plus dexmedetomidine in ponies.

OBJECTIVE: To compare the effects of a constant rate infusion (CRI) of dexmedetomidine and morphine to those of morphine alone on the minimum end-tidal sevoflurane concentration necessary to prevent movement (MACNM ) in ponies. STUDY DESIGN: Prospective, randomized, crossover, 'blinded', experimental study. ANIMALS: Five healthy adult gelding ponies were anaesthetized twice with a 3-week washout period. METHODS: After induction of anaesthesia with sevoflurane in oxygen (via nasotracheal tube), the ponies were positioned on a surgical table (T0), and anaesthesia was maintained with sevoflurane (Fe'SEVO 2.5%) in 55% oxygen. Monitoring included pulse oximetry, electrocardiography and measurement of anaesthetic gases, arterial blood pressure and body temperature. The ponies were mechanically ventilated and randomly allocated to receive IV treatment M [morphine 0.15 mg kg⁻¹ (T10-T15) followed by a CRI (0.1 mg kg⁻¹ hour⁻¹)] or treatment DM [dexmedetomidine 3.5 µg kg⁻¹ plus morphine 0.15 mg kg⁻¹ (T10-T15) followed by a CRI of dexmedetomidine 1.75 µg kg⁻¹ hour⁻¹ and morphine 0.1 mg kg⁻¹ hour⁻¹]. At T60, a stepwise MACNM determination was initiated using constant current electrical stimuli at the skin of the lateral pastern region. Triplicate MACNM estimations were obtained and then averaged in each pony. Wilcoxon signed-rank test was used to detect differences in MAC between treatments (α = 0.05). RESULTS: Sevoflurane-morphine MACNM values (median (range) and mean ± SD) were 2.56 (2.01-4.07) and 2.79 ± 0.73%. The addition of a continuous infusion of dexmedetomidine significantly reduced sevoflurane MACNM values to 0.89 (0.62-1.05) and 0.89 ± 0.22% (mean MACNM reduction 67 ± 11%). CONCLUSION AND CLINICAL RELEVANCE: Co-administration of dexmedetomidine and morphine CRIs significantly reduced the MACNM of sevoflurane compared with a CRI of morphine alone at the reported doses.

Influence of lipopolysaccharide and interleukin-6 on RANKL and OPG expression and release in human periodontal ligament cells.

Recent research into periodontal disease pathology focuses on the role of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) in periodontal bone destruction processes. RANKL regulates the differentiation of osteoclast by binding to its specific receptor RANK, while OPG inhibits the differentiation of osteoclasts by binding RANKL and therefore preventing RANKL to bind RANK. The aim of the present study was to investigate the influence of Porphyromonas gingivalis lipopolysaccharide (LPS) and interleukin-6 (IL-6) on RANKL and OPG expression and release in periodontal ligament (PDL) cells. Human PDL cells were stimulated for 48 h with purified P. gingivalis LPS and IL-6. OPG and sRANKL release were assessed by using enzyme-linked immunosorbent assay technique. OPG and RANKL expression was quantitatively measured by using the real-time PCR technique. Whereas P. gingivalis LPS induced sRANKL release, expression was only slightly increased, IL-6 did not show an effect on RANKL expression or release. In conclusion the data demonstrate that stimulation of PDL cells with P. gingivalis LPS leads to an increased release of sRANKL, rather than increased RANKL expression. Through this action, P. gingivalis LPS may exert its biological effect on osteoclast formation and bone resorption.

Efficient gene transfer to periodontal ligament cells and human gingival fibroblasts by adeno-associated virus vectors.

OBJECTIVES: We explored for the first time the possibility to deliver a reporter gene (Green Fluorescence Protein) to human primary periodontal ligament (PDL) cells and human gingival fibroblasts (HGF) using shuttle vectors derived from adeno-associated virus (AAV). Since AAV transduction rates on other human primary fibroblasts have been previously shown to depend on the particular cell lineage and on the employed viral serotype, we determined the most effective AAV variant for periodontal cells comparing different vector types. METHODS: AAV serotypes 1-5 encoding GFP in single stranded (ss) and self-complementary (sc) vector genome conformations were used to infect primary HGF and PDL cells. Two days post-infection, the percentage of GFP expressing cells was determined by flow cytometry. RESULTS: Highest transduction rates for both cell types were achieved with self-complementary vectors derived from AAV-2, resulting in GFP expression in up to 86% of PDL cells and 50% of HGF. Transgene expression could be observed by optical microscopy for 2 months after infection. Lower but detectable rates were obtained with serotypes 1, 3 and 5. CONCLUSIONS: The efficacy demonstrated here and the safety and versatility of AAV technology indicated in previous studies clearly suggest the potential of AAV vectors as tools for gene transfer to periodontal tissues.