Henri Tenenbaum

Long-term implant survival and success: a 10–16-year follow-up of non-submerged dental implants

OBJECTIVES The aim of the present study was to evaluate the long-term results of dental implants using implant survival and implant success as outcome variables. METHODS Of the 76 patients who received 162 implants of the Straumann Dental Implant System during the years 1990-1997, 55 patients with 131 implants were recalled 10-16 years after implant placement for a complete clinical and radiographic examination, followed by a questionnaire that examined the degree of satisfaction. The incidence of biological and technical complications has been carefully analysed for each implant. Success was defined as being free of all these complications over the entire observation period. Associated factors related to peri-implant lesions were analysed for each implant. RESULTS The long-term implant cumulative survival rate up to 16 years was 82.94%. The prevalence of biological complications was 16.94% and the prevalence of technical complications was 31.09%. The cumulative complication rate after an observation period of 10-16 years was 48.03%, which meant that substantial amounts of chair time were necessary following implant placement. The majority of implant losses and biological complications were concentrated in a relatively small number of patients. CONCLUSION Despite a relatively high long-term survival rate, biological and technical complications were frequent. Patients with a history of periodontitis may have lower implant survival rates than patients without a history of periodontitis and were more prone to biological complications such as peri-implant mucositis and peri-implantitis.

Cathepsin C, Matrix Metalloproteinases, and their Tissue Inhibitors in Gingiva and Gingival Crevicular Fluid from Periodontitis-affected Patients

Successive active phases observed in periodontal diseases may be explained either by a sudden activation of the pro-forms of tissue-stored degradative enzymes such as metalloproteinases (MMPs) or by an imbalance between metalloproteinases and their tissue inhibitors (TIMPs). To discriminate between these two hypotheses, we quantified the levels, the percentage of active form, and the activities of four metalloproteinases (MMPs -1, -2, -3, and -9), as well as the levels of two tissue inhibitors of metalloproteinases (TIMP-1 and -2) and the activity of cathepsin C in tissue extract supernatants and their corresponding gingival crevicular fluid samples collected from periodontitis-affected and healthy patients. Our results supported evidence that tissue destruction results from an imbalance of metalloproteinases over their tissue inhibitors rather than from a sudden activation of the pro-forms of these enzymes. A significant reduction in the activity of cathepsin C also contributed to the degradative process.

Expression of mRNAs Encoding for α and β Integrin Subunits, MMPs, and TIMPs in Stretched Human Periodontal Ligament and Gingival Fibroblasts

The biological mechanisms of tooth movement result from the cellular responses of connective tissues to exogenous mechanical forces. Among these responses, the degradation of the extracellular matrix takes place, but the identification of the molecular basis as well as the components implicated in this degradation are poorly understood. To contribute to this identification, we subjected human fibroblasts obtained from the periodontal ligament (PDLs) and from the gingiva (HGFs) to a continuous stretch to quantify the mRNAs encoding for various metalloproteinases (MMPs), their tissue inhibitors (TIMPs), and a and β integrin subunits. Both cell lines reacted by inducing the expression of the mRNAs encoding for MMP-1, MMP-2, TIMP-1, and TIMP-2, while other mRNAs did not vary (MTI-MMP, TIMP-3) or were not expressed (MMP-9). PDLs expressed selectively the mRNAs encoding for a4 and av, with no difference measurable under stretching, while the mRNAs encoding for a6 and β1 were increased and the one encoding for a5 was decreased. HGFs increased the mRNAs encoding for α2, α6, β1, and β3 and decreased the one encoding for a3. Analysis of our data indicated that stretched HGFs and PDLs induced the same pattern of mRNAs encoding for MMPs and TIMPs but differed for those encoding various integrin subunits, known to act as protein receptors in mechanotransduction.

Variable Cell Responses to P. gingivalis Lipopolysaccharide

Porphyromonas gingivalis is a major etiological agent of chronic periodontal diseases, the virulence of which has been attributed to different factors, including lipopolysaccharide (LPS). We investigated the differential responses induced by P. gingivalis LPS stimulation of human umbilical vein endothelial cells and human oral epithelial cells. RT-PCR analysis showed that P. gingivalis LPS used Toll-like receptor 2 (TLR2) to activate epithelial cells and Toll-like receptor 4 (TLR4) to activate endothelial cells. Both cell types were stimulated by P. gingivalis LPS to produce pro-inflammatory cytokines. Cytokine Array assay showed that although patterns of cytokine expression were similar in both cell types, some cytokines were specifically secreted by the endothelial cells, and others were specific to epithelial cells. These results support the idea that the same LPS preparation can act as a TLR2 or TLR4 agonist, depending on TLR expression of the host cell, inducing cytokine profiles that differ according to the cell type.

Selective and uncoupled role of substrate elasticity in the regulation of replication and transcription in epithelial cells.

Actin cytoskeleton forms a physical connection between the extracellular matrix, adhesion complexes and nuclear architecture. Because tissue stiffness plays key roles in adhesion and cytoskeletal organization, an important open question concerns the influence of substrate elasticity on replication and transcription. To answer this major question, polyelectrolyte multilayer films were used as substrate models with apparent elastic moduli ranging from 0 to 500 kPa. The sequential relationship between Rac1, vinculin adhesion assembly, and replication becomes efficient at above 200 kPa because activation of Rac1 leads to vinculin assembly, actin fiber formation and, subsequently, to initiation of replication. An optimal window of elasticity (200 kPa) is required for activation of focal adhesion kinase through auto-phosphorylation of tyrosine 397. Transcription, including nuclear recruitment of heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1), occurred above 50 kPa. Actin fiber and focal adhesion signaling are not required for transcription. Above 50 kPa, transcription was correlated with αv-integrin engagement together with histone H3 hyperacetylation and chromatin decondensation, allowing little cell spreading. By contrast, soft substrate (below 50 kPa) promoted morphological changes characteristic of apoptosis, including cell rounding, nucleus condensation, loss of focal adhesions and exposure of phosphatidylserine at the outer cell surface. On the basis of our data, we propose a selective and uncoupled contribution from the substrate elasticity to the regulation of replication and transcription activities for an epithelial cell model.

Modified periodontal risk assessment score: long-term predictive value of treatment outcomes. A retrospective study.

OBJECTIVE The aim of this study was to evaluate the long-term clinical predictive value of the periodontal risk assessment diagram surface (PRAS) score and the influence of patient compliance on the treatment outcomes. MATERIALS AND METHODS Thirty subjects suffering from periodontitis were re-examined 6-12 years after the initial diagnosis and periodontal treatments. The baseline PRAS score was calculated from the initial clinical and radiograph records. Patients were then classified into a low-to-moderate (0-20) or a high-risk group (>20). Patients who did not attend any supportive periodontal therapy were classified into a non-compliant group. PRAS and compliance were correlated to the mean tooth loss (TL)/year and the mean variation in the number of periodontal pockets with a probing depth (PPD) >4 mm. RESULTS TL was 0.11 for the low-to-moderate-risk group and 0.26 for the high-risk group (p<0.05); PPD number reduction was 2.57 and 2.17, respectively, and bleeding on probing reduction was 6.7% and 23.3%, respectively. Comparing the compliance groups, the PPD number reduction was 3.39 in the compliant group and 1.40 in the non-compliant group (p<0.05). CONCLUSION This study showed the reliability of PRAS in evaluating long-term TL and patient susceptibility to periodontal disease. Our data confirmed the positive influence of patient compliance on periodontal treatment outcomes.

Periodontal diseases, preterm births, and low birth weight: findings from a homogeneous cohort of women in Madagascar.

BACKGROUND Studies on the possible influence of periodontal disease on preterm birth (PB) and/or low birth weight (LBW) remain inconclusive especially due to the difficulty of assessing the numerous pregnancy risk factors. The aim of this study is to compare periodontal parameters in non-smoking pregnant women in Madagascar. METHODS A cohort study with 204 pregnant women (mean age: 25.6 years) was conducted in public prenatal care health clinics in Madagascar. Socioeconomic and obstetric information was obtained. Periodontal parameters, such as periodontal probing depth and clinical attachment loss (AL), were recorded during the second semester of pregnancy. RESULTS The mean gestational age was 37.8 weeks. At delivery, 42 newborns (20.6%) were PBs (<37 weeks) and 22 newborns (10.8%) were of LBW (<2,500 g). Nine (4.4%) newborns were PBs and of LBW (PLBW), and 149 newborns (73%) were of normal birth. The mean plaque index and papillary bleeding index were significantly higher (P <0.05 and P <0.001, respectively) in the PB group than in the normal birth group. Periodontitis (at least three sites from different teeth with clinical AL >or=4 mm) was significantly associated with PB (P <0.001), LBW (P <0.001), and PLBW (P <0.01). The rates of periodontitis were considerably higher in PB (78.6%), LBW (77.3%), and PLBW (77.8%) groups than in the full-term (8.6%), normal weight (16.5%), and normal birth (2.7%) groups. CONCLUSION The strong association among periodontitis, PB, and LBW in this study highlights the need to consider the periodontal status of pregnant women in Madagascar.

Periodontal diseases and stress: a brief review

Periodontal diseases are common chronic inflammatory diseases caused by pathogenic microorganisms colonising the subgingival area and inducing local and systemic elevations of pro-inflammatory cytokines resulting in tissue destruction. Apparition and evolution of periodontal diseases are influenced by many local or systemic risk factors. Psychological stress has been suggested as one of them and may negatively influence the outcome of periodontal treatment. However, mechanisms explaining the possible relationship between stress and increased susceptibility to periodontal disease remain poorly understood. Several stress markers are found in blood and saliva of patients with periodontal diseases and influence the development of periodontal diseases by several mechanisms including modifications of the inflammatory response and changes in the composition of the dental biofilm. The aim of this review is to provide an insight into the relationship between psychological stress and periodontal diseases.

Relationship between Periodontal Diseases and Preterm Birth: Recent Epidemiological and Biological Data

For ten years, the incidence of preterm birth does not decrease in developed countries despite the promotion of public health programs. Many risk factors have been identified including ethnicity, age, tobacco, and infection. However, almost 50% of preterm birth causes remain unknown. The periodontal diseases are highly prevalent inflammatory and infectious diseases of tooth supporting tissues leading to an oral disability. They influence negatively general health worsening cardiovascular diseases and diabetes. Periodontal diseases have been also suspected to increase the rate of preterm birth, but data remain contradictory. The objective of this review is to present the principal results of epidemiological, biological, and interventional studies on the link between periodontal diseases and preterm birth. The conclusions of this work underline the importance for the physician/obstetrician to identify women at risk for preterm birth and to address these patients to dentist for periodontal examination and treatment in order to limit adverse pregnancy outcomes.

Periodontal and Systemic Responses in Various Mice Models of Experimental Periodontitis: Respective Roles of Inflammation Duration and Porphyromonas gingivalis Infection

BACKGROUND The great variability of periodontal and systemic responses to experimental periodontitis reflects the inherent pathogenic complexity of mice models and could limit the resulting interpretations and their extension to human diseases. This study compared the effect of Porphyromonas gingivalis (Pg) infection and experimental periodontitis duration at local and systemic levels in various models. METHODS Periodontitis was induced in C57BL/6J mice by ligatures previously incubated with Pg (LIGPG group) or not (LIG group) or by oral gavage (GAV) with Pg ATCC 33277. Blood samples were taken, and mice were euthanized at different times. Periodontal tissue destruction, osteoclast number, and inflammation were assessed by histomorphometry, tartrate-resistant acid phosphatase histoenzymology, and cathepsin B (CATB) and matrix metalloproteinase 9 (MMP9) immunochemistry. Serum levels of interleukin-6 (IL-6) and IL-1β were measured using enzyme-linked immunosorbent assay bioplex methods. RESULTS Periodontal tissue destruction and osteoclast numbers were significantly elevated in LIGPG models compared to LIG and GAV models. They increased with time with the exception of osteoclast numbers in the LIG model. CATB and MMP9 expression was related to bone destruction processes and Pg infection. The highest serum levels of IL-6 and IL-1β were observed in the LIGPG group. A decrease of IL-6 and an increase of IL-1β serum level were observed with time in LIGPG group contrary to LIG group. CONCLUSIONS These data indicate that Pg infection worsened periodontal tissue destruction through specific pathogenic pathways and modified systemic response to periodontal inflammation. Furthermore, the blood cytokine response to ligature models showed their relevance for evaluating the systemic impact of periodontal disease.