Bone loss in implants placed at subcrestal and crestal level: A systematic review and meta-analysis

Background: To assess differences in marginal bone loss in implants placed at subcrestal versus crestal level. Methods: An electronic and a manual research of articles written in English from Jaunary 2010 to January 2018 was performed by two independent reviewers. Clinical trials comparing bone loss for implants placed at crestal and subcrestal level were included. Pooled estimates from comparable studies were analyzed using a continuous random-effects model meta-analysis with the objective of assessing differences in crestal bone loss between the two vertical positions. Results: 16 studies were included; 10 studies did not encounter statistically significant differences between the two groups with respect to bone loss. Three articles found greater bone loss in subcrestal implants; while 3 found more bone loss in crestal implants. A meta-analysis for randomized control trial (RCT) studies reported an average and non-statistically different crestal bone loss of 0.028 mm. Conclusions: A high survival rate and a comparable bone loss was obtained both for crestal and subcrestal implants’ placement. Quantitative analysis considering a homogenous sample confirms that both vertical positions are equally valid in terms of perimplant bone loss. However, with respect to soft tissue; in presence of a thin tissue; a subcrestal placement of the implant should be preferred as it may reduce the probability for the implant to become exposed in the future and thus avoid the risk of suffering from peri-implant pathologies

Endocortical bone loss in osteoporosis: The role of bone surface availability

Age-related bone loss and postmenopausal osteoporosis are disorders of bone remodelling, in which less bone is reformed than resorbed. Yet, this dysregulation of bone remodelling does not occur equally in all bone regions. Loss of bone is more pronounced near and at the endocortex, leading to cortical wall thinning and medullary cavity expansion, a process sometimes referred to as "trabecularisation" or "cancellisation". Cortical wall thinning is of primary concern in osteoporosis due to the strong deterioration of bone mechanical properties that it is associated with. In this paper, we examine the possibility that the non-uniformity of microscopic bone surface availability could explain the non-uniformity of bone loss in osteoporosis. We use a computational model of bone remodelling in which microscopic bone surface availability influences bone turnover rate and simulate the evolution of the bone volume fraction profile across the midshaft of a long bone. We find that bone loss is accelerated near the endocortical wall where the specific surface is highest. Over time, this leads to a substantial reduction of cortical wall thickness from the endosteum. The associated expansion of the medullary cavity can be made to match experimentally observed cross-sectional data from the Melbourne Femur Collection. Finally, we calculate the redistribution of the mechanical stresses in this evolving bone structure and show that mechanical load becomes critically transferred to the periosteal cortical bone.Comment: 13 pages, 3 figures. V2: minor stylistic improvements in text/figures; more accurately referenced subsection "Internal mechanical stress distribution"; some improved remarks in the Discussion sectio

Vitamin C Prevents Hypogonadal Bone Loss

Epidemiologic studies correlate low vitamin C intake with bone loss. The genetic deletion of enzymes involved in de novo vitamin C synthesis in mice, likewise, causes severe osteoporosis. However, very few studies have evaluated a protective role of this dietary supplement on the skeleton. Here, we show that the ingestion of vitamin C prevents the low-turnover bone loss following ovariectomy in mice. We show that this prevention in areal bone mineral density and micro-CT parameters results from the stimulation of bone formation, demonstrable in vivo by histomorphometry, bone marker measurements, and quantitative PCR. Notably, the reductions in the bone formation rate, plasma osteocalcin levels, and ex vivo osteoblast gene expression 8 weeks post-ovariectomy are all returned to levels of sham-operated controls. The study establishes vitamin C as a skeletal anabolic agent. © 2012 Zhu et al

The effect of smoking on survival and bone loss of implants with a fluoride-modified surface: a 2-year retrospective analysis of 1106 implants placed in daily practice

Aim: To compare survival and peri-implant bone loss of implants with a fluoride-modified surface in smokers and nonsmokers. Materials and Methods: Patient files of all patients referred for implant treatment from November 2004 to 2007 were scrutinized. All implants were placed by the same experienced surgeon (BC). The only inclusion criterion was a follow-up time of at least 2 years. Implant survival and bone loss were assessed by an external calibrated examiner (SV) comparing digital peri-apical radiographs taken during recall visits with the post-operative ones. Implant success was determined according to the international success criteria (Albrektsson et al. 1986). Survival of implants installed in smokers and nonsmokers were compared using the log-rank test. Both non-parametric tests and fixed model analysis were adopted to evaluate bone loss in smokers and nonsmokers. Results: 1106 implants in 300 patients (186 females; 114 males) with a mean follow-up of 31 months (SD 7.15; range 24-58) were included. 19 implants in 17 patients failed, resulting in an overall survival rate of 98.3% on implant level and 94.6% on patient level. After a follow-up period of 2 years, the CSR was 96.7% and 99.1% with the patient and implant as statistical unit respectively. Implant survival was significantly higher for nonsmokers compared to smokers (implant level p = 0.025; patient level p = 0.017). The overall mean bone loss was 0.34 mm (n = 1076; SD 0.65; range 0.00-7.10). Smokers lost significantly more bone compared to nonsmokers in the maxilla (0.74 mm; SD 1.07 vs 0.33 mm; SD 0.65; p < 0.001), but not in the mandible (0.25mm; SD 0.65 vs 0.22mm; SD 0.50; p = 0.298). Conclusion: The present study is the first to compare peri-implant bone loss in smokers and nonsmokers from the time of implant insertion (baseline) to at least 2 years of follow-up. Implants with a fluoride-modified surface demonstrated a high survival rate and limited bone loss. However, smokers are at higher risk to experience implant failure and more prone to show peri-implant bone loss in the maxilla. Whether this bone loss is predicting future biological complications remains to be evaluated

Polymicrobial periodontal disease triggers a wide radius of effect and unique virome.

Periodontal disease is a microbially-mediated inflammatory disease of tooth-supporting tissues that leads to bone and tissue loss around teeth. Although bacterially-mediated mechanisms of alveolar bone destruction have been widely studied, the effects of a polymicrobial infection on the periodontal ligament and microbiome/virome have not been well explored. Therefore, the current investigation introduced a new mouse model of periodontal disease to examine the effects of a polymicrobial infection on periodontal ligament (PDL) properties, changes in bone loss, the host immune response, and the microbiome/virome using shotgun sequencing. Periodontal pathogens, namely Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum were used as the polymicrobial oral inoculum in BALB/cByJ mice. The polymicrobial infection triggered significant alveolar bone loss, a heightened antibody response, an elevated cytokine immune response, a significant shift in viral diversity and virome composition, and a widening of the PDL space; the latter two findings have not been previously reported in periodontal disease models. Changes in the PDL space were present at sites far away from the site of insult, indicating that the polymicrobial radius of effect extends beyond the bone loss areas and site of initial infection and wider than previously appreciated. Associations were found between bone loss, specific viral and bacterial species, immune genes, and PDL space changes. These findings may have significant implications for the pathogenesis of periodontal disease and biomechanical properties of the periodontium. This new polymicrobial mouse model of periodontal disease in a common mouse strain is useful for evaluating the features of periodontal disease

Iron-enriched diet contributes to early onset of osteoporotic phenotype in a mouse model of hereditary hemochromatosis

Osteoporosis is associated with chronic iron overload secondary to hereditary hemochromatosis (HH), but the causative mechanisms are incompletely understood. The main objective of this study was to investigate the role of dietary iron on osteoporosis, using as biological model the Hfe-KO mice, which have a systemic iron overload. We showed that these mice show an increased susceptibility for developing a bone loss phenotype compared to WT mice, which can be exacerbated by an iron rich diet. The dietary iron overload caused an increase in inflammation and iron incorporation within the trabecular bone in both WT and Hfe-KO mice. However, the osteoporotic phenotype was only evident in Hfe-KO mice fed the iron-enriched diet. This appeared to result from an imbalance between bone formation and bone resorption driven by iron toxicity associated to Hfe-KO and confirmed by a decrease in bone microarchitecture parameters (identified by micro-CT) and osteoblast number. These findings were supported by the observed downregulation of bone metabolism markers and upregulation of ferritin heavy polypeptide 1 (Fth1) and transferrin receptor-1 (Tfrc), which are associated with iron toxicity and bone loss phenotype. In WT mice the iron rich diet was not enough to promote a bone loss phenotype, essentially due to the concomitant depression of bone resorption observed in those animals. In conclusion the dietary challenge influences the development of osteoporosis in the HH mice model thus suggesting that the iron content in the diet may influence the osteoporotic phenotype in systemic iron overload conditions.National Funds through Foundation for Science and Technology (FCT) Norte-01-0145-FEDER-000012 Portuguese Foundation for Science and Technology (FCT) SFRH/BD/77056/2011 European Regional Development Fund (FEDER) Norte-01-0145-FEDER-000012info:eu-repo/semantics/publishedVersio

Retrospective comparative study of bone loss in implants with and without immediate loading in the Egas Moniz university clinic

To evaluate bone loss after three years in implants placed at the implantology consult at the Egas Moniz University Clinic, relating bone loss to the type of loading (conventional or immediate load). A comparative and retrospective study, performed on a sample of 65 implants, placed in 24 of 327 patients, who attended the implantology consult at the Egas Moniz University Clinic in 2015, representing 7.3% of the study population through the measurement of distance between implant platform and bone using radiographs. Three years after implant placement with and without immediate loading there is statistically significant bone loss mesially and distally. It was found that when compared bone loss in loaded vs unloaded mesially and distally implants, there were no statistically significant differences. The bone loss of the unloaded implants was compared three years after being placed, with the bone level of the loaded implants also three years later. No significant difference was found. Although no statistically significant differences were found between bone loss in loaded implants vs unloaded mesially and distally, as it is supported by the literature, it was possible to conclude that there was, in fact, a statistically significant bone loss, mesially and distally, three years after implant placement with and without immediate loading. This may be due to poor oral hygiene, a history of periodontitis, smoking and peri-implantitis.info:eu-repo/semantics/publishedVersio

Importance of geometry of the extracellular matrix in endochondral bone differentiation.

Subcutaneous implantation of coarse powders (74-420 micron) of demineralized diaphyseal bone matrix resulted in the local differentiation of endochondral bone. However, implantation of matrix with particle size of 44-74 micron (Fine matrix) did not induce bone. We have recently reported that the dissociative extraction of coarse matrix with 4 M guanidine HCl resulted in a complete loss of the ability of matrix to induce endochondral bone; the total loss of biological activity could be restored by reconstitution of extracted soluble components with inactive residue. To determine the possible biochemical potential of fine matrix to induce bone, the matrix was extracted in 4 M guanidine HCl and the extract was reconstituted with biologically inactive 4 M guanidine HCl-treated coarse bone matrix residue. There was a complete restoration of the biological activity by the extract of fine matrix upon reconstitution with extracted coarse matrix. Polyacrylamide gel electrophoresis of the extract of fine matrix revealed similar protein profiles as seen for the extract of coarse matrix. Gel filtration of the 4 M guanidine HCl extract of fine powder on Sepharose CL-6B and the subsequent reconstitution of various column fractions with inactive coarse residue showed that fractions with proteins of 20,000-50,000 mol wt induced new bone formation. These observations demonstrate that although fine bone matrix contains, osteoinductive proteins, matrix geometry (size) is a critical factor in triggering the biochemical cascade of endochondral bone differentiation. Mixing of coarse matrix with Fine results in partial response and it was confined to areas in contact with coarse particles. The results imply a role for geometry of extracellular bone matrix in anchorage-dependent proliferation and differentiation of cells

New mutations at the imprinted Gnas cluster show gene dosage effects of Gsα in postnatal growth and implicate XLαs in bone and fat metabolism, but not in suckling

The imprinted Gnas cluster is involved in obesity, energy metabolism, feeding behavior, and viability. Relative contribution of paternally expressed proteins XLαs, XLN1, and ALEX or a double dose of maternally expressed Gsα to phenotype has not been established. In this study, we have generated two new mutants (Ex1A-T-CON and Ex1A-T) at the Gnas cluster. Paternal inheritance of Ex1A-T-CON leads to loss of imprinting of Gsα, resulting in preweaning growth retardation followed by catch-up growth. Paternal inheritance of Ex1A-T leads to loss of imprinting of Gsα and loss of expression of XLαs and XLN1. These mice have severe preweaning growth retardation and incomplete catch-up growth. They are fully viable probably because suckling is unimpaired, unlike mutants in which the expression of all the known paternally expressed Gnasxl proteins (XLαs, XLN1 and ALEX) is compromised. We suggest that loss of ALEX is most likely responsible for the suckling defects previously observed. In adults, paternal inheritance of Ex1A-T results in an increased metabolic rate and reductions in fat mass, leptin, and bone mineral density attributable to loss of XLαs. This is, to our knowledge, the first report describing a role for XLαs in bone metabolism. We propose that XLαs is involved in the regulation of bone and adipocyte metabolism