Wound healing around endosseous implants in experimental diabetes

Nevins, M; Karimbux, Nadeem Y.; Webe, Hans Peter; Giannobile, William V.; Fiorellini, Joseph P.

doi:10.1016/s1079-2104(99)70236-2

Cited by 81 publications

(149 citation statements)

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“…Animal studies have shown that uncontrolled diabetes hinders bone formation, bone remodeling, and wound healing (Nevins et al, 1998) and causes reduction in bone-to-implant contact (BIC) and bone thickness (Takeshita et al, 1998), while insulin upregulates bone formation (Siqueira et al, 2003) and maintains BIC (Kwon et al, 2005). The effects of a hyperglycemic state have been shown to include inhibition of osteoblastic cell proliferation and collagen production during the early stages of callus development, resulting in reduced bone formation as well as diminished mechanical properties of the newly formed bone (Lu et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Diabetes and Oral Implant Failure

2014

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The aim of this systematic review and meta-analysis was to investigate whether there are any effects of diabetes mellitus on implant failure rates, postoperative infections, and marginal bone loss. An electronic search without time or language restrictions was undertaken in March 2014. The present review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Eligibility criteria included clinical human studies. The search strategy resulted in 14 publications. The I 2 statistic was used to express the percentage of total variation across studies due to heterogeneity. The inverse variance method was used for the random effects model when heterogeneity was detected or for the fixed effects model when heterogeneity was not detected. The estimates of an intervention for dichotomous outcomes were expressed in risk ratio and in mean difference in millimeters for continuous outcomes, both with a 95% confidence interval. There was a statistically significant difference (p = .001; mean difference = 0.20, 95% confidence interval = 0.08, 0.31) between diabetic and non-diabetic patients concerning marginal bone loss, favoring non-diabetic patients. A meta-analysis was not possible for postoperative infections. The difference between the patients (diabetic vs. non-diabetic) did not significantly affect implant failure rates (p = .65), with a risk ratio of 1.07 (95% confidence interval = 0.80, 1.44). Studies are lacking that include both patient types, with larger sample sizes, and that report the outcome data separately for each group. The results of the present metaanalysis should be interpreted with caution because of the presence of uncontrolled confounding factors in the included studies.

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Section: Discussionmentioning

confidence: 99%

Diabetes and Oral Implant Failure

2014

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“…They are involved in the synthesis and secretion of bone matrix and contribute to matrix mineralization, thereby forming bone tissue (Krentz and Bailey, 2005;Mellado-Valero et al, 2007). It has been reported in animal and clinical experiments that osteoblasts can differentiate and form new bone (Nevins et al, 1998;Zimmet et al, 2003;Seo et al, 2004). Therefore, culturing osteoblasts in vitro is of interest for bone tissue engineering.…”

Section: Discussionmentioning

confidence: 99%

Proliferation and differentiation of human osteoblasts from a type 2 diabetic patient in vitro

Li¹,

Liu²,

Jiang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We investigated the proliferation and differentiation potential of human osteoblasts from a type 2 diabetic patient in vitro. Human osteoblasts were obtained from a healthy subject and a type 2 diabetic patient and were cultured in vitro using the tissue explant adherent method. Differences in cell morphology were observed under a phase contrast microscope. The osteogenic differentiation capacity was evaluated by alizarin red staining, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, alkaline phosphatase (ALP) staining, and detection of bone Gla-protein (BGP) and Col-1. Expression of Runx-2 and Col-1 was detected using RT-PCR and western blot. Our data indicated that alveolar bone osteoblasts from the type 2 diabetic patient exhibited poorer growth, smaller calcium nodule formation, slower proliferation, and lower ALP, BGP, and Col-1 concentrations in the cell culture supernatant, as compared to control 11293 Osteoblasts from a type 2 diabetic patients ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 11292-11299 (2015) cells (P < 0.05). Combined, our study indicated that alveolar bone osteoblasts from a type 2 diabetic patient exhibited slower proliferation and decreased differentiation, as compared to healthy control, when cultured in vitro.

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“…The investigation of the effect of diabetes on implants has exposed an alteration in bone remodelling processes and deficient mineralization, leading to less bone absorption. The amount of bone formed is analogous when comparing diabetes-induced animals with controls but there is a decline in the bone-implant contact in diabetics [52,53]. The decrease in the levels of bone-implant success in diabetics confirms that diabetes reduces bone integration.…”

Section: Impact Of Diabetes On Osseointegration-is a Contraindicationmentioning

confidence: 96%

Bone Restoration in Diabetic Osteolysis and Therapeutic Targets

Thenmozhi¹,

Nagalakshmi²,

Samuel³

et al. 2017

Diabetes Case Rep

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Bone, being a key structural support of the body, undergoes dynamic micro structural remodelling all over life to control automatic stress and calcium requirement. Neurovascular, visual, renal complications added with osteopenia and osteoporosis are main unbearable problems in diabetes mellitus (DM). It is clear that hyperglycaemia in diabetes mellitus leads to glucose toxicity which directly suppresses adipogenic delineation of the osteoblast precursors which depreciate bone feature and strength which augment propensity to fracture. A number of risk factors including oxidative stress, apoptosis and abnormal intracellularCa 2+ metabolism have been postulated to play a function in the inception and progress of osteoporosis within diabetes. This review determines to discuss the most recent findings of mechanisms concerned in the progression of osteoporosis in diabetes. We emphasize the role of signalling molecules in osteoclastogenesis as therapeutic targets in the prevention and treatment of diabetic osteolysis. Increasing validation during the last decade suggests that zinc as neutraceutical suppresses calcium/calcineurin pathway and many compounds are potent inhibitors of osteoclast synthesis by blocking RANKL pathway, an emerging concept that is gaining acceptance. The characteristic of impediment and management of DM-induced osteolysis should be an effective glycaemic control. Hence, we propose to accentuate that Zinc combined with suitable anti-diabetic drugs and inhibitors of osteoclastogenesis may represent a potential therapeutic target in Diabetes mellitus for the prevention, reduction of fracture risk and treatment of osteolysis by suppressing osteoclastogenesis via calcium, calcineurin and RANKL pathway.

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Wound healing around endosseous implants in experimental diabetes

Cited by 81 publications

References 0 publications

Diabetes and Oral Implant Failure

Diabetes and Oral Implant Failure

Proliferation and differentiation of human osteoblasts from a type 2 diabetic patient in vitro

Bone Restoration in Diabetic Osteolysis and Therapeutic Targets

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