Bone fracture nonunion rate decreases with increasing age: A prospective inception cohort study

Zura, Robert; Braid-Forbes, Mary Jo; Jeray, Kyle J.; Mehta, Samir; Einhorn, Thomas A.; Watson, John T.; Rocca, Gregory J. Della; Forbes, Kevin F.; Steen, R. Grant

doi:10.1016/j.bone.2016.11.006

Cited by 87 publications

(82 citation statements)

References 36 publications

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“…Even though obesity was thought to be a protecting factor for the skeleton due to its association with increased bone mineral density [23], it has been recently shown that obesity is associated with increased prevalence of bone fractures [24]. A recent prospective cohort study using data from 56,492 fractures of Medicare patients identified obesity as a risk factor for fracture nonunion [25]. The reduced bone turnover seems to be related with progressive insulin resistance induced by weight gain [26].…”

Section: Discussionmentioning

confidence: 99%

Influence of weight gain on the modulation of wound healing following tooth extraction

Furuse

Almeida

Costa

et al. 2018

Bone

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Introduction: Obesity is characterized by extreme body fat accumulation related to lean body mass. The low-grade systemic inflammation induced by weight gain may influence wound healing. This study assessed the association between obesity and alveoli repair after tooth extraction. Methods: Forty-two male Wistar rats were randomly divided into two groups: weight gain (n = 21), animals fed with hyperlipidic cafeteria diet in order to gain weight; and control (non-obese; n = 21) regularly fed rats. After twelve weeks, the upper right central incisor was extracted and animals were sacrificed after 7, 14 and 28 days. Slides were obtained for histological analysis. Bone formation and protein expression at the different periods were compared using Kruskal-Wallis test and Dunn post-test. Results: Bone area was higher in the control group all over the experiment with more TRAP-positive cells and TRAP-positive labeling in the weight gain group. RANKL was homogeneously expressed along the experiment with no differences among the groups; conversely OPG levels reduced in the weight gain groups 14 and 28 days after tooth extraction. Osteocalcin labeling was higher in the control group after 7 days of extraction, with no differences at later time points. VEGF labeling was higher in the control group after 14 days of tooth extraction while the strongest immunolabeling in the weight gain group was observed 21 days post-extraction. Conclusion: Weight gain induced a delay in bone repair after tooth extraction. The increase in the number of TRAP-positive cells observed in the extraction site seems to be mediated by the reduction in the expression of OPG rather than an overexpression of RANKL. In addition, the late expression of VEGF in the weight gain group might have delayed osteoblast migration and differentiation.

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Section: Discussionmentioning

confidence: 99%

Influence of weight gain on the modulation of wound healing following tooth extraction

Furuse

Almeida

Costa

et al. 2018

Bone

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“…The US Food and Drug Administration (FDA) define a nonunion as a fracture that does not heal within nine months and reports nonunion occurring in 1 out of 40 fractures (20). A lack of healing progression within three consecutive months is the clinical definition of a delayed union (21).…”

Section: Discussionmentioning

confidence: 99%

Adenovirus-mediated bone morphogenetic protein-2 promotes osteogenic differentiation in human mesenchymal stem cells in vitro

Cao

Sun

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Delayed and failed bone union following fracture is a common clinical complication that requires treatment in orthopedics. Cell-based therapies and tissue-engineering approaches are potential therapeutic strategies for bone repair and fracture healing. However, the effect of adenovirus expressing bone morphogenetic protein-2 (Ad-BMP-2) on the osteogenic ability of human mesenchymal stem cells (hMSCs) has remained to be fully elucidated. Therefore, in the present study, hMSCs were transduced using Ad-BMP-2 to assess the effects of its application and to determine whether Ad-BMP-2 promotes the osteogenic differentiation of hMSCs. The purity of the hMSC cultures was assessed using flow cytometric analysis. In order to assess the osteogenic activity, alkaline phosphatase activity (ALP) was measured and to estimate the osteoblastic mineralization and calcification, von Kossa staining for phosphates was performed. Cells positive for Src homology 2 domain were determined to be hMSCs and the presence of CD34 was used to distinguish hematopoietic lineages. Following treatment, the Ad-BMP-2 and control group had significantly increased ALP levels (P<0.05). Compared to the blank group and the group transfected with adenoviral vector containing LacZ, the phosphate deposition in the Ad-BMP-2 group and the positive control group treated with dexamethasone was markedly increased. The results of the present study suggested that Ad-BMP-2 promotes osteogenic differentiation in hMSCs and may have a potential application in treating delayed union and nonunion following bone fracture.

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“…An inadequate blood supply may also originate from central cardiovascular (stroke, cardiac arrest) insufficiency and peripheral vascular (i.e. atherosclerosis, venous thrombosis) diseases [43] (Figure 3).…”

Section: Trauma Surgerymentioning

confidence: 99%

Fracture Repair: Its Pathomechanism and Disturbances

Szczęsny¹

2018

Trauma Surgery

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Healing of the bone fracture is a biological process that is based on various cell lineages recruited, activated and regulated by molecular mediators, namely chemokines, growth factors, and cytokines, cooperating in a cascade of events aimed to fill the fracture gap with callus. Remodeling of the callus rebuilds the microarchitecture to the mature bonecancellous or compact, depending on the type of the bone that was primarily at the fracture gap. Restitution of the bone continuity requires activation of mesenchymal stem cells that transform into osteoblasts and mature into osteocytes. It is activated and regulated by molecules released from blood platelets from posttraumatic hematoma, traumatized tissues, nerve endings, and inflowing inflammatory cells. The significance of the inflammatory cells in this process is inappreciable, as they eradicate pathogens, remove wound debris, and supply the fracture gap with molecules regulating forthcoming cellular events. They also provide immune regulation of the healing. To proceed uneventfully, healing requires an adequate bone contact and biomechanical environment, proper oxygenation, and nutrition. Unfortunately, up to 15% of bone fractures show some kinds of disturbances that may result in cessation of reparative processes leading to non-union. Factors, responsible for that, are brought to date based on current literature and clinical observations.

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Bone fracture nonunion rate decreases with increasing age: A prospective inception cohort study

Cited by 87 publications

References 36 publications

Influence of weight gain on the modulation of wound healing following tooth extraction

Influence of weight gain on the modulation of wound healing following tooth extraction

Adenovirus-mediated bone morphogenetic protein-2 promotes osteogenic differentiation in human mesenchymal stem cells in vitro

Fracture Repair: Its Pathomechanism and Disturbances

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