Population study evaluating fracture risk among patients with chronic osteomyelitis

Lo, Chyi; Sung, Fung‐Chang; Mou, Chih-Hsin; Lin, Tzeng‐Jih; Tseng, Chun-Huang; Tzeng, Ya‐Ling

doi:10.1371/journal.pone.0189743

Cited by 1 publication

(1 citation statement)

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“…Osteomyelitis, age, poor diet or inherited genetic diseases can all reduce bone density or quality and lead to heightened fracture susceptibility, which can be debilitating and life-shortening (Cauley, 2017; Tsuchiya et al, 2017). Osteogenesis imperfecta (OI) is a rare inherited syndrome, mostly caused by mutations in collagen I or enzymes required for its maturation (Rauch and Glorieux, 2004).…”

Section: Introductionmentioning

confidence: 99%

Clinical pathologies of bone fracture modelled in zebrafish

Tomecka

Ethiraj

Sánchez

et al. 2019

Disease Models &Amp; Mechanisms

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Reduced bone quality or mineral density predict susceptibility to fracture and also attenuate subsequent repair. Bone regrowth is also compromised by bacterial infection, which exacerbates fracture site inflammation. Because of the cellular complexity of fracture repair, as well as genetic and environmental influences, there is a need for models that permit visualisation of the fracture repair process under clinically relevant conditions. To characterise the process of fracture repair in zebrafish, we employed a crush fracture of fin rays, coupled with histological and transgenic labelling of cellular responses; the results demonstrate a strong similarity to the phased response in humans. We applied our analysis to a zebrafish model of osteogenesis imperfecta (OI), which shows reduced bone quality, spontaneous fractures and propensity for non-unions. We found deficiencies in the formation of a bone callus during fracture repair in our OI model and showed that clinically employed antiresorptive bisphosphonates can reduce spontaneous fractures in OI fish and also measurably reduce fracture callus remodelling in wild-type fish. The csf1ra mutant, which has reduced osteoclast numbers, also showed reduced callus remodelling. Exposure to excessive bisphosphonate, however, disrupted callus repair. Intriguingly, neutrophils initially colonised the fracture site, but were later completely excluded. However, when fractures were infected with Staphylococcus aureus, neutrophils were retained and compromised repair. This work elevates the zebrafish bone fracture model and indicates its utility in assessing conditions of relevance to an orthopaedic setting with medium throughput.

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Section: Introductionmentioning

confidence: 99%