Human atrophic fracture non‐unions are not avascular

Abstract

A sinall proportion of fractures progress to non-union. Non-uiiioiis are routinely classified into two groups either hypertrophic or atrophic according to their radiological appearance. It is a coiiimon preconception that non-unions with a hypertrophic appearance on X-ray are biologically active and vascular with potential to heal given the correct stable environment. Atrophic nonunions are considered to be avascular aiid inert and will not heal even under the correct stable environment. Non-unions are either infected or aseptic. I n the present study, we tested the liypothesis that aseptic atrophic tion-uiiioiis are less vascular than aseptic hypertrophic lion-unions aiid healing fractures. Biopsies were taken from the fracture gap of patients with healing fractures. hypertrophic lion-unions aiid atrophic non-unions. A dual labelling technique was used with antibodies against CD3 1 (JC70) and Collagen IV. Blood vessels were quantified using a Chalkley point eyepiece graticule. There was no statistically significant difference in the median vessel count between the three fracture groups. These findings do not support tlie hypothesis that established atrophic fracture non-union are less vascular than hypertrophic non-unions or healing fractures.

NOTCH signaling in skeletal progenitors is critical for fracture repair

“…Therefore, these results support the concept that BMSCs and potentially NOTCH signaling are key cellular and signaling participants in the pathogenesis of both hypertrophic and atrophic nonunion. Fracture nonunions are sometimes considered to be avascular, although recent data suggest that no statistically significant change in the median vessel counts of biopsies from the fracture gap of patients with healing fractures, hypertrophic nonunions, or atrophic nonunions can be identified (47). These findings are supported by preclinical models, which have demonstrated the highly vascular nature of many nonunions, including atrophic nonunions (48,49).…”

Bone mineral metabolism in patients with neurofibromatosis type 1 (von Recklingausen disease)

“…Other cellular elements can be involved into altered bone growth, such as chondrocytes, fibroblasts and endothelial cells, all expressing physiologically neurofibromin [12,30,40]. In NF1 patients a significant reduction of endochondral bone formation [24], increased collagen synthesis, proliferation, migration and reduced apoptosis of fibroblast can be clearly observed [4,15,21,35,39].…”

In silicobiology of bone modelling and remodelling: regeneration

“…An example of an atrophic non-union based on Reed et al (2002) and several treatment strategies are shown in figure 4. Non-union was achieved experimentally by removing the periosteum and bone marrow at both sides of the fracture gap, which was numerically simulated by removing the boundary condition for mesenchymal stem cells in these areas.…”