Abstract
The healing of bone defects may be hindered by systemic conditions such as osteoporosis. Calcium phosphates, with or without ion substitutions, may provide advantages for bone augmentation. However, the mechanism of bone formation with these materials is unclear. The aim of this study was to evaluate the healing process in bone defects implanted with hydroxyapatite (HA) or strontium-doped calcium phosphate (SCP) granules, in non-ovariectomised (non-OVX) and ovariectomised (OVX) rats. After 0 (baseline), six and 28d, bone samples were harvested for gene expression analysis, histology and histomorphometry. Tumour necrosis factor-α (TNF-α), at six days, was higher in the HA, in non-OVX and OVX, whereas interleukin-6 (IL-6), at six and 28d, was higher in SCP, but only in non-OVX. Both materials produced a similar expression of the receptor activator of nuclear factor kappa-B ligand (RANKL). Higher expression of osteoclastic markers, calcitonin receptor (CR) and cathepsin K (CatK), were detected in the HA group, irrespective of non-OVX or OVX. The overall bone formation was comparable between HA and SCP, but with topological differences. The bone area was higher in the defect centre of the HA group, mainly in the OVX, and in the defect periphery of the SCP group, in both non-OVX and OVX. It is concluded that HA and SCP granules result in comparable bone formation in trabecular bone defects. As judged by gene expression and histological analyses, the two materials induced different inflammatory and bone remodelling responses. The modulatory effects are associated with differences in the spatial distribution of the newly formed bone.
Highlights
Bone tissue has an inheritable self-healing capacity
The aim of this study was to evaluate the differences in biological response to hydroxyapatite (HA) and strontium-doped calcium phosphate (SCP) granules in both normal and compromised bone conditions at two different time points
The SEM images show that the obtained HA and SCP granules had the same shape and granule size (Figure 2C and E, respectively)
Summary
Bone tissue has an inheritable self-healing capacity. This may fail in some situations where the deficiency is too large to be regenerated spontaneously. The process may be further hindered when the bone microstructure is compromised due to systemic diseases, e.g. osteoporosis. These situations traditionally require augmentation procedures where auto- or allografts represent the gold standard. The limited material supply, donor-site morbidity, transmission of infectious diseases and the risk of immunological rejection are still drawbacks [1]. It is a need to develop new or to modify existing materials, which further augment and/or accelerate bone healing and regeneration
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