Accelerated fracture healing with teriparatide

Abstract

Satisfactory healing of the osteoporotic fracture is critically important to functional recovery, morbidity, and quality of life. Some therapies for osteoporosis may affect the processes associated with bone repair. For example, bisphosphonates in experimental models are associated with increased callus size and mineralization, reduced callus remodeling, and improved mechanical strength. Local and systemic bisphosphonate treatment may improve implant fixation. No negative impact on fracture healing has been observed, even after major surgery or when administered immediately after fracture. For the osteoanabolic agent teriparatide, case reports and a randomized trial have produced mixed results, but they are consistent with a positive impact of teriparatide on fracture healing. Some of the agents currently being developed for osteoporosis, notably sclerostin and DKK1 antibodies have shown a beneficial effect on fracture healing. At this point, therefore, there is no evidence that osteoporosis therapies are detrimental to fracture healing with some promising experimental evidence for positive effects on healing, notably for those agents whose actions are primarily anabolic.

The use of biomarkers in clinical osteoporosis

“…Studies conducted recently suggest that this drug may be effective to speed up the healing of fractures, as well as to stimulate the process in patients with delayed healing. 13 According to Jakob et al this corroborates previous observations when concluding that women after menopause diagnosed with severe osteoporosis benefited from the use of teriparatide even with the interruption of therapy 18 months beforehand. 14 We observed that the most prevalent formation biomarkers were P1NP (procollagen 1 amino-terminal propeptide) and BAP, while CTX was applied the greatest number of times among resorption biomarkers.…”

Structural properties of fracture haematoma: current status and future clinical implications

“…Following a fracture, a crosslinked fibrin meshwork is formed by a platelet clump and initiation of the clotting cascade, with generation of thrombin stimulating the cleavage of fibrinogen to fibrin. Consequently, a cohort of cytokines and growth factors, such as vascular endothelial growth factor (VEGF), transforming growth factor‐ β 1 (TGF β 1) and bone morphogenetic protein (BMPs), are released from platelet degranulation and the periosteum, and are trapped by the developing haematoma (Binder et al ., ; Borges et al ., ). Besides releasing osteogenic factors, the periosteum has also been shown to have a vital role in the maturation of fracture haematomas by mediating chondrogenesis and endochondral ossification (Ozaki et al ., ).…”

Does Teriparatide Improve Fracture Union?: A Systematic Review

“…[8,9,44,45] PTPD up-regulate gene markers associated with osteoblast differentiation and an inhibitor of the Wnt pathway. [6,46] Successful attempt to use of TPTD even after revision surgery of nonunion has been published. [47] Surgeons can be very frustrated when nonunion not allowing its healing even if revision is well-performed according to the principles (surgical restabilization and provision of biological https://doi.org/10.11005/jbm.2020.27.3.167 stimulation).…”