How faithfully does intramembranous bone regeneration recapitulate embryonic skeletal development?

Postnatal intramembranous bone regeneration plays an important role during a wide variety of musculoskeletal regeneration processes such as fracture healing, joint replacement and dental implant surgery, distraction osteogenesis, stress fracture healing, and repair of skeletal defects caused by trauma or resection of tumors. The molecular basis of intramembranous bone regeneration has been interrogated using rodent models of most of these conditions. These studies reveal that signaling pathways such as Wnt, TGFß/BMP, FGF, VEGF, and Notch are invoked, reminiscent of embryonic development of membranous bone. Discoveries of several skeletal stem cell/progenitor populations using mouse genetic models also reveal the potential sources of postnatal intramembranous bone regeneration. The purpose of this review is to compare the underlying molecular signals and progenitor cells that characterize embryonic development of membranous bone and postnatal intramembranous bone regeneration.

Programming of osteoporosis and impact on osteoporosis risk.

Osteoporosis is a skeletal disorder characterized by reduced bone quantity and quality and an increased susceptibility to fracture, and seems to be one of many chronic conditions that might be influenced by events early in life. Specifically, there is growing evidence of an interaction between the genome and the environment in the expression of the disease.

Shoulder dystocia.

The frequency of shoulder dystocia in different reports has varied, ranging 0.2-3% of all vaginal deliveries. Once a shoulder dystocia occurs, even if all actions are appropriately taken, there is an increased frequency of complications, including third- or fourth-degree perineal lacerations, postpartum hemorrhage, and neonatal brachial plexus palsies. Health care providers have a poor ability to predict shoulder dystocia for most patients and there remains no commonly accepted model to accurately predict this obstetric emergency. Consequently, optimal management of shoulder dystocia requires appropriate management at the time it occurs. Multiple investigators have attempted to enhance care of shoulder dystocia by utilizing protocols and simulation training.

Review: developmental origins of osteoporotic fracture.

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterised in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content (BMC), but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birth weight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the HPA and GH/IGF-1 axes. Maternal smoking, diet (particularly vitamin D deficiency), and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimisation of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Epidemiology of osteoporotic fracture: looking to the future.

This paper reviews the recent literature on candidate genes, anthropometric and environmental factors, and the evolving area of intrauterine fetal programming with regard to the development of osteoporosis.