As 2012 fades into memory, it is a good time to reflect on events of the past twelve months that influenced to our field. As is typical, the past year brought both high and low points. The best news is that our Society continues to be strong. Both our Annual Meeting and Journal remain the leaders of their respective categories and our membership is strong. In addition, the last twelve months brought exciting new advances in both clinical and basic research related to diseases of bone and mineral metabolism. However, there are also a number of challenges to the continued advancement of our field. Perhaps the most difficult issue is uncertainty about funding for scientific research. For most scientists, the majority of their financial support comes from national governments. However, in most developed countries the economic slowdown that occurred after the global financial crisis of 2008 has put a significant strain on the treasuries of national government and this, in turn, has affected the research budgets of the government agencies that fund science. While global economies continue to recover slowly, uncertainty about research funding will likely remain with us for at least in the near future. This affects all scientists but is most challenging for junior investigators, who have yet to establish a track record of accomplishments and hence, are more vulnerable to the vagaries of research support.
This year brought advancement in our ability to identify those individuals who are at the greatest risk for developing osteoporosis. We found new risk factors for future fractures, like serum sclerostin levels, and made progress developing high resolution imaging technologies for bone. These make it hopeful that we will soon be able to better decide whom and when to treat patients to prevent osteoporotic fragility fractures. However, the elusive concept of “bone quality” remains to be measured in a way that will allow health care providers to identify individuals with modest decreases in bone density who are most likely to develop fragility fractures.
In basic science we continue to identify new factors and mechanisms that affect bone cell function. Advances in our understanding of the genetic code and its epigenetic modification have greatly advanced our perception of normal bone physiology and the derangements that produce clinical diseases. Perhaps no advance will more affect our field than the rapid increases in our ability to sequence the genome and identify specific polymorphisms in DNA that link to disease states. With the surprising discovery that up to eighty percent of the genome is active and many different forms of non-coding RNA play a significant role in controlling gene expression, it is becoming apparent that defining the sequences that cause specific genetic diseases like osteoporosis or Paget’s disease requires a full interrogation of the entire genome. As we advance in our appreciation of the links between genetics and functions of bone, it is almost certain that areas of the genome, which are remote from those coding proteins, will have significant effects on the development of bone diseases.
Next year holds additional hope for advancement in our field. At least one new therapeutic for osteoporosis appears to be near final review and others are in the late stages of development. Additionally, new areas of research that combine studies of bone with studies of muscle or immune cells promise to provide a more integrated approach to understanding the skeleton and may lead to a better appreciation of bone physiology and the mechanisms of skeletal diseases.
Farmington, CT, USA
The Year in Review
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