Orthopedic Innovation

Innovation within medicine more often arises via persistence and determination than from dramatic breakthroughs.  In fact, many paradigm shifting advancements are not initially embraced by the medical establishment.  In orthopedics, total joint replacement and arthroscopy are two excellent examples.  Sir John Charnley deserves much of the credit for the modern development of hip replacement surgery.  His initial designs used Teflon and those implants typically failed early.  He redesigned his implant to use a novel liner that significantly improved  its longevity.  Use of other materials and techniques over several decades via the hard work of many have led us to the point where we complain when a total hip lasts less than 10 or even 15 years.  (Read more)

Arthroscopy, one of the first minimally invasive types of surgery, at its beginning took longer and was more complicated than open surgery.  The first examination of joint via a "scope" was close to 100 years ago.    Over the last 30 years, it has become the standard of care for evaluating and treating many joint injuries such as ACL reconstruction and Rotator Cuff Repair.  This innovation is the result of contributions of thousands of researchers, surgeons and their patients.  It is also led to less invasive surgery for spine disorders.  (See Spine Surgery Video) (Read more/source)

We are now about a decade into "Biologic Orthopedics".  Therapies such as Platelet Rich Plasma, Stem Cells, Genetic Engineering, and Genome Sequencing are revolutionizing how we evaluate and treat patients.  As we surf the choppy waters of innovation, however, we will not always embrace ideal ideas.  Some "innovations" will fade as fads but others will emerge as commonplace treatments that significant improve the lives of millions of patients.  We need to balance our approach to novel methods of helping our patients.  We must seek their safety and benefit first.   In doing so, we are obligated to consider emerging biologic treatment options because they may be the best and most appropriate.

Allan Mishra, MD
@BloodCure

Genes Identified that are Associated with Risk of Fracture

In the study outlined below, genes were identified that are associated with increased risk of fracture.  Importantly, six genes NOT known to have a role in bone biology were found to correlate with bone mineral density.  This speaks to the importance of looking for diseases related genes within AND outside of known pathways.  See abstract below.

AM

Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture

• Karol Estrada,
• Unnur Styrkarsdottir,
• Evangelos Evangelou,
• Yi-Hsiang Hsu,
• Emma L Duncan,
• Evangelia E Ntzani,
• Ling Oei,
• Omar M E Albagha,
• Najaf Amin,
• John P Kemp,
• Daniel L Koller,
• Guo Li,
• Ching-Ti Liu,
• Ryan L Minster,
• Alireza Moayyeri,
• Liesbeth Vandenput,
• Dana Willner,
• Su-Mei Xiao,
• Laura M Yerges-Armstrong,
• Hou-Feng Zheng,
• Nerea Alonso,
• Joel Eriksson,
• Candace M Kammerer,
• Stephen K Kaptoge,
• Paul J Leo
• et al.

Nature Genetics

 

44,

 

491–501

 

(2012)

Received

 

07 October 2011 

Accepted

 

16 March 2012 

Published online

 

15 April 2012

Bone mineral density (BMD) is the most widely used predictor of fracture risk. We performed the largest meta-analysis to date on lumbar spine and femoral neck BMD, including 17 genome-wide association studies and 32,961 individuals of European and east Asian ancestry. We tested the top BMD-associated markers for replication in 50,933 independent subjects and for association with risk of low-trauma fracture in 31,016 individuals with a history of fracture (cases) and 102,444 controls. We identified 56 loci (32 new) associated with BMD at genome-wide significance (P < 5 × 10⁻⁸). Several of these factors cluster within the RANK-RANKL-OPG, mesenchymal stem cell differentiation, endochondral ossification and Wnt signaling pathways. However, we also discovered loci that were localized to genes not known to have a role in bone biology. Fourteen BMD-associated loci were also associated with fracture risk (P < 5 × 10⁻⁴, Bonferroni corrected), of which six reached P < 5 × 10⁻⁸, including at 18p11.21 (FAM210A), 7q21.3 (SLC25A13), 11q13.2 (LRP5), 4q22.1 (MEPE), 2p16.2 (SPTBN1) and 10q21.1 (DKK1). These findings shed light on the genetic architecture and pathophysiological mechanisms underlying BMD variation and fracture susceptibility.