Whole-Slide View of Rare Orthopaedic Tumor
JBJS Case Connector debuted digital whole-slide images back in 2016, and the February 27, 2019 case report by Lans et al. put that ability to link to and navigate an entire microscope slide to good use again.
The 27-year-old man described in this case report presented with a progressively painful right forearm. Conventional radiographs and MRI led clinicians to suspect a rare desmoplastic fibroma of the proximal aspect of the radius, but it was not until a CT-guided core biopsy was analyzed histologically that the diagnosis could be confirmed. The histologic findings, depicted in a digital whole-slide image, revealed a fibrous to fibro-osseous lesion composed of fibroblast-like cells with varying degrees of hypercellularity.
The patient subsequently underwent a wide-margin resection that preserved the radial head but created an 8.5-cm defect, which surgeons reconstructed with a vascularized fibular autograft. At the 2-year follow-up, the patient’s QuickDASH score was 2.7 and his PROMIS Upper Extremity and Physical Function Short Form score was 42.
For more information about JBJS Case Connector, watch this video featuring JBJS Editor-in-Chief Dr. Marc Swiontkowski.
A CRISPR/Cas9 Tutorial
This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson.
Understanding recent gene technology can be very daunting. The CRISPR/Cas9 method for gene editing is a prominent example. CRISPR stands for Clustered Regularly Interspersed Short Palindromic Repeats, and Cas9 is an acronym for the CRISPER-Associated Protein 9. Scientists became aware of CRISPR in E. coli in 1987, but they only recently realized that CRISPR constituted an adaptive immune system for bacteria and archae, which are primitive bacteria-like cells.
When infected by a virus (phage), a bacteria’s Cas genes are activated. Cas gene products cut viral DNA sequence sites called protospacers and then insert those sequences into the bacterial DNA. The host bacterium identifies the viral sequences by a protospacer adjacent motif (PAM), which is rarely seen in the host genome. Hence, replication of this sequence will not adversely affect the host. In the event of a second phage attack, Cas genes are activated and they generate CRISPR RNA (crRNA), which recognizes the phage sequence. crRNA associates with Cas nucleases to cleave both DNA strands of the invader.
There are numerous CRISPR modules. Type II CRISPR is one of an expanding number of naturally existing CRISPR families that has have been used for gene editing in eukaryotes. The type II CRISPR family uses crRNA and an additional tracrRNA to target specific DNA sequences. These have been combined to create a single guide RNA (gRNA) to direct sequence-specific Cas9 double-stranded DNA cleavage. The result is a simple, programmable RNA method that has been used for genome targeting and genome editing in eukaryotes.
The accuracy of this system has been markedly enhanced to avoid unwanted mutations. The system is being fashioned to block existing gene expression, modify gene expression by inserting DNA sequences, and activate expression of single or multiple genes. CRISPR technology enables researchers to develop mouse models of disease much more quickly and less expensively than traditional approaches. Larger animal models of disease can also now be produced.
Successful treatment of mouse models of human diseases with CRISPR suggests that the technology can be applied to directly treat human diseases in the future. Preclinical research is underway using CRISPR-ed stem cells or mouse models to study human diseases such as retinitis pigmentosa, Fanconi anemia, Duchenne muscular dystrophy, sickle-cell anemia, and cystic fibrosis.
Thanks to Dr. Gary Gibson for his help with this tip.
Reference
Gibson GJ, Yang M. What rheumatologists need to know about CRISPR/Cas9. Nat Rev Rheumatol. 2017 Apr;13(4):205-216. doi: 10.1038/nrrheum.2017.6. Epub 2017 Feb 9.
Microbiomes, OA, and Diabetic Foot Ulcers
This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson.
We hear the term “microbiome” with increasing frequency nowadays. Merriam-Webster’s online dictionary defines it as “a community of microorganisms (such as bacteria, fungi, and viruses) that inhabit a particular environment and especially the collection of microorganisms living in or on the human body.” Two recent studies suggest how the microbiome can affect musculoskeletal health.
Incorporating the term “the arthritis of obesity,” Rochester, New York researchers1 used obese mice with trauma-induced knee osteoarthritis (OA) to provide evidence that there is a “gut-joint connection” in the OA degenerative process. After supplementing the diets of some of the mice with oligofructose (a prebiotic fiber), the authors found reduced systemic inflammation, reduced obesity-associated macrophage migration to the synovium, and suppressed obesity-induced joint-structure changes.
Another recent study investigated the on-body microbiome as it relates to diabetic foot ulcers (DFUs). Despite clinical signs and nonspecific biomarkers of infection, there is no specific and sensitive measure available to monitor or prognosticate the success of foot salvage therapy (FST) in patients with DFUs. These investigators hypothesized that the initial microbiomes of healed versus nonhealed DFUs are distinct and that the changes in the DFU microbiome during FST are prognostic of clinical outcome.2
Twenty-three DFU patients undergoing FST had wound samples collected at 0, 4, and 8 weeks following wound debridement and antibiotic treatment. Eleven ulcers healed and 12 did not. Healed DFUs had a larger abundance Actinomycetales and Staphylococcaceae (p < 0.05), while nonhealed ulcers had a higher abundance of Bacteroidales and Streptococcaceae (p < 0.05).
In the future, assessment of the initial microbiome and monitoring changes in the prevalence of specific microbiome constituents in patients with diabetic foot ulcers may be a clinical tool for predicting treatment response to foot salvage therapy. It’s also conceivable that microbiome analysis could eventually help patients and surgeons decide between FST and amputation.
References
- Schott EM, Farnsworth CW, Grier A, Lillis JA, Soniwala S, Dadourian GH, Bell RD, Doolittle ML, Villani DA, Awad H, Ketz JP, Kamal F, Ackert-Bicknell C, Ashton JM, Gill SR, Mooney RA, Zuscik MJ. Targeting the gut microbiome to treat the osteoarthritis of obesity. JCI Insight. 2018 Apr 19;3(8). pii: 95997. doi: 10.1172/jci.insight.95997. [Epub ahead of print] PMID: 29669931, PMCID: PMC593113
- MacDonald A, Brodell JD Jr, Daiss JL, Schwarz EM, Oh I. Evidence of differential microbiomes in healing versus non-healing diabetic foot ulcers prior to and following foot salvage therapy. J Orthop Res. 2019 Mar 25. doi: 10.1002/jor.24279. [Epub ahead of print] PMID: 30908702
Autophagy: A Culprit in Aseptic Implant Loosening?
This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson.
Periprosthetic membranes are fibrous granulomatous tissues composed of wear debris and numerous cell types, including fibroblasts, macrophages, osteoclasts (OCs), osteoblasts (OBs), osteocytes (OSTs), mesenchymal stem cells (MSCs), synovial cells, endothelial cells, and, rarely, lymphocytes. Macrophages ingest wear debris, resulting in the production of proinflammatory factors such as tumor necrosis factor (TNF); interleukin (IL)-1, IL-6, IL-17; macrophage colony-stimulating factor (M-CSF); and reactive oxygen species. In addition, macrophages can differentiate into OCs, which can induce the fibroblast cytokines that contribute to bone resorption.
Autophagy is the basic catabolic mechanism that degrades/recycles unnecessary or dysfunctional cellular components through the action of lysosomes. The breakdown of cellular components promotes cellular survival during stress, such as starvation, by maintaining cellular energy levels. In most instances, autophagy does not lead to cell death. Although the products of autophagy are typically recycled intracellularly, they may also be secreted.
Autophagy is also important for the differentiation of OBs, OSTs, and OCs. In addition, autophagy is involved in OB mineralization, and autophagy proteins are required for OC bone resorption. Autophagy appears to be triggered by wear debris in OCs, OBs, and macrophages, where the process promotes the secretion of proinflammatory proteins associated with the development of aseptic loosening. Autophagy can also be involved in the secretion of proteins such as chemokine (C-C motif) ligand 2 (CCL2) and leukemia inhibitory factor (LIF), which were both overexpressed in aseptic loosening in a rat model.
Autophagy inhibition has been shown to decrease osteolysis severity in animal models. For example, 3-methyladenine inhibition of the autophagy response to TiAl6V4 particles improved bone microarchitecture in a murine calvaria resorption model. Although autophagy will probably not be the final answer for prosthetic loosening, it is an avenue that should prompt future research into new therapeutic approaches.
Reference
Camuzard O, Breuil V, Carle GF, Pierrefite-Carle V. Autophagy Involvement in Aseptic Loosening of Arthroplasty Components. J Bone Joint Surg Am. 2019 Mar 6;101(5):466-472. doi: 10.2106/JBJS.18.00479. PMID: 30845042
Rabbit Study Suggests Antibiotic-Releasing Implant Coating Could Cut Infection Risk
A study by Miller et al. in the February 20, 2019 issue of JBJS provides preclinical proof of concept that antibiotic-loaded coatings on orthopaedic implants could eventually reduce the incidence of implant-associated infection.
The researchers used in vivo bioluminescence imaging (BLI) and ex vivo analysis of colony-forming units (CFUs) to show the efficacy of an implant coating that released linezolid-rifampin over a 7-day period. Through a parapatellar arthrotomy, researchers reamed the femoral canal of 12 rabbits and inoculated the canals with a bioluminescent strain of MRSA. They then inserted a surgical grade titanium peg into each canal. All of the pegs were coated with a nanofiber coating; 6 of the pegs were loaded with the antibiotic coating and 6 were not.
Implants coated without antibiotics were associated with significantly increased in vivo BLI signals and significantly increased knee width, relative to implants with the antibiotic-releasing coatings. The animals were killed on day 7, and ex vivo analysis of CFUs isolated from soft tissue, bone, and implant specimens showed significantly increased CFUs in the specimens without the antibiotic-releasing coating, while CFUs were undetectable in the implants with antibiotics.
This larger-animal model to assess bacterial burden employed a clinically used orthopaedic implant and replicated a medial parapatellar arthrotomy in humans. According to the authors, the coating used is “highly versatile, and the polymers or drug concentrations could be modified for more rapid or longer release.” This rabbit model should be amenable to studying additional antibiotic-releasing strategies for possible translation to clinical research in humans.
Residual Pain after Joint Replacement
This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson.
In the absence of infection and aseptic loosening, significant postoperative pain persists in up to 20% of joint-replacement patients. In one study related to this predicament, investigators studied 3 groups of individuals: 1) those without a total joint replacement (TJR) and no self-reported pain, 2) patients with a well-functioning TJR and no self-reported pain (mean implant time of 1.5 years), and 3) patients with a painful TJR (self-reported pain of >8 on a 0 to10 VAS scale; mean implant time of 1.76 years)1.
Peripheral blood mononuclear cells were collected for use in a lymphocyte reactivity assay to detect anti-inflammatory (IL-1ra, IL-10, IL-13 and IL-11) and inflammatory cytokines or receptors (IL-1rII and TNFR1). In general, anti-inflammatory cytokine markers in patients with post-TJR pain were decreased compared to controls and to individuals with no pain following TJR, with IL-10 and IL-13 significantly decreased among painful TJR patients. TNFR1 was significantly elevated in those with painful TJRs, and IL-1rII was modestly elevated. The authors note that treating this “1-2 punch” of elevated proinflammatory cytokines and decreased anti-inflammatory cytokines may require “a complex pattern” of both inhibition of proinflammatory mechanisms as well as anti-inflammatory medications.
In a separate study, investigators used scanning electron microscopy (SEM) to try to determine whether implant corrosion was secondary to inflammatory cellular reactions or to the effects of electrocautery used in near proximity to metallic surfaces2. Twelve knee prostheses taken at necropsy were compared to an off-the-shelf cobalt-chromium knee implant intentionally exposed to Bovie and Aquamantys electrocautery sources. SEM data was collected using an identical method to that of the retrieved implants. Five of the 12 necropsy retrievals showed signs of inflammatory cell-induced corrosion. Compared to the necropsy-retrieved implants, the iron/carbon ratio of the Bovie electrocautery-damaged implant was significantly higher, suggesting that the mechanism by which immune cells corrode implants is different than the mechanism of electrocautery damage.
In a third study, which compared results of lymphocyte transformation testing (LTT) for metal sensitivity with histological and clinical findings in 27 cases of primary total knee arthroplasty (TKA), researchers found that LTT results alone were insufficient for the diagnosis of TKA pain-relief failure due to an immune reaction3. A positive LTT might not indicate that an immune reaction is the cause of pain and stiffness post-TKA.
It will take more research to determine whether there is a connection between surface pitting and chronic knee pain in metal-sensitive persons, whether the elevated macrophage response is an associated risk factor, and whether that is associated with metallic material response.
References
- Lauryn S, Caicedo M, Jacobs J, Hallab NJ. Do TJR Patients with High Self-Reported Pain Levels Exhibit Decreased Serum Anti-inflammatory Cytokine Markers? Abstract 0135 Orthopaedic Research Society 2019
- Sorrels JA, Heise G, Morrow B, Arnholt C, Kurtz S, Mihalko WM. Inflammatory Cell- Induced Corrosion and Electrocautery Damaged TKA Implants. Abstract 0131 Orthopaedic Research Society 2019
- Yang S, Dipane M, Lu CH, Schmalzried TP, McPherson EJ. Lymphocyte Transformation Testing (LTT) in Cases of Pain Following Total Knee Arthroplasty: Little Relationship to Histopathologic Findings and Revision Outcomes. J Bone Joint Surg Am. 2019 Feb 6;101(3):257-264. doi: 10.2106/JBJS.18.00134. PMID: 30730485
In Chronic Sciatica, Gabapentin Quells Nerve Pain Better than Pregabalin
This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson.
Orthopaedic surgeons may not be at the forefront of dealing with nonoperative nerve pain, but many of our patients who are not candidates for surgery suffer from spine-related nerve pain in their limbs, such as sciatica. Both gabapentin (GBP, Neurontin) and pregabalin (PGB, Lyrica) are used to treat chronic sciatica (CS).
Gamma-aminobutyric acid (GABA) is an important pain-related neurotransmitter, although neither GBP nor PGB affect the GABA receptor. Instead, both drugs associate with the ligand of the auxiliary α2δ-1 and α2δ-2 subunits of certain voltage-dependent calcium channels in nerves. Among other uses, Neurontin is prescribed to treat diabetic peripheral neuropathy, and Lyrica is commonly used to treat fibromyalgia.
Investigators reporting in JAMA Neurology sought to help guide practitioners in the initial choice of drug. Eighteen patients with MRIs corroborating single-sided nerve-root sciatic pain of at least 3 months duration were evaluated in an interim analysis as part of a randomized, double-blind, double-dummy crossover trial of PGB vs GBP (8 weeks of exposure to each drug with a 1-week washout in between). The primary outcome was pain intensity measured with a 10-point visual analog scale (VAS) at baseline and 8 weeks. Secondary outcomes included disability as measured with the Oswestry Disability Index and the severity and frequency of adverse events.
Relative to baseline, both drugs showed significant VAS pain reductions and disability-score improvements, However, head-to-head, GBP showed superior VAS pain reduction (mean [SD], GBP: 1.72 [1.17] vs PGB: 0.94 [1.09]; P = 0.035), regardless of the order in which it was given. There were no between-drug differences in disability scores, but adverse events for PGB were more frequent (PGB, 31 [81%] vs GBP, 7 [19%]; P = 0.002), especially when PGB was taken first.
The authors conclude that GBP was superior with fewer and less severe adverse events, and they suggest that gabapentin should be commenced before PGB to permit optimal crossover of medicines.
Reference
Robertson K, Marshman LAG, Plummer D, Downs E. Effect of Gabapentin vs Pregabalin on Pain Intensity in Adults WIth Chronic Sciatica: A Randomized Clinical Trial. JAMA Neurol. 2018 Oct 15. doi: 10.1001/jamaneurol.2018.3077. [Epub ahead of print] PMID: 30326006
Keeping Your Bones Pumped Up
This post comes from Fred Nelson, MD, an orthopaedic surgeon in the Department of Orthopedics at Henry Ford Hospital and a clinical associate professor at Wayne State Medical School. Some of Dr. Nelson’s tips go out weekly to more than 3,000 members of the Orthopaedic Research Society (ORS), and all are distributed to more than 30 orthopaedic residency programs. Those not sent to the ORS are periodically reposted in OrthoBuzz with the permission of Dr. Nelson.
While a reasonable amount of “pumping iron” exercise has proven beneficial for musculoskeletal health, long-term use of acid-suppressing proton pump inhibitors (PPIs) may have the opposite effect on bone. Many people are currently taking PPIs, most commonly for gastrointestinal disorders such as heartburn and gastroesophageal reflux. Fortunately, many are occasional PPI users, taking the drugs only when symptoms arise. However, PPIs are often prescribed long term for preventive reasons.1
The same proton-pump mechanism present in the GI tract is seen in the vacuolar H+-ATPases that are present in high concentrations on the ruffled border of osteoclasts.2 Years of PPI use may therefore interfere with normal and essential bone remodeling. PPIs are also prescribed in the pediatric population for reflux symptoms. The effect of PPIs on future fracture or long-term osteoporosis in these very young patients is not clear.
The consequences for adult and elderly patients are clearer. Femoral bone mineral density is significantly decreased in PPI users. Also, patients with peptic ulcer disease using PPIs have a higher risk for osteoporosis than peptic ulcer patients not using PPIs. Among younger adults, the risk of fracture was significantly higher in those using PPIs than in those not using PPIs.
In 2010, the FDA issued a communication alerting healthcare professionals that users of PPIs have a possible increased risk of fractures of the hip, wrist, and spine, and that they should weigh the known benefits against the potential risks when recommending use of these medications. In 2011, the FDA refined its language somewhat: “Following a thorough review of available safety data, FDA has concluded that fracture risk with short-term, low dose PPI use is unlikely.” Still, when fractures are the outcome of interest, the data implicates long-term use of PPIs in having deleterious effects on bone.
Although data on human fracture healing in association with PPI use are sparse, animal studies do show that PPIs have a negative impact on normal fracture healing, with a decrease in the expression of important markers of bone formation, including bone morphogenetic protein (BMP)-2, BMP-4, and cysteine-rich angiogenic inducer (CYR)61.
It is time to question the need for chronic use of PPIs by our patients. Orthopaedists should encourage their patients who take PPIs to discuss this matter with their primary care physician.
References
- Eom CS, Park SM, Myung SK, Yun JM, Ahn JS. Use of acid-suppressive drugs and risk of fracture: a meta-analysis of observational studies. Ann Fam Med. 2011 May-Jun;9(3):257-67. doi: 10.1370/afm.1243. PMID: 21555754
- Wagner SC. Proton Pump Inhibitors and Bone Health: What the Orthopaedic Surgeon Needs to Know. JBJS Rev. 2018 Dec 18. doi: 10.2106/JBJS.RVW.18.00029. [Epub ahead of print] No abstract available. PMID: 30562209
Epiphyseal Etiology for Juvenile Osteochondritis Dissecans?
Most patients with clinically apparent juvenile osteochondritis dissecans (JOCD) are between 12 and 19 years of age. Often the disease can be treated successfully with nonoperative modalities, but even in cases where the initial lesion resolves, patients may be predisposed to osteoarthritis later in life. While repetitive microtrauma is suspected to be involved in the development of JOCD, the exact etiology remains poorly understood, even 130 years after the condition was first described.
In the December 19, 2018 issue of The Journal, Toth et al. histologically examined 59 biopsy samples from the central condyles of 26 pediatric cadavers to look for areas of epiphyseal cartilage necrosis. Hypothesizing that such evaluation would reveal some lesions similar to those found in animals, the authors did indeed identify 6 samples with 1 or more areas of necrotic cartilage, which were either incorporated into subchondral bone or associated with focal failure of endochondral ossification. Those characteristics are consistent with a similar disease process called osteochondrosis manifesta seen in pigs and horses. While the clinical significance of these findings remains to be determined, the authors suggest that they may help explain an epiphyseal etiology of JOCD, and the data suggest that these microscopic changes (some of which are rendered in this article as whole-slide images) are probably present in young people 5 to 10 years prior to the clinical manifestations of JOCD.
These findings lend credence to the theory that the underlying etiology of JOCD primarily involves the epiphyseal growth plate rather than subchondral bone. Furthermore, the similarities between these cadaveric specimens and osteochondrosis manifesta lesions in porcine and equine femoral condyles may help us develop improved models to better diagnose, prevent, and treat this pathology.
Chad A. Krueger, MD
JBJS Deputy Editor for Social Media
What’s New in Musculoskeletal Basic Science 2018
Every month, JBJS publishes a Specialty Update—a review of the most pertinent and impactful studies published in the orthopaedic literature during the previous year in 13 subspecialties. Click here for a collection of all OrthoBuzz Specialty Update summaries.
This month, Matthew J. Allen, VetMB, PhD, author of the December 5, 2018 Specialty Update on Musculoskeletal Basic Science, focuses on the five most compelling findings from among the more than 60 noteworthy studies summarized in the article.
Gene Editing in Orthopaedics
–Gene-editing tools such as CRISPR-Cas9 have great potential as a means of introducing therapeutic genes into mesenchymal stem cells that can then be targeted to tissues in vivo. These researchers1 reported on genetically modified stem cells that have the potential to differentiate into chondrocytes encoding a natural inhibitor of interleukin-1, providing an opportunity for localized release of immunomodulatory factors.
Managing Orthopaedic Infections
–A novel study2 in which transmission electron microscopy was used to identify viable bacteria deep within the canalicular structure of cortical bone, remote from the site of an infected implant, suggests that effective debridement requires the removal of not just necrotic tissue, but also of adjacent, apparently unaffected bone.
Computational Modeling of Human Movement
–This report3 presented a human musculoskeletal model that provided extremely accurate predictions of ground reaction forces during simulated walking and squatting. As similar models are developed and validated, surgeons will have improved tools for evaluating patients, planning surgery, and making decisions about which procedure/implant is most appropriate for an individual patient.
Sex-Related Differences
–This report4 demonstrated sexually dimorphic regulation of gene-expression profiles in bone marrow osteoprogenitor cells that could partly explain clinical observations in sex differences in peak bone mass, bone remodeling, and immunomodulation.
Biological Enhancement of Ligament Healing
–Among several basic science papers focused on the optimal healing and durable fixation of tendons and ligaments, this notable work5 reported on the translation of bridge-enhanced ligament repair for the anterior cruciate ligament.
References
- Brunger JM, Zutshi A, Willard VP, Gersbach CA, Guilak F. CRISPR/Cas9 editing of murine induced pluripotent stem cells for engineering inflammation-resistant tissues. Arthritis Rheumatol.2017 May;69(5):1111-21. Epub 2017 Mar 31.
- de Mesy Bentley KL, Trombetta R, Nishitani K, Bello-Irizarry SN, Ninomiya M, Zhang L, Chung HL, McGrath JL, Daiss JL, Awad HA, Kates SL, Schwarz EM. Evidence of Staphylococcus aureus deformation, proliferation, and migration in canaliculi of live cortical bone in murine models of osteomyelitis. J Bone Miner Res.2017 May;32(5):985-90. Epub 2017 Jan 26.
- Jung Y, Koo YJ, Koo S. Simultaneous estimation of ground reaction force and knee contact force during walking and squatting. Int J Precis Eng Manuf.2017;18(9):1263-8.
- Kot A, Zhong ZA, Zhang H, Lay YE, Lane NE, Yao W. Sex dimorphic regulation of osteoprogenitor progesterone in bone stromal cells. J Mol Endocrinol.2017 Nov;59(4):351-63. Epub 2017 Sep 4.
- Perrone GS, Proffen BL, Kiapour AM, Sieker JT, Fleming BC, Murray MM. Bench-to-bedside: bridge-enhanced anterior cruciate ligament repair. J Orthop Res.2017 Dec;35(12):2606-12. Epub 2017 Jul 9.
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