Category: Skeletal System

Categories : Ageing Skeletal SystemTags :

The Brain Forces Muscles to ‘Hit the Brakes’ in Hip Osteoarthritis

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Muscle activation in people suffering from hip osteoarthritis might be a case of ‘mind over matter’, new research from Edith Cowan University (ECU) has shown.

Research undertaken by ECU post-doctoral research fellow Dr Myles Murphy investigated muscle function in people with hip osteoarthritis and found that these patients were unable to activate their muscles as efficiently. The findings are published in Sports Medicine and Health Science.

“Previous research has well established that the degree to which a joint degenerates is not directly related to the amount of pain a person with arthritis will experience. In fact, the stronger your muscles are, the more protected your joint is, and the less pain you will experience.

“Our research has shown that people with hip osteoarthritis were unable to activate their muscles as efficiently, irrespective of strength.”

As part of this research, Dr Murphy and his team studied the brain function of people with hip arthritis, finding that the mind played an enormous part in this equation.

“Basically, people with hip arthritis are unable to activate their muscles properly because the brain is actively putting on the brake to stop them from using the muscle. We don’t know why that is, yet. But the brain seems to really be hampering the progress of rehabilitation and the muscles to protect the joint,” Dr Murphy said.

“We suspect that it is a short-term, protective response gone wrong. Unlike a rolled ankle or a hurt knee, chronic pain like osteoarthritis tends to hang around for a long time.  Instead of being a protective response in the short term, the brain’s protective response becomes a really problematic and maladaptive response in the long term.”

Hip osteoarthritis is more prevalent in people over the age of 45, and women are much more like to develop the condition. People who have reported previous joint damage, from a sports injury or accident, are more likely to present with hip osteoarthritis, as are those with joint abnormalities, such as developmental dysplasia of the hip.

People living with hip arthritis often presents with different walking patterns than those without and could struggle with everyday activities like getting out of a chair, or vehicle.

“The impact on their daily lives is the biggest burden of osteoarthritis. The condition also results in substantial time-loss from work, and is associated with a high economic cost,” Dr Murphy said.

“The level of disability for normal activity within our study cohort was about 25%, compared to the 0% reported in our healthy control group.”

Dr Murphy is currently investigating novel ways in which to overcome this automatic muscle inhibition to effectively rehabilitate patients.

In the meantime, those living with hip osteoarthritis have been urged to continue strength training and to work with a qualified physiotherapist or exercise physiologist.

“You will need to work quite hard to build the strength in those muscles, but it can be done. There is no quick fix. Staying strong is something that people with hip osteoarthritis will need to actively keep working on,” he said.

Source: Edith Cowan University

Categories : Skeletal SystemTags :

Sustained Device Use Alters the Spine And Muscles, Causing Pain

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Learning new languages, sending emails, attending a virtual class, or speaking to loved ones halfway around the world are just some of the tasks accomplished by touching a button on a smartphone. Unfortunately, the ease and convenience of modern devices have also come with a painful crick in the neck. The sedentary nature of work and prolonged use of hand-held devices and computers have contributed to a sharp increase in neck pain.

While fatigue in neck muscles has long been suspected of causing pain, the actual mechanical changes in the spine and muscles that precede weakness remain an outstanding question.

Now, using high-precision X-ray imaging to track spine movements during neck exertion tasks, Texas A&M University researchers have discovered that sustained neck exertions cause muscle fatigue that then exaggerate the cervical spine curvature. This leads to neck pain.

Their results are published in the Proceedings of the National Academy of Sciences.

“We are talking about subtle movements of the neck in statically held positions, which are hard to capture. They are also highly complex because there are so many individual pieces in the neck, or as we call, motion segments,” said Dr Xudong Zhang, professor in the Department of Industrial and Systems Engineering. “With this study, we have, for the first time, provided unequivocal evidence that fatigue causes mechanical changes that increase the risk.”

Zhang said this understanding can help to make informed decisions about how we work and the design of products (e.g., head-mounted wearables) that can potentially reduce the risk of neck pain.

Neck pain is prevalent

Neck pain is one of the most common musculoskeletal disorders, and globally, around 2500 people out of 100 000 have some form of neck pain. In fact, by 2050, the estimated global number of neck pain cases is projected to increase by 32.5%. An important risk factor for neck pain is bad posture sustained over long periods. Consequently, working long hours on the computer in a stooped position or prolonged use of smart devices are important contributors to neck pain.

Neck posture is maintained dynamically by the bones of the spine pulled into position by the muscles that attach to them.  Although the neck is highly flexible, it is also very unstable.

“The muscle drives movements by producing force,” said Zhang. “We hypothesised that when different muscles’ force production abilities diminish, the bone positions change and that can be captured.”

Measuring fatigue

To test their idea, they recruited healthy volunteers in a “sustained-till-exhaustion” neck exertion task. The subjects maintained their necks in the neutral, 40° extended (bent backwards) and 40° bent forward for a certain duration. The investigators used electromyography (EMG) to measure muscle electrical activity. In particular, they objectively measured muscle fatigue through changes in the frequency of the EMG signal. In addition, they used high-precision, dynamic X-ray technology to track small-amplitude cervical spine movements that were of the order of a few degrees.

“We imagined the cervical spine as a cantilever bridge,” said Zhang. “If there is excessive and/or repeated stress on the bridge, it might sag or buckle; similarly, if the muscles get fatigued, the cervical spine may deflect.”

The researchers’ experimental paradigm validated that sustained exertions indeed lead to EMG signals of fatigue. Biomechanically, the muscular fatigue modified the spine’s mechanics, which then increases the propensity for injury.

Further investigations

As a next step, the researchers will develop dynamic biomechanical models, a novel approach that promises to provide a more realistic understanding of the muscular events that precede fatigue. Unlike the model in this study that assumes static neck exertions, the dynamic model will capture subtle but consequential changes in the muscles and bones over time.

Source: Texas A&M University

Categories : Exercise Skeletal SystemTags :

The Arms and Torso of Human Males Evolved to Throw a Punch

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Photo by Hermes Rivera on Unsplash

In the animal kingdom, males develop specialised weapons such as deer antlers for competition when winning a fight is critical. Humans do too, according to new research from the University of Utah. Males’ upper bodies are built for more powerful punches than females’, says the study, published in the Journal of Experimental Biology, suggesting that fighting may have long been a part of our evolutionary history.

“In mammals in general,” says professor David Carrier of the School of Biological Sciences, “the difference between males and females is often greatest in the structures that are used as weapons.”

Assembling evidence

For years, Carrier has been exploring the hypothesis that generations of interpersonal male-male aggression long in the past have shaped structures in human bodies to specialise for success in fighting. Past work has shown that the proportions of the hand aren’t just for manual dexterity- they also protect the hand when it’s formed into a fist. Other studies looked at the strength of the bones of the face (as a likely target of a punch) and how our heels, planted on the ground, can confer additional upper body power.

“One of the predictions that comes out of those,” Carrier says, “is if we are specialised for punching, you might expect males to be particularly strong in the muscles that are associated with throwing a punch.”

Jeremy Morris, then a doctoral student and now an assistant professor at Wofford College, designed an experiment with Carrier, doctoral student Jenna Link and associate professor James C. Martin to explore the sexual dimorphism, or physical differences between men and women, of punching strength. It’s already known that males’ upper bodies, on average, have 75% more muscle mass and 90% more strength than females’. But it’s not known why.

“The general approach to understanding why sexual dimorphism evolves,” Morris says, “is to measure the actual differences in the muscles or the skeletons of males and females of a given species, and then look at the behaviours that might be driving those differences.”

Cranking through a punch

To avoid potential hand injury from a using punching bag, the researchers instead rigged up a hand crank that would mimic the motions of a punch. They also measured participants’ strength in pulling a line forward over their head, akin to the motion of throwing a spear. This tested an alternative hypothesis that males’ upper body strength may have developed for the purpose of throwing or spear hunting.

Twenty men and 19 women participated. “We had them fill out an activity questionnaire,” Morris says, “and they had to score in the ‘active’ range. So, we weren’t getting couch potatoes, we were getting people that were very fit and active.”

But even with roughly uniform levels of fitness, the males’ average power during a punching motion was 162% greater than females’, with the least-powerful man still stronger than the most powerful woman. Such a distinction between genders, Carrier says, develops with time and with purpose.

“It evolves slowly,” he says, “and this is a dramatic example of sexual dimorphism that’s consistent with males becoming more specialised for fighting, and males fighting in a particular way, which is throwing punches.”

They didn’t find the same magnitude of difference in overhead pulling strength, lending additional weight to the conclusion that males’ upper body strength is specialised for punching rather than throwing weapons.

Breaking a legacy of violence

It’s an uncomfortable thought to consider that men may be designed for fighting. That doesn’t mean, however, that men today are destined to live their ancestor’s violent lives.

“Human nature is also characterized by avoiding violence and finding ways to be cooperative and work together, to have empathy, to care for each other, right?” Carrier says. “There are two sides to who we are as a species. If our goal is to minimise all forms of violence in the future, then understanding our tendencies and what our nature really is, is going to help.”

Source: University of Utah

Categories : Skeletal SystemTags :

Patients with Osteoarthritis are Often Prescribed NSAIDs Despite Contraindications

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Photo by Towfiqu barbhuiya

A new study published in the journal Osteoarthritis and Cartilage has found that people with newly diagnosed osteoarthritis (OA) of the knee or hip with contraindications to or precautions for NSAIDs still continue to be prescribed these drugs. Additionally they had higher use of opioids and slightly lower physical therapy (PT) use within the first year of OA diagnosis, both of which are not consistent with treatment guidelines for OA.

“We found individuals with contraindications to NSAIDs were still commonly prescribed them, placing them at risk for NSAID-related adverse events,” explains corresponding author Tuhina Neogi, MD, PhD, the Alan S. Cohen Professor of Rheumatology and professor of medicine at the school. “Additionally, they were not more likely to receive safer alternatives like PT despite its widespread recommendation as first-line intervention.”

The researchers used population-based register data to identify adults residing in Sweden (between 2004-13) without a previous knee or hip OA diagnosis. Among this group, between 2014-18, they identified people with knee or hip OA diagnosis and presence of contraindications to or precautions for oral NSAIDs at the time of OA diagnosis. They then estimated the risk of: 1) regular oral NSAID use; 2) regular opioid use; 3) PT during the first year after diagnosis among those with versus without contraindications or precautions.

Despite having contraindications to NSAIDs, 21% of those in the study were regular users of NSAIDs within the first year of their OA diagnosis. Similarly, 21% of those with precautions for using NSAIDs were also regular users. They also found a higher proportion of persons with contraindications were regular users of opioids than those without a contraindication or precaution, while a slightly lower proportion received PT.

Neogi stresses that more options for effective and safe management of OA symptoms are urgently needed, and greater work is required in narrowing and ultimately closing the evidence-knowledge-practice gap.

Source: Boston University

Categories : Skeletal SystemTags :

Radiology’s Role in Monitoring the Silent Disease – Osteoporosis

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Images of a hip and lumbar spine, where bone density is typically measured.

Osteoporosis is often called a ‘silent disease,’ because it progresses, without symptoms, until a fracture occurs most commonly in your hips, spine and wrists.  However, a bone density scan can alert doctors to the disease before a patient has experienced any symptoms.

Radiology imaging techniques play a crucial role in the early diagnosis, management and monitoring of low bone density. The rapid evolution of high-quality imaging techniques, using reduced radiation doses, has positioned radiology ideally for this role.

What is osteoporosis

A healthy bone viewed under a microscope, looks like honeycomb. Osteoporosis, put simply, is when the ‘holes and spaces’ in the honeycomb increase in size, causing the bones to lose density or mass and develop abnormal tissue structure. This is caused by the body losing too much bone or making too little bone because of a lack of calcium, vitamin D and not doing any weight-bearing exercises or both. This can lead to a decrease in bone strength which, in turn, can increase the risk of broken or fractured bones.

There are degrees of bone density loss which are determined by radiologists doing a DEXA scan.

‘The standard method of determining your bone density,’ says Dr Hein Els, director at SCP Radiology, ‘is a DEXA scan (dual-energy X-ray absorptiometry). This involves using two X-ray beams, at different energy levels. to measure the bone mineral density. It has a high accuracy for overall bone density and is commonly found in clinics and hospitals.’ 

The scan uses a low radiation exposure making it safer for routine screening and follow-up.

‘The amount of radiation is minimal,’ says Dr Els, ‘it’s equivalent to 1 or 2 days of background radiation at sea level.’ 

Osteoporosis vs osteopenia

Osteoporosis and osteopenia are both conditions measured on a DEXA scan and characterised by decreased bone density. While they are related, they differ in severity and implications for bone health.

The fracture risk is higher in osteoporosis due to more significant bone fragility.

Understanding and managing both conditions are crucial for maintaining bone health and preventing fractures.

Measuring bone density

‘We measure your bone mass density by comparing it to that of a healthy, young adult. The result will tell us how much lower (or higher) your bone mass score,’ explains Dr Els. ‘Software is also used to calculate a predicted 10-year fracture risk for a major osteoporotic fracture and a hip fracture. The result is a T-score which you will be given by your doctor.’

Who is at greater risk

The vast majority of patients referred for a DEXA scan are women.  However, men over the age of 50 are also at risk, though not to the same degree as women.  The aim is to prevent fractures later in life by maintaining healthy bone mineral density, which means it is beneficial to know your bone mineral density. Fractures in the elderly population are a significant cause of morbidity and mortality.

Apart from diagnosing osteoporosis and osteopenia and assessing fracture risk, DEXA scans are helpful in the following ways:

  • Monitoring bone density changes over time: For individuals diagnosed with osteoporosis or those undergoing treatment for bone loss, DEXA scans are used to monitor changes in bone density. This helps in evaluating the effectiveness of treatment
  • Postmenopausal women: Are at a higher risk of developing osteoporosis due to decreased oestrogen levels. DEXA scans are recommended for postmenopausal women, especially those with additional risk factors
  • Men over 50 can also be at risk of osteoporosis
  • A family history of osteoporosis or fractures can increase an individual’s risk. DEXA scans can help assess bone density in those with a genetic predisposition
  • Individuals with a low body mass index (BMI) are at a higher risk for osteoporosis and may benefit from bone density testing
  • Smokers and heavy alcohol users are risk factors for osteoporosis
  • Patients with fragility fractures: Individuals who have experienced fractures from minor falls or injuries may undergo DEXA scans to determine if osteoporosis is the underlying cause

How do you treat low bone mass density?

This can be done through medication such as bisphosphonates, hormone-related therapy and other bone-building medications or through lifestyle changes. This includes an adequate intake of calcium and vitamin D, regular weight-bearing exercise, quitting smoking and limiting alcohol.

The DEXA scan is the safest, most reliable method of determining your bone loss and whether your bones are normal or if you are osteopenic or osteoporotic – the precursor to osteoporosis or full-blown osteoporosis. Regular medical check-ups and proactive lifestyle changes can significantly mitigate the risks associated with these conditions.

‘There is no need to be harbouring this silent disease,’ says Dr Els, ‘when radiography is available to test for these and can put you on a path to wellness.’  

Categories : Skeletal SystemTags :

New Study Reveals Promising Drug Target for Osteoporosis Treatment

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In a recent study published in Journal of Cellular Physiology, researchers from Tokyo University of Science discovered a new target for the treatment of osteoporosis, which is responsible for 8.9 million fractures globally each year. They focused on improving a common bone-strengthening drug, teriparatide, which has a tendency to also increase bone resorption. By targeting a newly identified gene, they were able to suppress teriparatide’s bone resorption effect.

Induction of parathyroid hormone (PTH) signalling using the synthetic PTH-derived peptide – teriparatide, has demonstrated strong bone-promoting effects in patients with osteoporosis. These effects are mediated by osteogenesis, the process of bone formation involving the differentiation and maturation of bone-forming cells called osteoblasts. However, PTH induction is also associated with the differentiation of macrophages into osteoclasts, which resorb bone. Although, bone remodelling by osteoblasts and osteoclasts is crucial for maintaining skeletal health, PTH-induced osteoclast differentiation can decrease treatment efficacy in patients with osteoporosis. However, precise molecular mechanisms underlying the dual action of PTH signaling in bone remodelling are not well understood.

To bridge this gap, Professor Tadayoshi Hayata and Ms Chisato Sampei, from Tokyo University of Science, along with their colleagues, conducted a series of experiments to identify druggable target genes downstream of PTH signalling in osteoblasts. Explaining the rationale behind their study , corresponding author, Prof. Hayata says, “In Japan, it is estimated that 12.8 million people, or one in ten people, suffer from osteoporosis, which can significantly deteriorate their quality of life. Teriparatide is classified as a drug that promotes bone formation, but it also promotes bone resorption, which may limit bone formation. However, the full scope of its pharmacological action remains unknown.”

The researchers treated cultured mouse osteoblast cells and mice with teriparatide. They then assessed gene expression changes induced by PTH in both the cultured cells and bone cells isolated from the femurs of the treated animals, using advanced RNA-sequencing analysis. Among several upregulated genes, they identified a novel PTH-induced gene – ‘Gprc5a’, encoding an orphan G protein-coupled receptor, which has been previously explored as a therapeutic target. However, its precise role in osteoblast differentiation had not been fully understood.

PTH induction has been known to activate the cyclic adenosine monophosphate (cAMP) and protein kinase C (PKC) signaling pathways. Interestingly, the team found that in addition to PTH induction, activation of cAMP and PKC also resulted in overexpression of Gprc5a, albeit to a lesser extent, underscoring the potential involvement of other molecular pathways. Notably, upregulation of Gprc5a was suppressed upon inhibition of transcription, but, remained unaffected upon suppressing protein synthesis, suggesting that Gprc5a could be transcribed early on in response to PTH signaling and serves as a direct target gene.

Furthermore, the researchers examined the effect of Gprc5a downregulation on osteoblast proliferation and differentiation. Notably, while PTH induction alone did not affect cell proliferation, Gprc5a knockdown resulted in an increase in the expression of cell-cycle-related genes and osteoblast differentiation markers. These findings suggest that Gprc5a suppresses osteoblast proliferation and differentiation.

Diving deeper into the molecular mechanisms underlying the effects of Gprc5a, in PTH-induced osteogenesis, the researchers identified Activin receptor-like kinase 3 (ALK3) – a bone morphogenetic protein (BMP) signalling pathway receptor, as an interacting partner of Gprc5a. In line with their speculation, overexpression of Gprc5a indeed, led to suppression of BMP signalling via receptors including ALK3.

Overall, these findings reveal that Gprc5a – a novel inducible target gene of PTH, negatively regulates osteoblast proliferation and differentiation, by partially suppressing BMP signaling. Gprc5a can thus, be pursued as a novel therapeutic target while devising treatments against osteoporosis. The study sheds light on the complex process of bone remodeling and explains the bone-promoting and bone-resorbing effects of PTH signaling.

“Our study shows Gprc5a may function as a negative feedback factor for the bone formation promoting effect of teriparatide. Suppressing Gprc5a function may, therefore, increase the effectiveness of teriparatide in non-responding patients. In the future, we hope that our research will lead to improved quality of life and healthy longevity for people suffering from osteoporosis,” concludes Prof Hayata.

Source: Tokyo University of Science

Categories : Skeletal SystemTags :

Poor Sleep When Young may Drive Osteoporosis in Later Life

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Photo by Andrea Piacquadio

Adequate sleep can help prevent osteoporosis, according to a growing body of research. As part of the University of Colorado Department of Medicine’s annual Research Day, held on April 23, faculty member Christine Swanson, MD, MCR, described her clinical research on how sleep interacts with osteoporosis.

“Osteoporosis can occur for many reasons such as hormonal changes, aging, and lifestyle factors,” said Swanson, an associate professor in the Division of Endocrinology, Metabolism, and Diabetes. “But some patients I see don’t have an explanation for their osteoporosis.

“Therefore, it’s important to look for novel risk factors and consider what else changes across the lifespan like bone does – sleep is one of those,” she added.

How bone density and sleep change over time

In people’s early- to mid-20s, they reach what is called peak bone mineral density, which is higher for men than it is for women, Swanson said. This peak is one of the main determinants of fracture risk later in life.

Bone density mostly plateaus for a couple of decades. Then, when women enter the menopausal transition, they experience accelerated bone loss. Men also experience bone density decline as they age.

Sleep patterns also evolve over time. As people get older, their total sleep time decreases, and their sleep composition changes. For instance, sleep latency, which is the time it takes to fall asleep, increases with age. On the other hand, slow wave sleep, which is deep restorative sleep, decreases as we age.

“And it’s not just sleep duration and composition that change. Circadian phase preference also changes across the lifespan in both men and women,” Swanson said, referring to people’s preference for when they go to sleep and when they wake up.

How is sleep linked to bone health?

Genes that control our internal clock are present in all of our bone cells, Swanson said.

“When these cells resorb and form bone, they release certain substances into the blood that let us estimate how much bone turnover is going on at a given time,” she said.

These markers of bone resorption and formation follow a daily rhythm. The amplitude of this rhythm is larger for markers of bone resorption than it is for markers of bone formation, she said.

“This rhythmicity is likely important for normal bone metabolism and suggests that sleep and circadian disturbance could directly affect bone health,” she said.

Researching the connection between sleep and bone health

To further understand this relationship, Swanson and colleagues researched how markers of bone turnover responded to cumulative sleep restriction and circadian disruption.

For this study, participants lived in a completely controlled inpatient environment. The participants did not know what time it was, and they were put on a 28-hour schedule instead of a 24-hour day.

“This circadian disruption is designed to simulate the stresses endured during rotating night shift work and is roughly equivalent to flying four time zones west every day for three weeks,” she said. “The protocol also caused participants to get less sleep.”

The research team measured bone turnover markers at the beginning and end of this intervention and found significant detrimental changes in bone turnover in both men and women in response to the sleep and circadian disruption. The detrimental changes included declines in markers of bone formation that were significantly greater in younger individuals in both sexes compared to the older individuals.

In addition, young women showed significant increases in the bone resorption marker.

If a person is forming less bone while still resorbing the same amount – or even more – then, over time, that could lead to bone loss, osteoporosis, and increased fracture risk, Swanson said.

“And sex and age may play an important role, with younger women potentially being the most susceptible to the detrimental impact of poor sleep on bone health,” she said.

Research in this area is ongoing, she added.

Source: University of Colorado Anschutz Medical Campus

Categories : Neurology Skeletal SystemTags :

A Single Gene Variant that Gave Rise to Humans’ Unique Skull Base

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One of the unique features that Homo sapiens have compared with other closely related hominin species and primates is the shape of the base of the skull, which enabled larger brains to evolve. Now, in a study recently published in the American Journal of Human Genetics, a team from Tokyo Medical and Dental University (TMDU), the University of Helsinki, and the University of Barcelona has analysed a genomic variant responsible for this unique human skull base morphology.

Most of the genomic changes that occurred during human evolution did not occur directly to genes themselves, but in regions responsible for controlling and regulating the expression of genes. Variants in these same regions are often involved in genetic conditions, causing aberrant gene expression throughout development. Identifying and characterising such genomic changes is therefore crucial for understanding human development and disease.

The development of the basicranial region, the base of the skull where it joins the vertebra, was key in the evolution of Homo sapiens, as we developed a highly flexed skull base that allowed our increased brain size. Therefore, variants that affect the development of this region are likely to have been highly significant in our evolution.

First, the team searched for variants in just a single letter of the DNA code, called single nucleotide polymorphisms (SNPs), that caused different regulation of genes in the basicranial region in Homo sapiens compared with other extinct hominins. One of these SNPs stood out, located in a gene called TBX1.

They then used cell lines to show that the SNP, called “rs41298798,” is located in a region that regulates the expression levels of the TBX1 gene, and that the “ancestral” form of the SNP, found in extinct hominins, is associated with lower TBX1 expression, while the form found in Homo sapiens gives us higher levels of TBX1.

“We then employed a mouse model with lower TBX1 expression,” explains lead author Noriko Funato, “which resulted in distinct alterations to the morphology at the base of the skull and premature hardening of a cartilage joint where the bones fuse together, restricting the growth ability of the skull.” The changes in the Tbx1-knockout mice were reminiscent of the known basicranial morphology of Neanderthals.

These morphological changes are also reflected in human genetic conditions associated with lower TBX1 gene dosage, such as DiGeorge syndrome and velocardiofacial syndrome, further indicating the significance of this genetic variant in the evolution of our unique skull base morphology.

The identification of this genomic variant sheds light on human evolution, as well as providing insight into common genetic conditions associated with lower expression of the TBX1 gene, paving the way for greater understanding and management of these conditions.

Source: Tokyo Medical and Dental University

Categories : IT in Healthcare Skeletal SystemTags :

AI Helps Clinicians to Assess and Treat Leg Fractures

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Photo by Tima Miroshnichenko on Pexels

By using artificial intelligence (AI) techniques to process gait analyses and medical records data of patients with leg fractures, researchers have uncovered insights on patients and aspects of their recovery.

The study, which is published in the Journal of Orthopaedic Research, uncovered a significant association between the rates of hospital readmission after fracture surgery and the presence of underlying medical conditions. Correlations were also found between underlying medical conditions and orthopaedic complications, although these links were not significant.

It was also apparent that gait analyses in the early postinjury phase offer valuable insights into the injury’s impact on locomotion and recovery. For clinical professionals, these patterns were key to optimising rehabilitation strategies.

“Our findings demonstrate the profound impact that integrating machine learning and gait analysis into orthopaedic practice can have, not only in improving the accuracy of post-injury complication predictions but also in tailoring rehabilitation strategies to individual patient needs,” said corresponding author Mostafa Rezapour, PhD, of Wake Forest University School of Medicine. “This approach represents a pivotal shift towards more personalised, predictive, and ultimately more effective orthopaedic care.”

Dr. Rezapour added that the study underscores the critical importance of adopting a holistic view that encompasses not just the mechanical aspects of injury recovery but also the broader spectrum of patient health. “This is a step forward in our quest to optimize rehabilitation strategies, reduce recovery times, and improve overall quality of life for patients with lower extremity fractures,” he said.

Source: Wiley

Categories : Metabolic Disorders Skeletal SystemTags :

Type 2 Diabetes Alters the Behaviour of Discs in the Vertebral Column

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Type 2 diabetes alters the behaviour of discs in the vertebral column, making them stiffer, and also causes the discs to change shape earlier than normal. As a result, the disc’s ability to withstand pressure is compromised. This is one of the findings of a new rodent-based study published in PNAS Nexus.

Low back pain is a major cause of disability, often associated with intervertebral disc degeneration. People with type 2 diabetes face a higher risk of low back pain and disc-related issues. Yet the precise mechanisms of disc degeneration remain unclear.

Investigating the biomechanical properties of the intervertebral disc is crucial for understanding the disease and developing effective strategies for managing low back pain.

“These findings provide novel insight into the potential mechanisms underlying diabetes-related disc tissue damage and may inform the development of preventative and therapeutic strategies for this debilitating condition,” the research team wrote. The team consisted of engineers and physicians from the University of California San Diego, UC Davis, UCSF and the University of Utah.

The study emphasises that nanoscale deformation mechanisms of collagen fibrils accommodate compressive loading of the intervertebral disc.

In the context of type 2 diabetes, these mechanisms are compromised, resulting in collagen embrittlement.

These findings provide novel insight into the potential mechanisms underlying diabetes-related disc tissue damage and may inform the development of preventative and therapeutic strategies for this debilitating condition.

Researchers employed synchrotron small-angle x-ray scattering (SAXS), an experimental technique that looks at collagen fibril deformation and orientation at the nanoscale.

They wanted to explore how alterations in collagen behaviour contribute to changes in the disc’s ability to withstand compression.

They compared discs from healthy rats to those from rats with type 2 diabetes (UC Davis rat model). The healthy rats showed that collagen fibrils rotate and stretch when discs are compressed, allowing the disc to dissipate energy effectively.

“In diabetic rats, the way vertebral discs dissipate energy under compression is significantly impaired: diabetes reduces the rotation and stretching of collagen fibrils, indicating a compromised ability to handle pressure,” the researchers write.

Further analysis showed that the discs from diabetic rats exhibited a stiffening of collagen fibrils, with a higher concentration of non-enzymatic cross-links.

This increase in collagen cross-linking, induced by hyperglycaemia, limited plastic deformations via fibrillar sliding.

These findings highlight that fibril reorientation, straightening, stretching, and sliding are crucial mechanisms facilitating whole-disc compression.

Type 2 diabetes disrupts these efficient deformation mechanisms, leading to altered whole-disc biomechanics and a more brittle (low-energy) behaviour.

Source: University of California – San Diego