RECONSTRUCTION OF THE ANTERIOR CRUCIATE LIGAMENT: How to move after surgery?

 The long-term success of anterior cruciate ligament (ACL knee) reconstruction is tied to how you "move" after surgery, finds this team from Brigham Young University in Utah, who set out to understand why many ACL patients end up with knee osteoarthritis. This study, presented in the journal Medicine & Science in Sports & Exercise, shows the importance of avoiding both underload and overload, which are harmful to the cartilage, and therefore of restoring the mechanics of movement, through physiotherapy for example, so as to improve the chances of avoiding osteoarthritis.

 

One in 3 patients who undergo ACL reconstruction surgery will suffer from knee osteoarthritis within 10 years of their surgery. And one in two patients has a very high risk of suffering from an irrecoverable physical handicap. Seeking to explain this difficulty in recovery, the team explored 2 theories:

• the knee injury itself can cause persistent and chronic inflammation leading to underlying tissue changes;
• patients who sustain this ACL injury end up moving differently during activities like running, jumping, and walking, which worsens cartilage damage over time.

 

Based on these theories, Brigham Young University researchers with their colleagues at the University of North Carolina observed the gait biomechanics of 130 subjects who underwent ACL reconstruction surgery, between 6 months and 13 months old. years before. The participants, fitted with retroreflective markers on their legs, captured by cameras, were asked to walk as if they were walking normally and quietly on a sidewalk, at a constant speed. In particular, the researchers collected data on the reaction force of the ground on the injured leg during walking. This analysis concludes with a determining factor for the symptoms of pain and osteoarthritis, the underload or the overload of the operated leg:

• people who report persistent symptoms after surgery overload or underload walking their injured leg;
• specifically, the symptomatic group overloads or underloads the injured leg 4 to 5% more than the asymptomatic group.

 

A difference of 5% load at each step: thus, the effectiveness of the reconstruction of the ACL is obviously not called into question here, it is rather the mode of recovery that holds the attention: "The way you move is linked to the outcome of your surgery,” summarize the authors. "At first glance, these load differences may seem relatively small, however, a difference of 5% at each step, during each month, each year and then over a lifetime can lead to a progressive and chronic disease such as osteoarthritis. Posttraumatic ".

 

What are the implications for patients? the authors recommend that patients who have undergone this ACL reconstruction surgery take care to "restore the mechanics of movement in such a way as to improve the chances of avoiding osteoarthritis".

Concretely, this involves joining a physiotherapy or strength-building program. Under surveillance, of course.

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EXERCISE: How it removes toxic proteins from muscles

  This study from the University of São Paulo (USP) will certainly contribute to the development of alternatives to treat muscle weakness and atrophy. The Brazilian researchers, in partnership with American and Norwegian colleagues, show here, in Scientific Reports, that the absence of muscle stimulus results in an accumulation of toxic proteins in the cells which leads to muscle weakness or loss. of muscle mass. It is typically this type of muscle dysfunction that affects the elderly or people with sciatic nerve damage, bedridden patients or even workers who spend long hours sitting, specify the authors.

 

This buildup of toxic proteins is found to be linked to impaired autophagy, the cellular process responsible for identifying and eliminating damaged proteins and toxins. The study deciphers this process on a group of rats subjected to an exercise program preceding an injury and shows that physical exercise can keep the autophagic system working, optimizing its activity if necessary, as in the case of a dysfunction. muscle related to an injury or a temporary lack of exercise.

 

Without autophagy, a molecular cascade leads to cell death:  Here, the demonstration is performed in rats undergoing sciatic nerve ligation surgery, to create an effect equivalent to that of sciatic nerve compression in humans. The pain prevents the human or animal subject from using the affected leg and the muscles involved weaken and atrophy. During the 4 weeks preceding the surgery, the rats had been divided into 2 groups, one sedentary and the other trained to run at 60% of maximal aerobic capacity for 1 hour a day, 5 days a week. The experiment shows that the muscular dysfunction induced by the lesion of the sciatic nerve turns out to be less aggressive in the “aerobic” group than in the sedentary group. The researchers observe that the physical training increases autophagic flow and thus reduces dysfunctional protein levels in the muscles. At the same time, exercise improves the contractility of muscle tissue.

 

Thus, daily exercise sensitizes the autophagic system , facilitates the elimination of proteins and organelles that are not or no longer functional in the muscles. Elimination of these dysfunctional components is essential, because when built up, they become toxic and contribute to the breakdown and death of muscle cells.

 

Muscles work like a refrigerator , which needs electricity to operate. If this signal ceases because you remove the plug from the refrigerator or block the neurons that innervate the muscles, the foods, such as the proteins in the muscles, will start to “spoil”. Initially, an early warning mechanism present in the cells activates the autophagic system, which identifies, isolates and eliminates faulty material but if the mechanism ceases to function properly, the cells also malfunction. The proteins that then form toxic aggregates begin to damage and cause cell death.

Exercise is a transient stress that leaves a memory in the body, here via the autophagic system. When the body is subjected to other stresses, it is then better prepared to react and combat the effects.

 

The idea, at the end of this work, would be to be able to identify a molecule that selectively keeps the autophagic system on alert, similar to what happens during physical exercise, and to develop a drug to treat muscle dysfunction. . In particular, in bedridden or immobilized patients, or suffering from degenerative muscular diseases.

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CHILDHOOD OBESITY: A major factor in slipped capital femoral epiphysis and hip fragility

 Obesity in children is the main risk factor for serious hip disease later in life and sometimes as early as adolescence, these Liverpool researchers warn, so that increasing rates of obesity in children lead to the increase in urgent surgeries among adolescents, due to debilitating hip disease. A study presented in the journal Pediatrics, specifically focused on slipped capital femoral epiphysis, a disease that affects 1 in 2,000 children.

 

This disease, frequently confused with a severe dislocation of the hip, is characterized by a real deformation, even “collapse” of the hip, which leads to pain and lifelong disability. Early detection and treatment of the disease is important to minimize its severity. Slipped capital femoral epiphysis is one of the most common causes of hip replacements in young adults, and sometimes even children. Surgeons have long suspected that obesity may be the cause, and this study adds to the evidence of its responsibility.

 

The study looked at the body mass index (BMI) of nearly 600,000 children in Scotland, where BMI measurements are collected through routine school health screening. Analysis of data from this very large cohort of children shows that:

• children who are obese at age 5 have a 75% risk of remaining obese by age 12;
• and above all, children suffering from severe obesity at the age of 5 years are 20 times more likely to develop epiphysiolysis femoris than a child of normal weight;
• Finally, the higher the BMI of the child, the higher the risk of slipped capital femoral epiphysis.

 

 

Crucial Implications for Physicians: Lead author Dr. Daniel Perry, pediatric orthopedic surgeon at Alder Hey Hospital comments on these findings: "Surgeons have long suspected that obesity in children is at the root of this disease, and these results show it very clearly. These are very important data for doctors who treat children with slipped capital femoral epiphysis, especially in obese children. Early identification of the disease means children usually only need relatively simple surgery, while later identification most often involves high-risk reconstructive surgery.”

 

While slipped capital femoral epiphysis has a profound impact on the quality of life of adolescents, the link with obesity is striking, here is therefore a new reason to ensure the healthy weight of children, and this from an early age.

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MECANOBIOLOGY: Why knee joint injury leads to osteoarthritis

 These scientists from the University of Eastern Finland and the Massachusetts Institute of Technology have discovered why injury to the knee joint usually leads to osteoarthritis. By deciphering this process mediated by inflammation of the joint and by an increase in the flow of fluids from the cartilage, this study, presented in Scientific Reports, opens up a new way of detecting the risk of post-traumatic osteoarthritis. A track to improve rehabilitation protocols and personalize them according to each patient.

 

Injuries to the knee joints are usually related to the practice of certain sports such as football, rugby, hockey or athletics, however most athletes are unaware that such injuries can lead to inflammation of the joints and, ultimately, a post-traumatic osteoarthritis. In advanced post-traumatic osteoarthritis, the articular cartilage is completely degraded, causing severe joint pain, lack of mobility and these symptoms can lead to a significant deterioration in quality of life, autonomy and even isolation. social. However, these mechanisms leading to osteoarthritis and its severe consequences remain poorly understood. Additionally, a doctor examining a post-trauma patient remains today. hui unable to predict the evolution of his joints and the risk of possible development of osteoarthritis. This study finally deciphers the underlying process leading from trauma to osteoarthritis and, in doing so, paves the way for prediction and earlier management.

 

It is a new mechanobiological model of cartilage degeneration that the team describes to us: after a knee trauma, the articular cartilage degenerates around the damaged areas and the tissues deform with the faster flow of fluid around the cartilage and this , even under normal dynamic pressure on the joint, such as when walking. Cell death is accelerating, note these experimental observations carried out in cartilage samples. "  Our results indicate that after knee injury and tissue overload, osteoarthritis is caused by a significant leak of proteoglycans at the surface of the injury  " summarizes the lead author, researcher Gustavo A. Orozco from the University of Eastern Finland.

 

A model that can be used to predict the progression of post-traumatic osteoarthritis and to evaluate the results of the clinical interventions performed:

Specifically, this model should eventually make it possible to identify knee lesions at low, moderate or high risk of osteoarthritis and allow the choice, for each subject, of an optimal and personalized rehabilitation protocol.

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