ORTHOBIOLOGICS DIGEST No. 6 October 12 2026 Longevity, Artificial Intelligence, PRP, and the Biology of Aging Joints

Updated: 12 hours ago
By Deborah Westergaard, MD
Board-Certified Anesthesiologist and Pain Medicine Physician
Medical Director, Regen Experts | Dallas & Plano, Texas

What Does It Really Mean to Age Well?
A few days ago, a video appeared in my TikTok feed featuring Bryan Johnson, the technology entrepreneur who has become famous for his efforts to reverse biological aging.
Johnson was discussing how some measurements of his cardiovascular and respiratory fitness resemble those of an 18-year-old.
My immediate thought was:
What about his joints?
That question sent me down another research rabbit hole.
It also brought me back to something I think about frequently in my work as an orthobiologic physician.
We are becoming increasingly sophisticated at measuring biological aging, manipulating cellular behavior, and developing technologies that may fundamentally change medicine.
But what happens if we succeed in extending human lifespan while our joints, tendons, muscles, and bones continue to deteriorate?
What good is living to 100 or beyond if we cannot move comfortably enough to enjoy those additional years?
This week's Digest explores that question from several directions.
We begin with Bryan Johnson's pursuit of biological youth and his own experience with experimental stem cell injections.
Then we examine a remarkable $1.8 billion initiative to develop artificial intelligence models capable of predicting cellular behavior.
We return to clinical medicine with a randomized trial investigating PRP for advanced knee osteoarthritis.
Finally, we examine two fascinating studies exploring how exercise and mechanical forces influence the behavior of cartilage and tendon cells.
These developments are exciting, but they also require perspective.
Scientific discovery, clinical evidence, and successful treatment are not interchangeable.
My goal with this Digest is to explore where the science is taking us, what we can reasonably conclude today, and what these developments might eventually mean for preserving musculoskeletal health.
This Week in Orthobiologics Digest No.6: Five Stories Worth Understanding
1. Can Your Heart Be 18 While Your Joints Are 49? Bryan Johnson's pursuit of biological youth raises questions about whether our joints age at the same rate as the rest of our bodies. His own musculoskeletal problems and experimental stem cell treatments provide an intriguing perspective.
2. What If We Could Predict How Your Cells Would Respond Before We Treated You? A $1.8 billion initiative involving Biohub, major technology companies, and federal research agencies aims to develop artificial intelligence models capable of predicting cellular behavior.
3. Can PRP Still Help When Knee Arthritis Is Advanced? A randomized clinical trial involving 90 patients with advanced knee osteoarthritis found encouraging improvements following intra-articular PRP injections. But what does this tell us about treating the entire joint?
4. Could Exercise Change the Biological Messages Your Cells Send? Researchers discovered that exercise changes tiny particles circulating in human blood. Those particles may influence aging cartilage cells, raising fascinating questions about cellular communication.
5. Why Are Some Tendon Injuries So Difficult to Heal? Researchers at Queen Mary University of London discovered that the stiffness of the environment surrounding tendon cells can dramatically change their behavior.
ARTICLE ONE
Can Your Heart Be 18 While Your Joints Are 49?
Bryan Johnson's pursuit of biological youth raises an important question about musculoskeletal aging.
A video featuring longevity entrepreneur Bryan Johnson recently appeared in my TikTok feed.
The interview was conducted by The School of Hard Knocks, a social media channel known for interviewing successful entrepreneurs about how they made their fortunes and what advice they would give others.
Although the original interview was recorded earlier, it appeared in my feed this week.
That is one of the interesting things about social media. An older interview can suddenly reach a new audience and introduce an entirely new group of people to an important subject.
Johnson discussed selling his payments company for approximately $800 million.
But what caught my attention was not his financial success.
It was his discussion of biological aging.
At the time of the interview, Johnson was 47 years old. He reported that measurements of his cardiovascular performance and lung capacity were comparable to those of an 18-year-old.
He also discussed his belief that humanity may eventually be able to extend life far beyond what we currently consider normal.
Those are extraordinary ambitions.
But as I listened, I found myself wondering:
If his cardiovascular system is functioning like that of an 18-year-old, what about his joints?
Who Is Bryan Johnson?
For readers unfamiliar with him, Bryan Johnson is an American technology entrepreneur who founded Braintree, a payment-processing company acquired by PayPal in 2013.
Over the past several years, he has become internationally recognized for his ambitious longevity program, Blueprint.
His approach involves intensive physiological monitoring, carefully controlled nutrition, exercise, sleep, supplements, and experimental medical interventions.
Johnson has invested substantial financial resources into measuring and attempting to slow biological aging.
His underlying premise is that aging should be studied and potentially modified rather than simply accepted as inevitable.
It is a fascinating undertaking.
But there is an important distinction between measuring physiological performance and demonstrating that every tissue in the body has become biologically younger.
Cardiovascular fitness, cartilage integrity, tendon health, bone quality, and muscle function are not necessarily interchangeable measures of aging.
And Johnson's own experience illustrates that distinction.
Johnson's Experiment With 300 Million Stem Cells
Interestingly, Johnson had already been investigating his musculoskeletal health.
On October 18, 2024, he published an article titled:
“I Injected My Joints With 300 Million Stem Cells.”
In that article, he described traveling to the Bahamas for experimental treatment involving approximately 300 million donor-derived mesenchymal stromal cells.
The cells originated from Swedish bone marrow donors and were manufactured by Cellcolabs.
They were not harvested from Johnson's own bone marrow.
According to his published account, the treatment involved six major joints: both shoulders, both hips, and both knees.
His physicians also targeted selected surrounding structures, including tendons, bursae, and labral tissue.
The injections were performed under ultrasound guidance.
Before treatment, Johnson underwent musculoskeletal imaging, including MRI and ultrasound examinations.
His reported findings included shoulder labral degeneration, rotator cuff tendinosis, patellar chondromalacia, gluteal tendon abnormalities, and hip impingement.
Although he described his symptoms as relatively minor, these findings demonstrated that his musculoskeletal system had experienced structural changes despite his intensive longevity program.
Importantly, his treatment was not limited to injecting cells into the joint spaces.
His physicians also addressed selected periarticular structures.
That suggests a more anatomically targeted approach than simply placing a biologic into a joint cavity.
However, his public account does not provide enough information to determine how each injection target was selected or whether treatment decisions were based on a comprehensive correlation of imaging, physical examination, symptoms, and biomechanics.
Nor does the account establish that his treatment regenerated cartilage or reversed joint aging.
Original source: Bryan Johnson — I Injected My Joints With 300 Million Stem Cells
Dr. Westergaard's Perspective
I find Bryan Johnson's pursuit of longevity fascinating.
He has brought considerable public attention to biological aging, preventive medicine, and the value of measuring physiological function.
But his experience illustrates something important.
Having the cardiovascular capacity of an 18-year-old does not necessarily mean having the joints of an 18-year-old.
Cartilage, subchondral bone, tendons, ligaments, and muscles are distinct tissues with different biological and mechanical demands.
Their condition cannot be determined by cardiovascular measurements alone.
Johnson's experience also raises an important distinction within orthobiologics.
The donor-derived, culture-expanded mesenchymal stromal cells he received are fundamentally different from the same-day autologous platelet-rich plasma and bone marrow concentrate used in my practice.
I personally prefer using a patient's own biological material whenever clinically appropriate.
One of my concerns with donor-derived cellular products is the potential for infectious disease transmission and other risks associated with sourcing, processing, and manufacturing.
Donor screening and quality-control procedures can reduce these risks, but no screening process can identify every conceivable biological hazard.
That does not mean every donor-derived product is unsafe. Properly regulated donor-derived therapies have important applications in medicine.
It does mean that the source, manufacturing process, and clinical evidence matter enormously.
What About Cultured Autologous Cells?
I have personally undergone both culture-expanded autologous cell treatments and same-day bone marrow concentrate procedures.
For my culture-expanded treatments, I chose the Regenexx Cayman program because of its established physician training, clinical experience, and research involvement.
I have also undergone same-day autologous bone marrow concentrate procedures, including intraosseous treatment of my shoulder and treatments involving my hand joints.
My personal experience with both approaches has been positive.
In particular, I experienced substantial improvement following intraosseous bone marrow concentrate treatment of my shoulder.
But I cannot conclude from my own experience that cultured cells are superior to freshly prepared bone marrow concentrate or vice versa.
Culture expansion can increase cell numbers.
However, cell number alone does not establish treatment superiority.
Culture conditions may alter cellular characteristics, signaling, and biological behavior. Fresh preparations have their own limitations, including variable cell populations and concentrations.
We still need well-designed comparative research to determine which approaches work best for particular conditions.
More cells do not automatically mean better treatment.
And equally important:
What we inject matters, but where we put it also matters.
In my practice, I evaluate the joint as a functional biological unit.
That includes cartilage, subchondral bone, menisci, ligaments, tendons, surrounding musculature, and biomechanics.
The goal is not simply to inject a biologic into a joint space.
It is to identify which structures are contributing to symptoms and determine whether an appropriately targeted treatment may help.
Ultimately, the question is not simply whether we can make biological-age measurements look younger.
It is whether we can preserve the structure, function, and longevity of our musculoskeletal system as we age.
After all, living longer is only part of the equation.
Maintaining the ability to move comfortably throughout those additional years matters just as much.
ARTICLE TWO
What If We Could Predict How Your Cells Would Respond Before We Treated You?
A $1.8 billion initiative could fundamentally change how scientists study disease.
Source: Reuters, October 7, 2026 Research initiative: Biohub Virtual Biology Initiative
Imagine visiting your physician and discovering that researchers could predict how your cells might respond to a treatment before you actually received it.
That sounds like science fiction.
But a major new research initiative is attempting to move biology in precisely that direction.
On October 7, 2026, Reuters reported that Biohub, the nonprofit research organization founded by Mark Zuckerberg and Priscilla Chan, was expanding its Virtual Biology Initiative into a coordinated effort valued at approximately $1.8 billion.
The initiative involves collaboration with major technology companies and federal scientific organizations, including the Department of Energy and National Institutes of Health.
Its objective is to generate enormous amounts of biological data that can be used to train artificial intelligence models to predict how cells behave.
This is not simply another medical chatbot.
The ambition is much larger.
Researchers want to develop computational models that can simulate aspects of cellular biology.
Original reporting: Reuters — $1.8 Billion Push for AI Biology
What Is a Virtual Cell?
To understand the idea, imagine that scientists want to know what happens when a particular drug interacts with a human cell.
Traditionally, researchers might grow cells in a laboratory, expose them to a substance, and observe the response.
They might repeat the experiment under different conditions.
Eventually, promising findings may progress into animal experiments and, much later, human clinical trials.
This process is expensive and time-consuming.
Now imagine creating a sophisticated computer model of cellular behavior.
Researchers could potentially ask the model:
What happens if we change a particular gene?
What happens if we expose the cell to a drug?
What happens when the cell is older?
What happens when inflammation is present?
The computer would generate predictions based on patterns learned from enormous biological datasets.
Scientists would then test those predictions in real experiments.
The goal is not to eliminate laboratory research.
It is to help researchers identify which experiments are most promising before committing substantial time and resources.
A virtual cell would therefore function somewhat like a sophisticated biological simulator.
But unlike a flight simulator, which operates according to relatively well-established physical principles, cellular biology contains enormous complexity that scientists are still trying to understand.
Building reliable predictive models will require much more than simply feeding existing research papers into artificial intelligence.
Researchers need standardized experimental data describing how real cells respond to carefully controlled changes.
That is one of the central objectives of the Virtual Biology Initiative.
AI-Designed Drugs Are Already Entering Human Trials
Interestingly, another recent story provides a glimpse of what AI-assisted biological discovery can already accomplish.
A YouTube video titled Please Stay Alive for Five More Years appeared in my feed recently.
It described a drug developed by Insilico Medicine for idiopathic pulmonary fibrosis, a serious disease involving progressive lung scarring.
The drug, rentosertib, was developed using artificial intelligence to help identify a biological target and design a molecule intended to act on that target.
In a randomized Phase 2a study involving 71 patients, investigators reported encouraging changes in lung function in the highest-dose group compared with placebo.
The results were published in Nature Medicine in 2025.
This was an important development, although the trial was too small and short to establish definitive clinical efficacy.
It also illustrates an important distinction.
AI-assisted drug discovery is already producing compounds tested in humans. Fully predictive virtual-cell medicine remains a much more ambitious goal.
The two technologies are related through computational biology, but they are not identical.
What Could This Mean for Orthobiologics?
In orthobiologics, one of the most important unanswered questions is why patients respond differently to similar treatments.
Two individuals may have comparable MRI findings and receive similar PRP preparations, yet experience different clinical outcomes.
Age, inflammation, metabolic health, tissue degeneration, mechanical loading, and other factors may influence those responses.
Imagine eventually developing computational models that help researchers understand how chondrocytes, tenocytes, osteoblasts, macrophages, and other cells respond under different biological conditions.
Could scientists eventually identify which patients are most likely to benefit from a particular intervention?
Could they identify cellular environments associated with poor tissue repair?
Could treatment strategies eventually become more individualized?
Those are fascinating possibilities.
But they remain future research questions.
Dr. Westergaard's Perspective
I find this development extraordinarily interesting.
We are witnessing technological changes that could dramatically accelerate the advancement of medicine, health, longevity, and healthspan.
The speed of these developments can be dizzying.
Sometimes it is difficult to comprehend how quickly our world is changing.
Artificial intelligence is already influencing scientific discovery, and increasingly sophisticated biological models may amplify that trajectory.
Will every development be beneficial?
Certainly not.
There will be mistakes, unintended consequences, ethical questions, and technologies that fail to deliver what their developers promise.
But I believe we need to stay informed.
As physicians, patients, and members of society, we should make an effort to understand the technologies that may shape our near future.
We may not be able to predict precisely where these developments will take us.
But understanding the science gives us a better opportunity to participate thoughtfully in decisions about how these technologies are developed and used.
For orthobiologics, the possibility of eventually understanding why one patient's tissues respond differently from another's is particularly exciting.
Perhaps the future of regenerative medicine will involve not simply developing better biologics, but understanding which biological approach is most appropriate for a particular patient.
That would represent a remarkable advancement.
ARTICLE THREE
Can PRP Still Help When Knee Arthritis Is Advanced?
A randomized clinical trial offers encouraging findings for patients facing knee replacement.
Original study: Lacko M, et al.Journal: Journal of Orthopaedic Surgery and Research Published: June 2, 2026
Patients with advanced knee osteoarthritis are frequently told that their remaining treatment options are limited.
For many, knee replacement becomes the primary recommendation.
But a recent randomized clinical trial raises an interesting question.
Could platelet-rich plasma still provide meaningful symptom relief when arthritis is already advanced?
Researchers in Slovakia investigated PRP in patients with late-stage knee osteoarthritis.
The study was published in June 2026 in the Journal of Orthopaedic Surgery and Research. PubMed
Original research: PRP Compared With Corticosteroids and NSAIDs in Advanced Knee Osteoarthritis
How Was the Study Conducted?
The researchers enrolled 90 patients between 40 and 80 years old.
All participants had symptomatic knee osteoarthritis classified as Kellgren-Lawrence grade 3 or 4.
These grades represent relatively advanced structural changes visible on radiographs.
Importantly, the participants were already on waiting lists for knee replacement surgery.
The researchers randomly assigned patients to three treatment groups.
One group received two injections of autologous PRP, administered one week apart.
The injections were intra-articular, meaning the PRP was placed directly into the knee joint space.
A second group received a single intra-articular corticosteroid injection using betamethasone.
The third group received the oral anti-inflammatory medication aceclofenac.
The investigators measured pain, stiffness, physical function, opioid use, and several blood biomarkers associated with inflammation and cartilage metabolism.
Patients were evaluated at baseline, three months, and six months.
Of the original 90 participants, 82 completed the six-month follow-up.
What Did the Researchers Find?
The PRP group experienced statistically significant improvements in pain and physical function.
At both three and six months, pain scores favored PRP over the corticosteroid and oral NSAID comparison groups.
Measures of stiffness and physical function also improved.
The researchers additionally identified changes in several blood biomarkers associated with inflammation and cartilage metabolism.
For example, they reported reductions in certain inflammatory mediators and cartilage-turnover markers.
These findings suggest that PRP may influence biological pathways involved in osteoarthritis.
However, biomarker changes do not establish that cartilage has regenerated.
The study did not demonstrate restoration of full-thickness cartilage defects or reversal of advanced structural osteoarthritis.
The investigators concluded that intra-articular PRP may provide a useful symptomatic treatment option for some patients awaiting arthroplasty.
What Are the Limitations?
This was a randomized controlled trial, which is an important strength.
However, it was relatively small, with only 82 patients completing follow-up.
The study lasted six months, so it cannot establish how long the improvements persist.
The comparator treatments also differed in administration and dosing.
Two PRP injections were compared with one corticosteroid injection or oral medication.
There was no sham-injection group.
These differences limit what can be concluded about comparative efficacy and placebo-related effects.
And perhaps most importantly for my clinical perspective:
The investigators studied intra-articular PRP. They did not study intraosseous bone marrow concentrate or comprehensive treatment of multiple joint structures.
That distinction matters.
Dr. Westergaard's Perspective
I find this study encouraging.
It suggests that patients with advanced knee osteoarthritis should not automatically be dismissed as having no potential nonoperative treatment options.
But it also illustrates why we need to distinguish between different orthobiologic techniques.
This trial evaluated PRP injected into the joint space.
It did not evaluate injections into subchondral bone.
It did not investigate treatment of individual meniscal lesions, ligament abnormalities, or other potentially symptomatic structures.
In advanced osteoarthritis, the joint is often affected at multiple anatomical levels.
Cartilage loss may coexist with subchondral bone abnormalities, meniscal degeneration, ligament laxity, synovitis, and altered biomechanics.
The underlying bone is particularly important.
Cartilage and subchondral bone form an interconnected functional structure often described as the osteochondral unit.
Changes in the bone beneath the cartilage may contribute to pain and disease progression.
That is one reason I have become particularly interested in intraosseous bone marrow concentrate treatment in appropriately selected patients.
In my clinical experience, some of the most striking and durable improvements I have observed have followed targeted intraosseous autologous bone marrow concentrate procedures.
However, those observations do not establish that intraosseous treatment is superior to intra-articular PRP.
Direct comparative research is still needed.
What we inject matters, but where we put it also matters.
For patients considering orthobiologic treatment for advanced knee arthritis, I believe a comprehensive evaluation is essential.
Learn about an individualized knee joint-preservation evaluation.
The goal should be to identify the structures contributing to symptoms and determine whether an individualized, nonoperative treatment strategy is appropriate.
Not every patient with advanced arthritis is a candidate for orthobiologic treatment.
Some patients will ultimately benefit most from joint replacement.
But advanced radiographic arthritis does not necessarily mean every nonoperative option has been exhausted.
And this study provides additional evidence that intra-articular PRP may offer meaningful symptomatic benefit for selected patients.
ARTICLE FOUR
Could Exercise Change the Biological Messages Your Cells Send?
New research suggests exercise may influence aging cartilage through microscopic cellular messengers.
Original research: Iijima H, et al.Journal: Nature Aging Published: September 29, 2026
Most of us understand that exercise is beneficial for joint health.
It strengthens muscles, improves balance, supports cardiovascular fitness, and helps maintain mobility.
But researchers at Harvard Medical School and Mass General Brigham asked a different question.
Could exercise actually change the biological messages circulating through our bodies—and could those messages influence aging cartilage?
Their findings, published in Nature Aging on September 29, 2026, suggest that the answer may be yes.
But to understand what they discovered, we need to look carefully at how the experiments were conducted.
Original research: Exercise Enhances Aged Chondrocyte Health Through MicroRNA-29-Enriched Extracellular Vesicles
First, the Researchers Started With Older Human Adults
The investigators examined older human adults who participated in a three-month aerobic exercise intervention.
They collected blood samples and analyzed tiny particles circulating in the blood called extracellular vesicles, or EVs.
So what exactly are extracellular vesicles?
They are microscopic packages surrounded by a membrane that cells naturally release.
These packages can carry proteins, lipids, and genetic material from one cell to another.
One important type of genetic material carried by extracellular vesicles is called microRNA.
MicroRNAs help regulate how genes are expressed.
You can think of extracellular vesicles as tiny delivery packages carrying molecular messages between cells.
Some of these messages may influence inflammation, metabolism, tissue maintenance, and other biological processes.
Are Extracellular Vesicles the Same as Exosomes?
Not exactly.
Exosomes are one type of extracellular vesicle, but not all extracellular vesicles are exosomes.
Other categories include microvesicles and apoptotic bodies.
The researchers characterized extracellular vesicles isolated from blood, but the study should not be interpreted as demonstrating that they had isolated a pure population of exosomes.
That distinction becomes important when we discuss commercially marketed exosome products.
What Happened After the Humans Exercised?
After the three-month exercise intervention, the investigators found changes in the molecular contents of circulating extracellular vesicles.
Of particular interest was an increase in a group of regulatory molecules called microRNA-29.
The researchers suspected that these molecules might influence how aging cartilage cells function.
But detecting a molecular change in human blood does not establish that the change benefits cartilage.
So they designed additional experiments.
Next, They Studied Cartilage Cells in the Laboratory
The researchers exposed cultured cartilage cells to extracellular vesicles associated with exercise.
These laboratory experiments included aged-like human chondrocytes.
To model aspects of an aging cartilage environment, investigators grew cells under experimentally altered mechanical conditions, including relatively stiff substrates.
They then examined whether exercise-associated extracellular vesicles could influence the cells' behavior.
The results suggested that these vesicles could counteract some changes associated with cellular aging.
The investigators identified a signaling pathway involving a gene called KL, which produces the protein alpha-Klotho.
Alpha-Klotho has attracted scientific attention because of its relationship to cellular aging and tissue homeostasis.
The investigators found evidence that microRNA-29-enriched extracellular vesicles could influence this pathway and promote characteristics associated with healthier cartilage cells.
This was an in vitro experiment.
In other words, the researchers were studying cells under controlled laboratory conditions, not treating human patients with arthritis.
Then They Moved to Aged Mice
The investigators also conducted experiments in aged mice.
They administered exercise-associated extracellular vesicles directly into mouse knee joints.
The mice subsequently demonstrated improvements in experimental measures of cartilage health and age-related degeneration.
Additional experiments using engineered extracellular vesicles enriched with microRNA-29 helped investigate the proposed signaling mechanism.
This combination of human exercise data, laboratory experiments, and animal studies provided evidence that exercise-related extracellular vesicles can influence cartilage biology.
But there are important limitations.
The researchers did not demonstrate that exercise regenerates cartilage in humans.
They did not establish that injecting extracellular vesicles into human arthritic knees improves symptoms or function.
And they did not demonstrate that commercially manufactured exosome products reproduce the biological effects observed in their experiments.
What they identified was a potentially important biological mechanism through which exercise may influence cartilage health.
That is fascinating.
It suggests exercise may benefit our joints not only through stronger muscles and improved biomechanics, but also through molecular communication between cells.
Dr. Westergaard's Perspective: Why This Study Raises Questions About Exosomes
I find this research intriguing.
Every important medical advancement has to begin somewhere.
The investigators began with observations in older human adults, then used laboratory and animal experiments to investigate a possible biological mechanism.
That is how scientific hypotheses develop.
But this study also brings up a subject that concerns me greatly.
Commercially marketed exosome treatments.
It pains me to see musculoskeletal practices offering products marketed as exosomes when fundamental questions about their composition, manufacturing, safety, and clinical effectiveness may remain unanswered.
An exosome is not a stem cell.
It is a type of extracellular vesicle.
Exosomes do not contain viable stem cells, although they can carry biologically active molecules.
The term exosome also does not tell us precisely what is inside a commercially manufactured preparation.
Patients deserve to know what they are receiving.
Where did the biological material originate?
Was it derived from umbilical cord tissue, placental tissue, or another source?
How was it processed?
How was the product characterized?
What testing established its identity, purity, potency, and safety?
And what clinical evidence demonstrates that the specific product improves the condition being treated?
These are important questions because products marketed as exosomes may originate from different biological sources and undergo substantially different manufacturing processes.
What Does the FDA Say?
The FDA has repeatedly warned about unapproved regenerative medicine products, including exosome preparations.
As of October 2026, there are no FDA-approved exosome products.
The agency has also reported serious adverse events involving unapproved products marketed as exosomes.
Products intended to treat orthopedic conditions generally require appropriate FDA authorization or approval under the applicable regulatory framework. U.S. Food and Drug Administration
FDA reference: FDA Consumer Alert on Stem Cells and Exosomes
Why I Prefer Autologous Orthobiologics
In my own practice, I prefer using autologous orthobiologic preparations, particularly platelet-rich plasma and bone marrow concentrate.
Autologous means the biological material comes from the patient receiving treatment.
PRP is prepared from the patient's blood.
Bone marrow concentrate is prepared from the patient's own bone marrow aspirate.
These approaches have different regulatory considerations from commercially manufactured donor-derived exosome products.
PRP is a blood-derived preparation rather than an exosome product.
Certain minimally manipulated bone marrow preparations may qualify for specific regulatory exclusions, depending on their processing and intended use.
However, autologous use does not automatically establish FDA approval or compliance for every orthopedic indication.
The evidence for PRP and bone marrow concentrate also varies by condition.
My preference is based partly on knowing the biological source and controlling the collection and preparation process.
That does not eliminate every risk or guarantee a successful outcome.
But it is an important consideration in how I practice.
I am enthusiastic about research into extracellular vesicles.
Studies like this may eventually help us understand how cellular communication influences tissue aging and repair.
However, there is an enormous difference between investigating extracellular vesicles under controlled research conditions and offering a commercially manufactured product as a proven treatment for osteoarthritis.
We can be excited about scientific discovery while remaining cautious about what we inject into patients.
ARTICLE FIVE
Why Are Some Tendon Injuries So Difficult to Heal?
New research suggests the mechanical environment surrounding tendon cells may influence their ability to function.
Original research: Grossemy SE, et al.Journal: Advanced Science Published: September 13, 2026, Institution: Queen Mary University of London
Tendon injuries can be frustrating.
Some respond well to rehabilitation and conservative treatment.
Others become chronic, producing persistent pain and impaired function.
Researchers at Queen Mary University of London recently investigated a fascinating question.
Could the physical environment surrounding tendon cells influence how those cells behave?
Their findings suggest that certain tendon cells are remarkably sensitive to the stiffness of their surroundings.
But the most interesting part is how the researchers demonstrated this.
Original research: Unravelling the Distinct Phenotype and Mechanosensitive Properties of Different Tendon Cell Populations
First, We Need to Understand Tendon Structure
Tendons are not simply solid ropes connecting muscles to bones.
They contain organized bundles of collagen fibers called fascicles.
Between those bundles is a softer, more flexible material called the interfascicular matrix, or IFM.
This material allows the collagen bundles to move relative to one another as the tendon stretches and recoils.
That movement helps distribute mechanical forces through the tendon.
The researchers suspected that cells living in the softer interfascicular matrix might respond differently to mechanical forces than cells located within the collagen bundles themselves.
They also knew that aging and tendon disease can alter the mechanical properties of the surrounding tissue.
So they designed an experiment to investigate what happens when the environment surrounding tendon cells becomes stiffer.
How Was the Experiment Conducted?
The researchers used tendon tissue obtained from rat tails.
They selected rat tail tendons because their anatomy allowed the investigators to separate different tendon compartments while preserving viable cells.
This was not a study involving human patients.
The researchers isolated two different populations of tendon cells.
One population came from the collagen fascicles themselves.
The second population came from the softer interfascicular matrix between those fascicles.
They then grew these cells in the laboratory on specially prepared surfaces with different mechanical stiffness.
Some surfaces were relatively soft, resembling the natural environment of the interfascicular matrix.
Others were considerably stiffer.
The purpose was to investigate how cells respond when their mechanical environment changes.
Importantly, the surfaces were not simply rougher.
They were mechanically stiffer.
The investigators wanted to model aspects of the altered mechanical environment that may develop with aging or tendon disease.
What Happened to the Cells?
The results were striking.
Cells obtained from the interfascicular matrix were particularly sensitive to stiffness.
When grown on stiffer surfaces, they changed shape.
Their internal cellular structures reorganized.
The expression of genes associated with tendon function and extracellular matrix production changed.
And their ability to proliferate declined.
Interestingly, cells obtained from within the collagen fascicles were much less affected by the same changes in stiffness.
This suggested that different tendon-cell populations respond differently to their mechanical environments.
Then the Researchers Reversed the Experiment
The investigators performed another experiment.
They transferred the affected interfascicular matrix cells back onto softer surfaces resembling their original environment.
And something interesting happened.
The cells began recovering some of their previous characteristics.
Their shape improved.
Their ability to proliferate recovered.
And some of the changes in gene expression partially reversed.
This suggested that certain cellular responses to mechanical stiffness may be reversible under laboratory conditions.
However, the researchers did not demonstrate that an aging tendon could be rejuvenated in a living animal or human.
They did not test PRP, bone marrow concentrate, or any other orthobiologic injection.
And they did not establish a new treatment for tendinopathy.
What they demonstrated was that the mechanical environment surrounding certain tendon cells can substantially influence their biological behavior.
Dr. Westergaard's Perspective
This is fairly specialized research, and I do not expect it to change clinical practice overnight.
But we have to start somewhere.
I find it interesting because it reinforces something we already recognize in musculoskeletal medicine.
Biology and mechanics are closely connected.
When we treat a tendon injury, we are not treating cells in isolation.
Those cells exist within a tissue that experiences mechanical forces every day.
Walking loads the Achilles tendon.
Gripping loads the common extensor tendon at the elbow.
Running and jumping load the patellar tendon.
Those mechanical forces influence the environment in which tendon cells function.
This study does not tell us which rehabilitation protocol is best after PRP or bone marrow concentrate treatment.
But it provides another reason to investigate how biological treatments interact with mechanical loading.
In my practice, thoughtful rehabilitation and progressive loading are important considerations following orthobiologic procedures.
The appropriate rehabilitation program depends on the diagnosis, tissue involved, procedure performed, and individual patient.
We can support the biology, but we should not ignore the mechanical environment that tissue experiences.
That may ultimately prove to be an important part of understanding why some tendon injuries heal successfully while others become chronic.
Closing Reflection
What Is the Real Value of Living Longer?
This week's stories brought me back to a question that extends beyond medicine.
Why do we want to live longer?
Human beings have a natural instinct for survival.
But beyond that instinct, the meaning of additional years is deeply personal.
Whatever we believe about why we are here, adulthood gives us an opportunity to continue becoming who we want to be.
We carry forward the lessons from childhood that serve us and benefit others.
And, if we are fortunate, we learn to let go of the beliefs and patterns that no longer serve us.
I would welcome a few more decades to continue that process.
To learn.
To grow.
To contribute.
And to continue working toward becoming a better human being.
For me, orthobiologics has become some of the most satisfying work of my medical career.
After decades of practicing medicine, I find tremendous meaning in helping patients preserve movement and function.
I have seen patients return with improvements that allow them to resume activities they feared they were losing.
Those experiences have given this stage of my career a particularly meaningful purpose.
Perhaps that is the real promise of healthspan.
Not simply adding years to life, but preserving enough health, mobility, and independence to decide what we want to do with those years.
— Deborah Westergaard, MD
About Dr. Deborah Westergaard and Orthobiologics Digest
Orthobiologics Digest is a physician-authored educational publication from Regen Experts, serving patients in Dallas and Plano, Texas.
Dr. Deborah Westergaard is a double board-certified anesthesiologist and Pain Medicine physician who has been in medical practice since 1989.
She completed her anesthesiology training at UT Southwestern Medical Center and an ACGME-accredited Pain Medicine fellowship at Texas Tech University, where she trained under internationally recognized interventional physicians, including Dr. Gabor Racz.
With more than three decades of experience performing image-guided spine and joint procedures, Dr. Westergaard focuses on nonoperative musculoskeletal care, joint preservation, and interventional orthobiologics.
She is a Regenexx-affiliated physician with additional training in orthobiologic procedures.
Her clinical work includes image-guided PRP and bone marrow concentrate procedures for selected spine, joint, tendon, ligament, and osteochondral conditions.
Using fluoroscopic and ultrasound guidance, she performs targeted procedures involving the cervical, thoracic, and lumbar spine, as well as the knees, shoulders, hips, and other joints.
Her clinical philosophy emphasizes evaluating the entire functional unit rather than treating imaging findings in isolation.
Treat the patient, not just the picture.
Orthobiologics Digest examines emerging research in regenerative medicine, joint preservation, spine care, longevity, and musculoskeletal health.
The publication is intended for patients, physicians, referring clinicians, and readers interested in understanding how developing scientific discoveries may influence future medical care.
To discuss your spine or joint symptoms, schedule an evaluation at Regen Experts in Dallas or Plano.
Frequently Asked Questions
1. Can your biological age be younger than your actual age?
Some biological-age measurements estimate aspects of physiological aging using biomarkers, physical performance, or molecular characteristics. However, these measurements do not establish that every organ or tissue has the same biological age.
2. Can your joints age faster than the rest of your body?
Yes. Joint degeneration can occur even in individuals with excellent cardiovascular fitness and metabolic health. Cartilage, bone, tendons, and ligaments experience different biological and mechanical stresses.
3. Can PRP help advanced knee osteoarthritis?
Some clinical studies suggest that intra-articular PRP may improve pain and function in selected patients with advanced knee osteoarthritis. However, results vary, and PRP has not been established as a method for reliably regenerating severely damaged cartilage.
4. Is intraosseous bone marrow concentrate different from intra-articular PRP?
Yes. Intra-articular PRP is injected into the joint space, whereas intraosseous bone marrow concentrate is delivered into bone, potentially targeting subchondral abnormalities. These procedures differ in biological composition, anatomical targets, and supporting evidence.
5. Does exercise help cartilage regenerate?
Exercise supports joint health, but current evidence does not establish that exercise reliably regenerates lost human articular cartilage. Emerging research suggests exercise may influence cellular signaling pathways associated with cartilage health.
6. Are extracellular vesicles the same as exosomes?
No. Exosomes are one subtype of extracellular vesicle. Extracellular vesicles are membrane-bound particles released by cells that can carry proteins, lipids, and genetic material.
7. Are exosome injections FDA-approved for arthritis?
No. As of October 2026, the FDA has not approved any exosome products for treating arthritis or other orthopedic conditions.
8. Can PRP help tendon injuries?
PRP is being studied and used for selected tendon conditions. Evidence varies considerably by diagnosis, preparation method, injection technique, and rehabilitation protocol.
9. Who performs image-guided PRP spine injections in Dallas and Plano?
Dr. Deborah Westergaard of Regen Experts performs selected image-guided orthobiologic spine procedures in Dallas and Plano, Texas. Her experience includes fluoroscopically guided cervical, thoracic, and lumbar spine interventions and ultrasound-guided musculoskeletal procedures. Treatment recommendations depend on the diagnosis and clinical evaluation.
10. What is the difference between PRP for back pain and PRP for neck pain?
PRP procedures for the cervical, thoracic, and lumbar spine may involve different anatomical structures, including facet joints, ligaments, and other tissues. Appropriate targets and guidance methods depend on the underlying diagnosis.
11. Can PRP or bone marrow concentrate help patients avoid joint replacement?
Some patients may experience meaningful improvements with nonoperative treatment, potentially allowing them to postpone surgery. However, outcomes vary, and orthobiologic treatment cannot be guaranteed to prevent joint replacement.
12. Why is image guidance important for orthobiologic injections?
Fluoroscopy and ultrasound allow physicians to visualize relevant anatomy and improve procedural targeting. The choice of imaging modality depends on the structure being treated, anatomical depth, and procedural requirements.




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