Orthobiologics Digest™ No. 7: Can PRP Delay Knee Replacement?
Updated: Oct 22
By Deborah Westergaard, MD
Board-Certified Anesthesiologist and Pain Medicine Physician
Medical Director, Regen Experts | Dallas & Plano, Texas
Orthobiologics Digest™
This is my periodic look at research, medicine, technology, and the stories that may change how we think about joint preservation, spine care, aging, and regenerative medicine.
In This Issue:
Can PRP really delay knee replacement? What happens when living human neurons become part of a computer? Is fatty replacement of the multifidus more biologically important than we thought? And if a herniated disc can shrink naturally, when does it make sense to vaporize part of it?
Before we alter biology, are we certain we understand what the biology is already trying to do?
1. Can PRP Delay Knee Replacement? What the Research Actually Shows
A new report suggests PRP may help patients with advanced knee osteoarthritis postpone knee replacement. But when the underlying study followed patients for only six months, how much can we really conclude about delaying surgery?
What Caught My Attention
A recent physician commentary distributed through EIN Presswire carried an intriguing headline: “Trial Suggests PRP May Delay Knee Replacement for Patients Already on the Surgical List.”
I followed that headline back to the actual randomized controlled trial, published June 2, 2026, in the Journal of Orthopaedic Surgery and Research.
The study included 90 patients between 40 and 80 years old with Kellgren-Lawrence grade 3 or 4 knee osteoarthritis who were already on knee-replacement waiting lists. They were randomized to two intra-articular PRP injections one week apart, a corticosteroid injection, or oral aceclofenac.
At three and six months, the PRP group had significantly better pain and WOMAC outcomes than the comparison groups. The investigators also reported changes in several inflammatory and cartilage-turnover biomarkers. The authors concluded that PRP could serve as a bridge therapy before arthroplasty.
That is encouraging.
But six months is a very short period when the question is whether a treatment can meaningfully delay a knee replacement.
Dr. Westergaard's Take
I think this is an interesting study, particularly because these were not patients with very early arthritis. They had advanced osteoarthritis and were already on surgical waiting lists.
If PRP allows an appropriate patient to function better and postpone knee replacement—even if the benefit is measured in months or perhaps a year—that can still have value.
But that is different from proving that PRP prevents knee replacement.
It also raises a larger issue in orthobiologic research: PRP is not one uniform treatment.
Platelet concentration, leukocyte concentration, preparation technique, number of injections, and the structures being treated can all differ.
And placement matters.
If the problem involves more than the joint space—perhaps a degenerative meniscus, lax or injured ligament, tendon pathology, or subchondral bone disease—simply injecting PRP into the joint may not address the entire problem.
So I think the better question is not:
“Does PRP work?”
It is:
What is wrong with this particular knee, what structures are contributing to the problem, what is the patient’s goal, and which biologic treatment and which anatomical targets make sense?
What Happens When We Look 10 to 20 Years Out?
This is where another body of research becomes particularly interesting.
Philippe Hernigou and colleagues studied 140 patients who were candidates for bilateral knee replacement. One knee underwent total knee arthroplasty (total knee replacement) while the opposite knee received bone marrow concentrate into subchondral bone lesions.
At an average follow-up of 15 years, only 25 of the 140 BMC-treated knees—about 18%—had eventually undergone knee replacement. The average time to replacement among those that eventually required it was about ten years.
That does not mean every patient with advanced knee arthritis can avoid replacement for 15 years. It does tell us that long-term joint-preservation research deserves serious attention.
Location May Matter
An additional Hernigou study may be even more provocative.
Sixty patients with bilateral knee osteoarthritis received the same bone marrow concentrate. In each patient, one knee received the concentrate intra-articularly while the other knee received it in the subchondral bone of the femur and tibia.
At an average of 15 years, 12 of 60 subchondral-treated knees had undergone knee replacement, compared with 42 of 60 knees treated intra-articularly.
Where we put an orthobiologic may be just as important as what is in the syringe.
These studies are not head-to-head trials of PRP versus bone marrow concentrate, so we cannot use them to claim that BMC is universally superior to PRP.
PRP may be entirely appropriate for someone seeking a less invasive treatment or a smaller initial financial commitment, particularly when the immediate goal is symptom improvement or buying time.
But when I evaluate an arthritic knee, I am looking beyond the cartilage surface. I am looking at the entire osteochondral unit, including the subchondral bone, menisci, ligaments, and tendons.
The new PRP trial is encouraging. But perhaps its most valuable contribution isn’t proving that PRP can prevent knee replacement. It doesn’t.
It reminds us that even in patients with advanced knee osteoarthritis who have already been told they are candidates for replacement, the conversation may not necessarily be over.
2. What If the Next Computer Is Alive?
This story is a little outside traditional orthobiologics. But it is fundamentally about biology, adaptation, and the extraordinary things living human cells may be capable of doing.
And I couldn’t stop reading about it.
In August, a biological data-center prototype began operating in Singapore through a collaboration involving NUS Medicine, DayOne, and Australia’s Cortical Labs.
It contains 20 CL1 biological computing units incorporating living human neurons derived from stem cells.
But the story actually goes back further.
Researchers at Cortical Labs previously created a system called DishBrain, integrating human and rodent neurons with a high-density multielectrode array and a simplified version of the computer game Pong.
The neurons did not watch a computer screen or understand Pong the way a person does.
Electrical information was delivered to the neuronal cultures through electrodes. Their electrical activity was recorded, feedback was returned, and the cultures demonstrated adaptive changes in activity. The researchers called the phenomenon synthetic biological intelligence.
Meanwhile, Switzerland’s FinalSpark has developed a remotely accessible Neuroplatform using three-dimensional human neural organoids on electrodes.
Its published system continuously records electrical activity, provides electrical stimulation, and uses microfluidics to maintain the cultures. The investigators reported that their best-performing organoids could remain active for around 100 days.
So What Is Actually Happening?
The simplest explanation is this:
Computer → living neurons → computer.
A conventional computer processes information by changing electrical states through silicon transistors.
An artificial neural network changes mathematical values—weights—in software.
A biological neural network is different.
These are actual living cells.
Neurons receive electrical information, generate action potentials, and communicate through networks of synapses. With learning and adaptation, the strength and architecture of those connections can change.
That is neuroplasticity.
Put very simply:
A conventional computer learns by changing numbers in software. A living neural network can learn by physically changing itself.
Dr. Westergaard's Take
First, I find this fascinating.
Then I find it a little creepy.
We are keeping human neurons alive, giving them information, recording their responses, sending feedback, and watching them adapt.
None of this proves that these neuronal cultures are conscious. It certainly does not mean that a dish of neurons understands that it is playing Pong.
But I keep returning to an uncomfortable question.
As these systems become larger, more complex, and capable of increasingly sophisticated adaptation, could we someday reach a point where we owe something to the living part of the machine?
I don’t know.
And I think that honesty is important.
For now, these are experimental neuronal cultures, not little conscious brains trapped inside computers.
But medicine and technology have a long history of creating capabilities before society has fully decided what those capabilities mean.
For now, the computer is alive in the biological sense. Whether it could ever become alive in the experiential sense may be one of the most important questions this technology eventually forces us to answer.
3. When Back Muscle Turns to Fat, It May Be More Than an MRI Finding
When most people look at a lumbar MRI, they expect to hear about discs, arthritis, spinal stenosis, bone spurs, or a pinched nerve.
But there is another structure on those images that I pay very close attention to:
the multifidus muscle.
The multifidus is one of the deep muscles running along the spine. It helps control movement and provides segment-by-segment stabilization of the vertebrae.
And sometimes on an MRI, healthy multifidus muscle has begun to disappear.
In its place is fat.
A fascinating study published October 4 in Advanced Science examined fatty-infiltrated paraspinal muscle at the cellular level.
The researchers found that intramuscular fat, rather than simply fat surrounding the muscle, was independently associated with trunk muscle strength. People with greater intramuscular fat had lower paraspinal muscle mass and strength.
But then they went deeper.
Muscle contains satellite cells. Think of them as part of the muscle’s resident repair crew. When muscle needs to repair or regenerate, these cells can become activated and participate in forming new muscle.
Muscle also contains fibro-adipogenic progenitors, or FAPs, which participate in the environment surrounding muscle repair.
Using single-nucleus RNA sequencing, the investigators identified substantial changes in the cellular environment of fatty-infiltrated paraspinal muscle. They identified signaling involving ANGPTL4 and SDC2 that appeared to impair myogenesis, and inhibiting SDC2 in laboratory experiments partially rescued that impairment. They also identified a FAP population with enhanced fat-forming characteristics.
So this may not simply be fat filling an empty space where muscle used to be.
The biological environment inside the muscle itself may be changing in ways that make regeneration more difficult.
That is what makes this paper so interesting.
Dr. Westergaard's Take
When I see significant fatty infiltration or atrophy of the multifidus on a lumbar MRI, I don’t consider it incidental.
It makes me concerned about the health and function of that muscle and whether normal neural input and neuromuscular function may have been compromised.
I see it frequently.
Interestingly, multifidus atrophy and fatty infiltration are not always emphasized in the radiology reports I review. That may partly reflect what conventional spine imaging is being asked to evaluate: disc herniation, stenosis, spondylolisthesis, nerve compression, and other structural findings that may influence surgical or interventional decisions.
That is one reason I want to see the actual MRI images rather than relying exclusively on the written report.
I want to see the whole system.
And age isn’t the whole story.
The multifidus isn’t simply a muscle sitting beside the spine. It is an important component of the spine’s active stabilization system.
I think about the lumbar spine as a functional spinal unit rather than as a collection of isolated discs and joints.
The vertebral bodies, discs, facet joints, multifidus muscles, supraspinous and interspinous ligaments, ligamentum flavum, and longitudinal ligaments all have roles in controlling movement and maintaining stability.
Think of the vertebrae almost as interconnected puzzle pieces.
When their normal relationships change, the geometry of the motion segment changes. Facet relationships can change. Neural foramina can become smaller. Depending on the anatomy, the spinal canal can narrow. Nerves may lose space.
So if we focus exclusively on a disc, facet joint, or compressed nerve while ignoring a severely dysfunctional stabilization system surrounding it, are we treating the whole problem?
And This Brings Me to Platelet-Poor Plasma
In 2017, Olga Miroshnychenko, Wen-Teh Chang, and Jason Dragoo published an intriguing laboratory study in the American Journal of Sports Medicine examining platelet-rich and platelet-poor plasma in human skeletal muscle cells.
PRP increased myoblast proliferation but did not produce evidence of differentiation. Platelet-poor plasma and platelet-depleted preparations, by contrast, induced myoblast differentiation and increased multinucleated myotube formation and myosin heavy-chain expression.
That study was not performed in the multifidus, and it does not prove that injecting platelet-poor plasma into an atrophied multifidus will reverse fatty infiltration.
But the biology matters to me.
When I treat multifidus muscle, my preference is platelet-poor plasma rather than a platelet-concentrated PRP product. Muscle is different from tendon, ligament, or joint tissue, and I don’t assume that the biologic preparation appropriate for one tissue is automatically appropriate for another.
There is laboratory evidence that PPP promotes skeletal-muscle myoblast differentiation, which is necessary for muscle regeneration, and that biology informs how I think about treating muscle.
Does that prove PPP reverses multifidus atrophy?
No.
We don’t have that evidence yet.
But it gives us a biologically plausible reason to study the approach.
And perhaps, as our understanding of spinal degeneration improves, we will stop thinking only about the most dramatic abnormality on an MRI and start thinking more seriously about the entire biological and mechanical system surrounding it.
Sometimes the most important finding is the muscle that’s quietly disappearing beside everything else.
4. If a Herniated Disc Can Shrink on Its Own, Should We Vaporize Part of It?
There is a minimally invasive treatment for lumbar disc herniation called percutaneous laser disc decompression, or PLDD.
A needle is placed into the intervertebral disc. A laser fiber is introduced through the needle, and laser energy vaporizes a small amount of material within the nucleus pulposus.
The objective is to reduce intradiscal pressure and potentially relieve symptoms associated with the herniation.
A 2026 systematic review and meta-analysis of PLDD sounds encouraging at first glance.
Fifteen publications representing 14 unique cohorts were included. Five studies involving 298 patients produced a pooled clinical success rate of 73.8%. Across eight cohorts involving 650 patients, the pooled reoperation rate was 10.3%, and the pooled complication rate across ten studies was 1.3%.
Those numbers caught my attention.
But then I started asking a different question.
How many of those patients would have improved anyway?
Lumbar disc herniations have a remarkable ability to regress naturally.
Published analyses have found that spontaneous regression is considerably more common with extruded and sequestrated discs than with contained protrusions. One widely cited analysis reported regression probabilities of approximately 52.5% for protrusions, 70.4% for extrusions, and 93% for sequestrations.
That creates an important interpretation problem.
Most studies in the PLDD meta-analysis were nonrandomized, single-arm studies, and there was substantial heterogeneity in several outcomes. The authors themselves called for better comparative research and better definition of long-term results and patient selection.
Without an appropriate comparison group, a fundamental question remains:
Did the procedure cause an improvement that would not otherwise have occurred?
Dr. Westergaard's Take
I am not saying PLDD doesn’t work.
Reducing intradiscal pressure may relieve symptoms in appropriately selected patients, and the published literature suggests that many patients improve.
My concern is different.
The nucleus pulposus is not scrap material.
It is part of a living intervertebral disc with important biological and mechanical functions. Its proteoglycan-rich matrix helps retain water, distribute loads, and maintain the mechanics of the motion segment.
PLDD intentionally vaporizes and thermally alters some of that tissue.
The amount treated is not expressed as one standardized percentage of the nucleus across every PLDD technique. Laser wavelengths, energy delivery, and procedural protocols vary.
So before intentionally altering nucleus pulposus in a disc that is already degenerating, I want answers to two questions:
How much benefit are we actually adding beyond the natural history of the herniation?
And:
What happens to that treated disc five, ten, or fifteen years later?
A 10% reoperation rate sounds impressive until we ask exactly what the denominator and follow-up mean.
Avoiding surgery for six or twelve months is not the same thing as disc preservation.
And spontaneous regression complicates the picture further.
If a substantial percentage of disc herniations—particularly extrusions and sequestrations—can become smaller without surgery, improvement after PLDD does not automatically prove that PLDD caused the improvement.
That doesn’t mean we dismiss the procedure.
It means we ask better questions.
For me, the endpoint isn’t simply whether someone’s leg pain is better six months later.
I want to know whether we relieved the patient’s symptoms while preserving as much normal biology and function of the spinal segment as reasonably possible.
That is a higher bar.
Until we have stronger comparative research and meaningful long-term follow-up, I think this is a question worth asking:
If the body may already be capable of shrinking a herniated disc on its own, when is intentionally vaporizing part of that disc actually necessary?
A Final Thought
Four very different stories.
One involves platelets and an arthritic knee. One involves living human neurons attached to computers. One looks at muscle quietly being replaced by fat. And one asks whether we should destroy a small amount of living disc tissue to treat a condition that may sometimes improve through the body’s own biology.
Yet I think they belong together.
Medicine has become extraordinarily good at identifying abnormalities and developing ways to intervene.
The harder question is sometimes knowing when intervention improves biology—and when biology deserves the opportunity to work first.
That doesn’t mean doing nothing.
It means understanding anatomy, physiology, natural history, and the goals of the individual patient before deciding what should be injected, stimulated, removed, burned, replaced—or preserved.
The future of regenerative medicine may depend as much on learning what not to destroy as on discovering what we can regenerate.
Frequently Asked Questions
Can PRP delay knee replacement?
Possibly, but current evidence does not establish that PRP prevents knee replacement. A 2026 randomized trial in patients with advanced knee osteoarthritis who were already on knee replacement waiting lists found better six-month outcomes with PRP than with corticosteroid injection or an NSAID. Longer-term research is needed to determine whether PRP can meaningfully delay knee replacement and for how long.
Can bone marrow concentrate help delay knee replacement?
Long-term studies of subchondral bone marrow concentrate in selected patients with knee osteoarthritis have reported substantial periods without knee replacement. In one long-term study, patients were followed for approximately 15 years. These studies are not direct comparisons between bone marrow concentrate and PRP, and their results should not be generalized to every patient with knee osteoarthritis.
Can orthobiologics help patients avoid knee replacement?
Orthobiologic treatments such as platelet-rich plasma (PRP) and bone marrow concentrate may be considered for selected patients when the goal is to improve function, address specific injured or degenerative tissues, and potentially postpone more invasive treatment. Whether an orthobiologic approach is appropriate depends on the diagnosis, severity of arthritis, condition of the cartilage and subchondral bone, other involved structures, overall health, and the patient's goals.
Can orthobiologics help patients avoid back surgery?
For some spine conditions, nonoperative treatment may be appropriate before surgery is considered. The decision depends on the cause of the symptoms, imaging findings, neurologic examination, spinal stability, and the patient's overall condition and goals. Progressive weakness, significant neurologic deficits, or certain structural problems may require prompt surgical evaluation. The goal is not to avoid necessary surgery, but to determine when tissue-preserving, nonoperative care is a reasonable option.
Can a herniated disc shrink without surgery?
Yes. Lumbar disc herniations can regress spontaneously, and research suggests that spontaneous regression is particularly common with extruded and sequestrated disc herniations. This natural history is important when evaluating procedures designed to remove, vaporize, or otherwise alter disc tissue. Whether observation or nonoperative treatment is appropriate depends on symptoms, neurologic findings, imaging, and the individual patient.
What does multifidus fatty infiltration mean on a lumbar MRI?
Multifidus fatty infiltration refers to fat accumulating within or replacing portions of the deep paraspinal muscle. The multifidus contributes to movement control and segmental stabilization of the spine. Research suggests that greater intramuscular fat may be associated with reduced paraspinal muscle mass and strength and with biological changes in the muscle's regenerative environment. It is one reason the muscles surrounding the spine may deserve attention along with discs, facet joints, nerves, and other structures on lumbar MRI.
What is biological computing with living human neurons?
Biological computing combines living neurons with electronic hardware so researchers can deliver electrical signals to neuronal networks, record their responses, and study how living cells adapt. Experimental systems have already connected human neurons with silicon-based computing technology. Terms such as biological computing, biocomputers, and synthetic biological intelligence are being used to describe this emerging field. Current research does not establish that these neuronal cultures are conscious or that they understand the tasks they perform.
Deborah Westergaard, MD
Board-Certified Anesthesiologist and Pain Medicine
Physician Medical Director, Regen Experts | Dallas & Plano, Texas
Orthobiologics Digest™ | Published by Regen Experts | Deborah Westergaard, MD | October 2026 | All rights reserved.
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