Can You Regrow Cartilage?

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Cartilage damage has long been viewed as a permanent condition, often leading to chronic pain and long-term disability. Conventional medical understanding was that the vital cushioning tissue permanently deteriorated with age, athletic trauma, or arthritis. 

However, a recent breakthrough from a Stanford Medicine-led study may offer a non-surgical solution for knee injuries and the prevention of arthritis by discovering how to block a key protein linked to ageing, raising the question: Can you regrow cartilage?

Scientists Successful in Cartilage Regeneration Treatment

Researchers at Stanford Medicine identified a single protein that acts as a master regulator of cartilage aging. The study focuses on a single injection blocking an aging-related protein called 15-hydroxy prostaglandin dehydrogenase (15-PGDH). This reversed the natural age-related deterioration of knee cartilage in older mice and prevented the onset of arthritis after knee joint injuries mimicking ACL tears.

What Is 15-PGDH?

  • Accumulates in cartilage as we age
  • Blocks regenerating adult tissue from repair
  • Scientists call it a “gerozyme” because it increases with aging
  • Interferes with molecules responsible for tissue repair and inflammation reduction

Why Current Surgeries Fall Short

Traditional surgical interventions like microfracture surgery create tiny fractures in the underlying bone to stimulate new tissue growth. The problem:

  • Produces non-high-quality fibrocartilage, similar to scar tissue
  • Lacks hyaline cartilage formation, which is needed for proper joint function
  • Lacks bounce and elasticity of natural cartilage
  • Degrades relatively quickly

Damaged Cartilage and the Growing Joint Health Concern

Osteoarthritis affects over 54 million people living with joint pain, stiffness, and reduced mobility. The economic burden of direct health care costs in the United States alone has reached approximately $303 billion annually. 

Yet despite this financial impact, no drug has ever been able to slow down or reverse the disease itself, and treatment options have remained frustratingly limited to pain management and surgical joint replacement.

The Three Types of Cartilage

The fundamental problem lies in cartilage’s unique biology. The human body contains three main types of cartilage, complicating how to treat the disease:

  • Elastic Cartilage: Soft and flexible, forming structures like the outer ear
  • Fibrocartilage: Dense and tough, making it absorbable to shock in areas like the spaces between the spinal vertebrae
  • Hyaline Cartilage/ also called Articular Cartilage: Smooth and glossy, allowing the hips, shoulders, ankles, and knee joints to move with low friction

Hyaline cartilage is the most commonly damaged and cannot regenerate naturally because it lacks blood vessels and stem cells. Developing osteoarthritis is a typical result of this.

While scientists have identified stem or progenitor cells capable of forming cartilage in bone, they haven’t successfully found similar cells within articular cartilage itself.

Understanding How Cartilage Deteriorates

Articular cartilage is composed primarily of collagen II and proteoglycans, which create a resilient, shock-absorbing cushion that allows bones to glide smoothly during movement. As we age or after sustaining an injury, chondrocytes begin functioning abnormally, resulting in:

  • The release of pro-inflammatory molecules
  • Breaking down collagen instead of maintaining it
  • Cartilage thinning and softening as collagen degrades
  • Inflammation leading to joint swelling and pain
  • A continuous cycle of more inflammation and more cartilage damage

Revolutionary Results in Regenerative Medicine Without Stem Cells or Orthopaedic Surgery

What makes this latest discovery remarkable is that blocking 15-PGDH triggers cartilage regeneration without involving stem or progenitor cells.

How the Treatment Works to Regrow Cartilage

The treatment reprograms already existing cells in the joint, specifically chondrocytes that make and maintain cartilage. It transforms them from an unhealthy, inflammatory state back into functional, cartilage-producing cells.

In studies with aged mice, researchers injected a small-molecule drug that blocks 15-PGDH activity directly into knee joints. The results included:

  • Cartilage that had thinned with age thickened across the entire joint surface
  • Prevention of osteoarthritis, a degenerative joint disease, after knee injuries similar to ACL tears
  • Reduction in the risk of arthritis, while previously 50% of patients developed arthritis within 10-20 years after an ACL injury

Dr. Nidhi Bhutani, associate professor of orthopaedic surgery and senior author of the study, explained: “Millions of people suffer from joint pain and swelling as they age… Until now, there has been no drug that directly treats the cause of cartilage loss. But this inhibitor causes dramatic regeneration of cartilage beyond what has been reported with any other intervention.”

Promising Results in Human Joint Cartilage Damage, Knee Cartilage Damage, and Aging Cartilage

The research team tested the treatment on human cartilage tissue removed from patients undergoing total knee replacement surgeries. After just one week of treatment with the 15-PGDH inhibitor, the human tissue showed:

  • Lower levels of cartilage degradation genes
  • Reduced inflammation markers
  • Beginning regeneration of articular cartilage

Treatment in mice demonstrated improved mobility with clear signs of reduced pain, as well as:

  • The capability to put more weight on previously injured legs
  • Maintained a steadier gait
  • Showed functional improvement, not just tissue regrowth

Continuing to Move Forward in Clinical Trials

A 15-PGDH inhibitor is already in human clinical trials. Phase 1 studies testing the drug for age-related muscle weakness have proven it’s safe and active in healthy volunteers.

Dr. Helen Blau, professor of microbiology and immunology at Stanford and leader of the Baxter Laboratory for Stem Cell Biology, expressed optimism, stating, “Phase 1 clinical trials of a 15-PGDH inhibitor for muscle weakness have shown that it is safe and active in healthy volunteers… We are very excited about this potential breakthrough. Imagine regrowing existing cartilage and avoiding joint replacement.” The research suggests two possible application methods, such as:

  • Oral medication: Patients could take a pill
  • Local injection: Direct injection into affected joints

Proactive Prevention Over Replacement

The Stanford researchers envision a “Jiffy Lube model” of cartilage replenishment, incorporating periodic treatments that boost articular cartilage before problems arise. This approach could potentially:

  • Prevent arthritis rather than treating it after it becomes debilitating
  • Benefit athletes who’ve experienced joint injuries
  • Help individuals with family histories of arthritis
  • Offer proactive rather than reactive care

This preventive approach will benefit individuals with a high risk of developing osteoarthritis, including those who may sustain work injuries through repetitive movement.

How Car Accident Cases and Workers’ Compensation Cases Will Be Impacted

This breakthrough has profound implications for two populations particularly vulnerable to cartilage damage.

Car Accident Injuries and Post-Traumatic Arthritis

Car accident injuries often result in meniscus tears, ligament damage, and cartilage fractures. Post-traumatic osteoarthritis develops in about 12% of these injuries. Additionally, victims of knee, hip, or shoulder car accident injuries face up to a 50% risk of developing arthritis in the future. 

Car accident victims often undergo surgery for joint injuries, leading to years of progressive cartilage loss and eventual joint replacement. The 15-PGDH inhibitor could immediately interrupt this by preventing inflammation and cartilage breakdown, ultimately stopping the progression of chronic arthritis and replacing the need for cartilage repair.

Workers’ Compensation and Repetitive Strain Injuries

Physically demanding jobs like construction work, warehousing, and healthcare frequently cause joint damage from repetitive strain injuries. This gradually wears away cartilage, leading to early-onset osteoarthritis development and often forcing workers into premature disability or career shifts. 

Workers’ compensation currently spends vast resources on arthritis treatment, including pain medication, physical therapy, and joint replacement surgeries. Cartilage regeneration before irreversible damage could significantly reduce pain and suffering and healthcare costs.

Early 15-PGDH inhibitor treatment for cartilage thinning could allow workers, such as warehouse workers with knee pain from lifting and kneeling, or construction workers with shoulder issues from overhead work, to stay productive rather than go on disability.

Next Steps for the Road Ahead

While further trials and regulatory approval are needed, the treatment shows significant clinical promise. Its strong safety profile from muscle weakness trials and compelling results in animal and human tissue suggest efficacy will translate to living patients.

For the millions suffering from injured joints—whether from aging, sports injuries, car accidents, or workplace wear and tear—the Stanford Medicine research represents genuine hope not just for treating arthritis or joint cartilage degeneration, but preventing the need for it.

Help From an Experienced Personal Injury Attorney

If you’ve suffered a car accident injury or workplace injury, resulting in chronic joint pain or requiring cartilage repair, our personal injury law firm can help. Backed by a dedicated legal team of award-winning abogados de accidentes automovilísticos y workers’ compensation attorneys, we specialize in helping clients overcome their injuries and any financial strain resulting from the incident. 

Contacto Abogado Jeff, abogado de accidentes automovilísticos a Programe una consulta gratuita. We can explore your legal options regarding your car accident case or workers’ compensation case. After an accident, Jeff te tiene

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