The Scientific Evidence Behind Inflammation-First Knee Arthritis Care

Posted by stemcelladmin on with 0 Comment
Share
  1. Scientific Basis of Inflammation-First Knee Arthritis Care

This page summarises the scientific evidence supporting an inflammation-first approach to knee osteoarthritis, as presented in the Inflammation Pillar Video. Each section corresponds directly to a key statement from the script, supported by peer-reviewed research.

1. Knee Arthritis Is Not Just Wear and Tear

Scientific Proof

Osteoarthritis is now recognised as a whole-joint inflammatory disease involving the synovium, cartilage, subchondral bone, ligaments, and infrapatellar fat pad.

Key References

  • Robinson WH et al., Nature Reviews Rheumatology – Osteoarthritis as an inflammatory disease
  • Berenbaum F, Osteoarthritis and Cartilage – Low-grade chronic inflammation in OA progression

Consensus

Mechanical damage alone does not explain pain severity or disease progression.

2. Inflammation Inside the Joint Drives Pain, Stiffness, and Progression

Scientific Proof

  • Synovitis strongly correlates with pain severity
  • Associated with effusion and stiffness
  • Predicts faster cartilage loss

Key References

  • Hill CL et al., Annals of the Rheumatic Diseases
  • Felson DT et al., Arthritis & Rheumatology

Consensus

Pain tracks inflammatory activity, not X-ray grade.

3. Two Patients With the Same X-Ray Can Have Very Different Pain

Scientific Proof

Radiographic severity correlates poorly with clinical symptoms.

Key References

  • Bedson J, Croft PR, Rheumatology
  • Hannan MT et al., Arthritis & Rheumatism

Consensus

Imaging underestimates biological disease activity.

4. Exercise Improves Support, Not Inflammation

Scientific Proof

  • Improves muscle strength and neuromuscular control
  • Does not suppress synovial cytokines when inflammation is active

Key References

  • Henriksen M et al., Osteoarthritis and Cartilage
  • Baker KR et al., Arthritis Care & Research

Consensus

Exercise is necessary but biologically insufficient when inflammation is uncontrolled.

5. Why Patients Plateau Despite Good Physiotherapy

Scientific Proof

  • Active synovitis predicts poor rehabilitation response
  • Associated with pain flares after loading
  • Reduces tolerance to strengthening

Key References

  • Scanzello CR et al., Clinical Orthopaedics and Related Research
  • Schaible HG, Nature Reviews Rheumatology

Consensus

Plateaus are biological, not motivational failures.

6. Painkillers Suppress Symptoms, Not Disease Biology

Scientific Proof

  • NSAIDs reduce pain temporarily
  • Do not halt cartilage degeneration
  • Do not modify disease progression

Key References

  • Zhang W et al., OARSI Guidelines
  • Hochberg MC et al., Arthritis Care & Research

Consensus

Symptom relief does not equal disease control.

7. Sequence Matters: Calm Inflammation Before Strengthening

Scientific Proof

  • Reducing inflammatory load improves pain thresholds
  • Improves exercise tolerance
  • Enhances functional outcomes

Key References

  • Atukorala I et al., Arthritis Research & Therapy
  • Bennell KL et al., British Journal of Sports Medicine

Consensus

Biological readiness determines rehabilitation success.

8. Joint Preservation Focuses on Biology, Not Just Mechanics

Scientific Proof

Modern OA management emphasises early biological modulation, load management, and individualised treatment sequencing.

Key References

  • Loeser RF et al., Osteoarthritis and Cartilage
  • Hunter DJ, The Lancet

Consensus

Joint preservation is proactive, not passive.

9. Inflammation Is Treatable

Scientific Proof

  • Inflammation in OA is measurable
  • Inflammation is modifiable
  • Inflammation is clinically meaningful

Key References

  • Mathiessen A, Conaghan PG, Arthritis Research & Therapy
  • Scanzello CR, Goldring SR, Arthritis & Rheumatology

Consensus

Osteoarthritis inflammation is manageable, not inevitable.

See the video here -https://youtu.be/IJFPdKUwpc0?si=5lN4781-zEmo3Xk0

FAQ’s

Q: Is knee osteoarthritis only caused by wear and tear?

A: No. Current research shows osteoarthritis is a whole-joint inflammatory disease. Mechanical wear alone does not explain pain severity or progression.

Q: Why does knee pain not match X-ray findings?

A: Pain correlates more strongly with synovial inflammation than with radiographic cartilage loss. X-rays underestimate biological disease activity.

Q: Does exercise reduce inflammation in knee arthritis?

A: Exercise improves strength and support but does not reliably suppress active synovial inflammation when it is present.

Q: Why do some patients plateau despite physiotherapy?

A: Active inflammation sensitises pain pathways and limits tolerance to loading, leading to biological—not motivational—plateaus.

Q: Are painkillers disease-modifying in knee arthritis?

A: No. NSAIDs reduce symptoms temporarily but do not alter the underlying disease process or progression.

Share

PRASAD Treatment for Knee Osteoarthritis: What It Is, Who It Helps, and How It Works

Posted by stemcelladmin on with 0 Comment
Share
  1. PRASAD Treatment for Knee Osteoarthritis: What It Is, Who It Helps, and How It Works

Most people believe knee osteoarthritis is simply a problem of worn-out cartilage. Modern research, however, shows that osteoarthritis is driven by chronic inflammation, metabolic imbalance, and altered cartilage cell behaviour.

The PRASAD Treatment was developed to address these deeper mechanisms. Rather than offering temporary pain relief, it aims to reset the joint’s biological environment so that function improves and disease progression slows.

Why Osteoarthritis Needs More Than Symptom Control

Osteoarthritis is now understood as a whole-joint disease involving cartilage, synovium, bone, muscles, and inflammatory signalling molecules. Persistent inflammation keeps the joint in a breakdown-dominant state, even when X-rays appear only mildly abnormal.

This explains why pain severity often does not correlate with imaging findings—and why isolated injections or painkillers rarely provide durable improvement.

What Is the PRASAD Treatment?

PRASAD is a structured regenerative protocol designed to:

  • Reset chronic joint inflammation
  • Improve cartilage and synovial metabolism
  • Enhance the joint’s internal repair environment
  • Restore strength-based load tolerance
  • Delay or avoid knee replacement in selected patients

Unlike single-shot therapies, PRASAD is a phased protocol tailored to the patient’s inflammatory status, metabolic profile, and stage of osteoarthritis.

The Biological Rationale Behind PRASAD

Inflammation Reset

Stressed cartilage cells release danger signals known as alarmins. These molecules perpetuate inflammation and accelerate tissue breakdown. PRASAD targets this inflammatory loop to calm the joint before regenerative stimulation is applied.

Metabolic Rebalancing

In osteoarthritis, cartilage cells shift toward a catabolic (breakdown-driven) state. PRASAD incorporates metabolic correction and biologic modulation to push the joint environment back toward repair and stability.

Targeted Regenerative Support

Depending on patient selection, PRASAD may integrate platelet-based or cell-supported biologics, always within a controlled protocol rather than as stand-alone injections.

How PRASAD Differs From Standard Knee Injections

Common Treatment Primary Action PRASAD Difference
Steroid injections Short-term inflammation suppression PRASAD avoids cartilage-weakening effects of repeated steroids
PRP Growth factor delivery Used only after inflammation is biologically controlled
Hyaluronic acid Lubrication PRASAD focuses on biological reset, not temporary viscosity

Who Is an Ideal Candidate?

PRASAD is most effective for patients with:

  • Early to moderate knee osteoarthritis
  • Inflammatory flares with activity-related pain
  • Stiffness that improves with movement
  • Metabolic risk factors such as weight gain or insulin resistance
  • A desire to delay or avoid knee replacement

Expected Outcomes

Patients commonly experience improvements in pain, swelling frequency, walking endurance, stair climbing, and confidence in knee function. Results are gradual but more durable because the underlying joint environment is altered.

Safety Considerations

PRASAD primarily uses autologous biologics combined with structured rehabilitation and metabolic correction. This results in a favourable safety profile when proper screening is followed.

Why PRASAD Represents the Future of Osteoarthritis Care

Modern osteoarthritis management is moving toward early biologic intervention, inflammation control, metabolic optimisation, and strength-based joint loading. PRASAD aligns with this evidence-driven direction.

For a simpler, patient-focused explanation of the PRASAD approach, read the detailed overview on drakvenkat.com.

Consultation

If you are exploring non-surgical regenerative options for knee arthritis, a personalised evaluation can determine whether the PRASAD protocol is appropriate for you.

Share