Major platelet growth factors (released from α-granules):
PDGF (AA, AB, BB) – Chemotaxis, fibroblast & smooth-muscle proliferation
TGF-β1 / TGF-β2 – Collagen synthesis, fibrosis control, immunomodulation
VEGF – Angiogenesis, endothelial cell proliferation
EGF – Epithelial regeneration, cell differentiation
IGF-1 – Cell growth, matrix synthesis, survival signaling
FGF (basic FGF) – Angiogenesis, fibroblast proliferation
HGF – Tissue regeneration, anti-fibrotic effects
PDGF (Platelet-Derived Growth Factor) = Primary driver of tenocyte chemotaxis, proliferation, collagen I synthesis
TGF-β (Transforming Growth Factor-β) = Extracellular matrix production, tendon remodeling (excess → fibrosis risk)
IGF-1 (Insulin-Like Growth Factor-1) = Tenocyte survival, anabolic collagen signaling
FGF-2 (Basic Fibroblast Growth Factor) = Fibroblast proliferation, early tendon healing
VEGF (Vascular Endothelial Growth Factor) = Neovascular support in hypovascular tendon
CTGF (Connective Tissue Growth Factor) = Late-phase matrix organization
HGF (Hepatocyte Growth Factor) = Anti-fibrotic modulation
EGF (Epidermal Growth Factor) = Minimal direct tendon impact
TGF-β = Chondrocyte differentiation, proteoglycan & collagen II synthesis
IGF-1 = Cartilage matrix production, chondrocyte survival
PDGF = Progenitor recruitment, early repair signaling
FGF-2 = Chondrocyte proliferation (dose-dependent effects)
CTGF = Cartilage–bone interface remodeling
HGF = Anti-inflammatory, protective signaling
VEGF = Limited role (excess may promote degeneration)
EGF = Minor relevance in mature cartilage
IGF-1 = Axonal growth, Schwann-cell survival, neuroprotection
HGF = Strong neurotrophic, anti-fibrotic regeneration effects
PDGF = Schwann-cell proliferation, nerve repair support
VEGF = Neurovascular coupling, perfusion-dependent regeneration
FGF-2 = Neuronal plasticity, glial proliferation
EGF = Supportive glial signaling
TGF-β = Scar modulation (excess inhibits regeneration)
CTGF = Often inhibitory via fibrosis
PDGF = Gold-standard wound healing signal; fibroblast migration
EGF = Keratinocyte proliferation, epithelialization
VEGF = Angiogenesis, granulation tissue formation
TGF-β = Matrix deposition, scar formation control
FGF-2 = Dermal fibroblast expansion
IGF-1 = Cellular survival, repair support
CTGF = Scar maturation
HGF = Anti-fibrotic modulation
Tendon & cartilage benefit most from PDGF + TGF-β + IGF-1
Nerve favors IGF-1 + HGF (often under-appreciated in PRP discussions)
Skin healing is PDGF-dominant, with EGF + VEGF synergy
Anatomic Areas of Injury:
Articular cartilage (knee, hip, shoulder, ankle joints)
Meniscus (knee)
Fibrocartilage structures
Chondral defects (full-thickness and partial-thickness)
Key Characteristics:
Cartilage is avascular tissue with limited healing capacity. Lacking the inflammatory response seen in other connective tissues, cartilage injuries frequently result in poor tissue repair with subsequent degeneration. Defects are often replaced by fibrocartilage rather than hyaline cartilage, which is mechanically inferior.
Growth Factors Involved in Healing:
Transforming Growth Factor-β (TGF-β)
Primary anabolic factor for cartilage repair
Stimulates chondrocyte differentiation and proteoglycan synthesis
Promotes collagen II production (the main structural protein in hyaline cartilage)
Can overrule interleukin-1 catabolic effects in diseased cartilage
Capable of enhancing cartilage repair in arthritic tissue
Temporal expression: Maximal at day 7 post-injury, lasting until day 14
Caution: Induces chondrophyte and osteophyte formation at joint margins, which may limit intra-articular application
Insulin-Like Growth Factor-1 (IGF-1)
Main cartilage anabolic factor under normal conditions
Stimulates cartilage matrix production and proteoglycan synthesis
Promotes chondrocyte survival and metabolic activity
Temporal expression: Maximal at day 7 post-injury
Limited contribution in diseased cartilage due to IGF-1 nonresponsiveness of arthritic chondrocytes
Shows great safety profile with minimal side effects
Insulin-Like Growth Factor-II (IGF-II)
Supports chondrocyte metabolic stimulation
Temporal expression: Maximal at day 7 post-injury
Works in autocrine/paracrine fashion to restore proteoglycan content
Fibroblast Growth Factor-2 (FGF-2)
Stimulates chondrocyte proliferation
Temporal expression: Maximal at day 7 post-injury
Dose-dependent effects on cartilage metabolism
Involved in early repair signaling
Bone Morphogenetic Protein-2 (BMP-2)
Enhances chondrocyte proteoglycan synthesis
Only capable of action in absence of interleukin-1
Cannot overcome catabolic effects in inflamed tissue
Induces chondrophyte formation at joint margins (similar to TGF-β)
Platelet-Derived Growth Factor (PDGF)
Supports progenitor cell recruitment
Contributes to early repair signaling
Less prominent role compared to TGF-β and IGF-1
Connective Tissue Growth Factor (CTGF)
Involved in cartilage-bone interface remodeling
Role in late-phase matrix organization
Vascular Endothelial Growth Factor (VEGF)
Limited and potentially detrimental role in cartilage
Excess may promote cartilage degeneration
Angiogenic effects may be counterproductive in avascular cartilage tissue
Anatomic Areas of Injury:
Medial collateral ligament (MCL) - knee
Anterior cruciate ligament (ACL) - knee
Posterior cruciate ligament (PCL) - knee
Lateral collateral ligament (LCL) - knee
Ankle ligaments (anterior talofibular, calcaneofibular, deltoid)
Periodontal ligament
Shoulder ligaments (glenohumeral, coracoclavicular)
Wrist and hand ligaments
Key Characteristics:
Ligament healing follows a classical healing response with site-dependent quality. Healing may be related to exposure to synovial fluid. Ligaments heal primarily by formation of granulation tissue and scarring, similar to tendons.
Growth Factors Involved in Healing:
Basic Fibroblast Growth Factor (bFGF/FGF-2)
Hastens healing and increases strength of ligaments after injury
Powerful stimulator of angiogenesis
Increases fibroblast proliferation in vitro
bFGF receptor proteins present and increase during early stages of MCL healing
Temporal expression: Peaks at days 3-7, remains elevated through day 14
Spatial distribution: Concentrated at wound edges and proliferating tissue
Epidermal Growth Factor (EGF)
Increases fibroblast proliferation in vitro
EGF receptor proteins present and increase during early healing stages
Temporal expression: Similar pattern to bFGF receptor
Potential for synchronized exogenous growth factor therapy with maximal receptor levels
Insulin-Like Growth Factor-I (IGF-I)
Active during early inflammatory phase
Aids fibroblast proliferation and migration
Increases collagen production
Similar mechanisms to tendon healing
Transforming Growth Factor-β (TGF-β)
Active during inflammation
Regulates cellular migration and proliferation
Modulates fibronectin binding interactions
Increases breaking energy of healing ligament
Platelet-Derived Growth Factor (PDGF)
Produced shortly after ligament damage
Stimulates production of other growth factors including IGF-I
Roles in tissue remodeling
Combined with IGF-I or FGF-2, stimulates periodontal ligament regeneration
Vascular Endothelial Growth Factor (VEGF)
Produced at highest levels after inflammatory phase
Powerful stimulator of angiogenesis
Supports vascular network formation in healing ligament
Anatomic Areas of Injury:
Skeletal muscle (all anatomic locations)
Musculotendinous junction injuries
Muscle contusions (blunt trauma)
Muscle strains and tears
Laceration injuries
Key Characteristics:
Muscle injury triggers inflammation followed by fiber regeneration and collagen synthesis. The inflammatory response involves neutrophils, ED1+ macrophages, and ED2+ macrophages. Satellite cells play an integral role by serving as a source of myoblasts for fiber regeneration. Simultaneous with fiber regeneration, types I and III collagen are expressed, which under certain circumstances can lead to scarring and fibrosis.
Growth Factors Involved in Healing:
Hepatocyte Growth Factor (HGF)
Primary activator of quiescent satellite cells
Released during muscle repair
Guides muscle regeneration process
Critical for initiating satellite cell proliferation
Fibroblast Growth Factors (FGFs)
Regulate satellite cell proliferation during myogenesis
Come from muscle, motor nerve, and inflammatory cells
Act as proliferative factors during in vitro myogenesis
Necessary for formation of new neuromuscular junctions
FGF-2 specifically promotes satellite cell activation and proliferation
Transforming Growth Factor-β (TGF-β)
Regulates satellite cell proliferation
Major influence on reorganization of extracellular matrix
Conditions collagen synthesis and scar formation
Can lead to fibrosis if dysregulated
Balances regeneration with matrix remodeling
Insulin-Like Growth Factors (IGF-I and IGF-II)
Promote satellite cell differentiation during myogenesis
Released during muscle repair
Guide muscle regeneration
IGF-I and IGF-II act predominantly as differentiation factors in vitro
Platelet-Derived Growth Factor (PDGF)
Regulates satellite cell proliferation during myogenesis
Acts as proliferative factor in vitro
Contributes to early inflammatory and repair phases
Leukemia Inhibitory Factor (LIF)
Acts predominantly as proliferative factor
Conditions the regeneration process
Supports satellite cell expansion
Tumor Necrosis Factor-α (TNF-α)
Released during muscle repair
Modulates inflammatory response
Exact functions in muscle remodeling remain under investigation
Neurotrophic Factors (HARP/PTN/HB-GAM)
Necessary for formation of new neuromuscular junctions
Critical for functional muscle regeneration
Support nerve-muscle interface restoration
Anatomic Areas of Injury:
Peripheral nerves (all anatomic locations)
Brachial plexus
Sciatic nerve
Median nerve
Ulnar nerve
Radial nerve
Peroneal nerve
Tibial nerve
Digital nerves
Facial nerve
Key Characteristics:
Peripheral nerve injuries pose significant clinical challenges with often incomplete functional recovery. Nerve regeneration is complex, requiring axonal growth, Schwann cell proliferation, myelin sheath regeneration, and angiogenesis. Growth factors promote nerve cell growth and survival, regulate the regenerative microenvironment, and stimulate plasticity changes post-injury.
Growth Factors Involved in Healing:
Nerve Growth Factor (NGF)
Successfully loaded onto nerve guidance conduits for peripheral nerve repair
Promotes nerve cell growth and survival
Stimulates axon regeneration
Regulates regenerative microenvironment
Brain-Derived Neurotrophic Factor (BDNF)
Successfully loaded onto nerve guidance conduits
Supports neuronal survival and differentiation
Promotes axonal growth
Enhances functional recovery
Neurotrophin-3 (NT-3)
Successfully loaded onto nerve guidance conduits
Supports specific neuronal populations
Promotes sensory and motor neuron survival
Glial Cell Line-Derived Neurotrophic Factor (GDNF)
Successfully loaded onto nerve guidance conduits
Strong neurotrophic effects
Supports motor neuron survival and regeneration
Insulin-Like Growth Factor-1 (IGF-1)
Contributes to neuron regeneration and pain alleviation
Successfully loaded onto nerve guidance conduits
Supports axonal growth and Schwann cell survival
Provides neuroprotective effects
Present in PRP formulations for nerve repair
Basic Fibroblast Growth Factor (bFGF)
Contributes to neuron regeneration and pain alleviation
Successfully loaded onto nerve guidance conduits
Supports neuronal plasticity and glial proliferation
Promotes angiogenesis to support nerve regeneration
Vascular Endothelial Growth Factor (VEGF)
Contributes to neuron regeneration
Successfully loaded onto nerve guidance conduits
Supports neurovascular coupling
Facilitates perfusion-dependent regeneration
Present in PRP formulations for nerve repair
Platelet-Derived Growth Factor (PDGF)
Supports Schwann cell proliferation
Aids nerve repair processes
Present in PRP formulations for nerve repair
Promotes cellular migration to injury site
Transforming Growth Factor-β (TGF-β)
Contributes to neuron regeneration
May modulate scar formation
Excess can inhibit regeneration through fibrosis
Present in PRP formulations for nerve repair
Balances repair with scar control
Hepatocyte Growth Factor (HGF)
Strong neurotrophic and anti-fibrotic regeneration effects
Reduces scar formation that can impede nerve regeneration
Supports functional recovery
Epidermal Growth Factor (EGF)
Provides supportive glial signaling
Contributes to Schwann cell function
Connective Tissue Growth Factor (CTGF)
Often inhibitory via fibrosis promotion
May impede nerve regeneration if overexpressed
Anatomic Areas of Injury:
Cutaneous wounds (all body surfaces)
Surgical incisions
Traumatic lacerations
Burn injuries
Pressure ulcers
Diabetic ulcers
Venous ulcers
Arterial ulcers
Key Characteristics:
Wound healing proceeds through four overlapping phases: hemostasis, inflammation, proliferation, and remodeling. Growth factors are released by platelets, inflammatory cells, fibroblasts, and keratinocytes to orchestrate cell migration, proliferation, differentiation, and extracellular matrix synthesis.
Growth Factors Involved in Healing:
Platelet-Derived Growth Factor (PDGF)
Gold-standard wound healing signal; FDA-approved for clinical use
Released by platelets upon injury (first growth factor at wound site)
Stimulates fibroblast and smooth muscle cell migration and proliferation
Promotes formation of granulation tissue
PDGF-BB specifically has well-defined safety profile
Currently used clinically: PDGF-BB approved for diabetic foot ulcers
Epidermal Growth Factor (EGF)
Promotes keratinocyte proliferation and epithelialization
Stimulates migration and proliferation of epithelial cells
Aids in re-epithelialization of wounds
Critical for restoring epidermal barrier
Vascular Endothelial Growth Factor (VEGF)
Promotes angiogenesis and granulation tissue formation
Facilitates formation of new blood vessels
Supplies oxygen and nutrients to healing tissue
Essential for transition from inflammation to proliferation
Transforming Growth Factor-β (TGF-β)
Regulates matrix deposition and scar formation control
Multiple isoforms (TGF-β1, TGF-β2, TGF-β3) with varying effects
Regulates inflammation, collagen deposition, and tissue remodeling
Modulates transition between healing phases
Dysregulation can lead to excessive scarring or fibrosis
Fibroblast Growth Factor (FGF)
Stimulates dermal fibroblast expansion
Promotes fibroblast proliferation and angiogenesis
Contributes to tissue regeneration
Basic FGF (bFGF) currently used clinically in some countries
Insulin-Like Growth Factor (IGF)
Supports cellular survival and repair
Enhances fibroblast function
Promotes matrix synthesis
Connective Tissue Growth Factor (CTGF)
Involved in scar maturation
Regulates late-phase matrix organization
Influences final wound strength and appearance
Hepatocyte Growth Factor (HGF)
Provides anti-fibrotic modulation
Helps prevent excessive scar formation
Balances matrix deposition
Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF
What is PRP?
PRP is a concentration of a patient’s own platelets prepared from blood and injected to support healing responses.
Is PRP FDA approved?
No. PRP is not FDA approved as a drug or biologic for pain, arthritis, or tissue regeneration.
What part is FDA regulated?
The PRP preparation devices (centrifuges/kits) are FDA 510(k) cleared to prepare PRP—not to treat disease.
Why do clinics say “FDA cleared”?
“FDA cleared” applies to the device, not the injection or medical claim.
Is PRP legal to use?
Yes. PRP is permitted under the practice of medicine, but it is considered off-label use.
Is PRP experimental?
PRP is investigational for many conditions; evidence varies by body part and diagnosis.
Does FDA allow PRP injections?
FDA allows use but does not approve treatment claims or standardized dosing.
Can PRP be advertised as regenerative or stem cell therapy?
No. The FDA warns against regenerative or stem-cell claims for PRP.
Is PRP the same as stem cells or exosomes?
No. PRP contains platelets and growth factors—not stem cells.
Is PRP safer than steroids?
PRP avoids steroid-related risks but has no FDA-approved efficacy claims.
Does insurance cover PRP?
Typically no. PRP is usually cash-pay.
Why might a patient still choose PRP?
Patients may seek PRP to avoid steroids or surgery, understanding it is not FDA approved.
What consent is required?
Patients must acknowledge PRP is not FDA approved, outcomes vary, and benefits are not guaranteed.
This FAQ addresses the regulatory status of common interventional pain treatments, with particular emphasis on platelet-rich plasma (PRP), stem cell therapies, and other regenerative medicine approaches.
Q: Is PRP FDA-approved for pain management?
No, PRP is not FDA-approved for interventional pain treatments. PRP falls under the FDA's Center for Biologics Evaluation and Research (CBER) jurisdiction and is exempt from the traditional FDA regulatory pathway under 21 CFR 1271.
[1]
Most PRP preparation systems have 510(k) clearance only for producing platelet-rich preparations intended to be mixed with bone graft materials to enhance handling properties in orthopedic practices.
[1]
Any use of PRP for intradiscal, epidural, facet joint, or sacroiliac joint injections is considered off-label use.
[1]
Q: What are my responsibilities when using PRP off-label?
When using PRP off-label, clinicians must "be well informed about the product, to base its use on firm scientific rationale and on sound medical evidence, and to maintain records of the product's use and effects".
[1]
All regenerative therapies must follow applicable FDA regulations.
[2]
Q: Are there any special regulatory concerns with activated PRP?
The language in 21 CFR 1271 has raised some regulatory concern regarding activated PRP, though the FDA has not attempted to regulate it to date.
[1]
Clinicians using activated PRP should remain informed about potential regulatory developments.
Q: What is the current evidence level for PRP in lumbar spine applications?
According to the 2025 ASIPP guidelines, intradiscal PRP injections have Level III (fair) evidence with a moderate consensus-based recommendation. Epidural PRP injections also have Level III evidence, while facet joint and sacroiliac joint PRP injections have Level IV (limited) evidence.
[2]
Q: Are stem cell therapies FDA-approved for pain management or musculoskeletal conditions?
No. The only FDA-approved stem cell products are derived from umbilical cord blood and are used to treat certain cancers and disorders of the hematopoietic system, such as leukemias, lymphomas, and sickle cell disease.
[3]
The FDA has not approved stem cell products to treat any other diseases or conditions, such as osteoarthritis, chronic pain, or aging.
[3]
Recently, an MSC therapy was approved for pediatric graft-vs.-host disease, marking the first MSC therapy approved by the U.S. FDA—but this is not for pain or musculoskeletal indications.
[4]
Q: What about bone marrow aspirate concentrate (BMAC)?
BMAC is considered to meet criteria for minimal manipulation and homologous use under FDA regulations, potentially qualifying for the same surgical exemption.
[5]
The 2020 ASIPP position statement provides strong evidence that BMAC preparation involves minimal manipulation and moderate evidence for homologous utility for various musculoskeletal and spinal conditions.
[5]
However, if the FDA does not accept BMAC as homologous, it would require an Investigational New Drug (IND) classification with FDA (351) cellular drug approval for use.
[5]
Q: What is the evidence level for stem cell therapies in lumbar spine applications?
According to the 2025 ASIPP guidelines, intradiscal injections of mesenchymal stem cells (MSCs) have Level III (fair) evidence with a moderate consensus-based recommendation.
[2]
For knee osteoarthritis, the evidence is highest with Level II evidence based on systematic reviews and randomized controlled trials.
[5]
Q: Are adipose-derived stem cells (stromal vascular fraction) FDA-approved?
No. Stromal vascular fraction (SVF) products are not FDA-approved, and the risks and efficacy are largely uncharacterized.
[6]
These products have skirted FDA regulation by claiming to be of low risk based on autologous use and minimal manipulation, but the FDA has issued warning letters to clinics utilizing SVF products, citing violations such as lack of a valid biologics license and deviations from current good manufacturing practice.
[6-7]
Q: Has the FDA issued warnings about stem cell clinics?
Yes. The FDA has issued multiple warnings that stem cell products for joint diseases, sports injuries, chronic pain, and other indications have not been proven safe or effective.
[3]
The FDA cautions that patients are vulnerable to the marketing of stem-cell treatments that are not supported by adequate study, are illegal, and may be harmful.
[6]
The FDA's Office of Criminal Investigations has worked with federal agencies to prosecute those who have manufactured, sold, and utilized stem-cell products without FDA approval.
[6]
Q: Have there been documented harms from unapproved stem cell products?
Yes. A 2021 CDC/FDA investigation documented bacterial infections in 20 patients who received umbilical cord blood-derived products marketed as stem cell treatments.
[3]
Of unopened, undistributed products sampled for testing, 65% (22 of 34 vials) were contaminated with at least 1 of 16 bacterial species, mostly enteric organisms including E. coli and Enterobacter cloacae.
[3]
All but one patient required hospitalization.
[3]
Q: How many stem cell clinics are operating in the United States?
As of March 2021, 1,480 U.S. businesses operating 2,754 clinics were found selling purported stem cell treatments—more than four times as many businesses as were identified 5 years earlier.
[8]
These clinics are selling stem cell products that are not FDA-approved and lack convincing evidence of safety and efficacy.
[8]
Q: What is the FDA's current enforcement stance?
The FDA offered a grace period for "stem cell clinics" until November 2020 to come into compliance by obtaining Investigational New Drug applications and working to secure premarket approval of their products.
[9]
The FDA needs to enforce adherence to their outlined standards to protect patients.
[9]
Q: Are corticosteroids FDA-approved for pain management?
Yes, corticosteroids are FDA-approved for numerous conditions including rheumatic disorders (rheumatoid arthritis, osteoarthritis, acute gouty arthritis, bursitis, tenosynovitis, epicondylitis), inflammatory conditions, allergic states, and many other indications.
[2]
Intra-articular corticosteroid injections use FDA-approved medications for approved indications including osteoarthritis and rheumatoid arthritis.
Q: What about epidural steroid injections?
Epidural steroid injections typically represent off-label use of FDA-approved medications (corticosteroids and local anesthetics). While the drugs themselves are FDA-approved, their epidural administration for specific spine pain indications may not have formal FDA approval for that route or indication.
[10]
Q: Are there FDA warnings about corticosteroid injections?
Yes, the FDA has warned that injection of corticosteroids into the epidural space may result in rare but serious adverse effects, including loss of vision, stroke, paralysis, and death.
[11]
These rare complications may be associated with particulate steroids, with no adverse outcomes reported when nonparticulate steroids were used.
[11]
Q: What is the FDA approval status of spinal cord stimulation?
Spinal cord stimulation (SCS) is FDA-approved for chronic pain and was initially introduced to market in 1967.
[2]
Dorsal root ganglion (DRG) stimulation received FDA approval in 2016 with specific mandated training requirements—physicians must complete both didactic and hands-on training before offering this therapy.
[12]
Q: What's the difference between FDA-cleared and FDA-approved devices?
Medical devices can enter the market through multiple FDA pathways: 510(k) clearance (demonstrating substantial equivalence to existing devices) or premarket approval (PMA) requiring more rigorous safety and efficacy data. Many neuromodulation devices are FDA-cleared rather than approved, representing a lower evidentiary threshold.
Q: Which medications are FDA-approved for intrathecal pain management?
Only morphine and ziconotide are FDA-approved analgesics for long-term intrathecal infusion.
[13]
Ziconotide is a selective N-type voltage-gated calcium channel blocker approved for intrathecal use in uncontrolled cancer pain.
[14]
Q: What about birth tissue products (umbilical cord, placental membranes, amniotic fluid)?
Birth tissue products are subject to different regulatory pathways depending on their processing and intended use.
[12][15]
The FDA has determined the need for varying degrees of regulation for these products for safety and efficacy.
[12]
The regulatory landscape for these products is frequently updated and federally enforced, so clinicians must stay informed to remain within FDA purview.
[12]
Q: Is radiofrequency ablation FDA-approved?
Radiofrequency ablation procedures (conventional, thermal, water-cooled) use devices that may be FDA-cleared but are applied to various anatomical targets without specific FDA approval for each indication.
Q: Are there any recommendations against radiofrequency ablation?
Yes, recent guidelines strongly recommend against facet joint radiofrequency ablation for chronic spine pain. A 2025 BMJ guideline issued strong recommendations against joint radiofrequency ablation with or without joint targeted injection for chronic axial spine pain.
[16]
These reflect evidence-based practice recommendations rather than FDA warnings.
FDA approval status varies significantly by device, drug, and indication rather than by procedure type
Off-label use is common and legal when clinicians meet their responsibilities for informed use based on scientific rationale and sound medical evidence
Stem cell products for pain and musculoskeletal conditions are NOT FDA-approved—the only approved stem cell products are for hematologic malignancies
[3]
PRP devices are FDA-cleared only for bone graft applications—all other uses are off-label
[1]
Recent guidelines recommend against many interventional procedures for chronic spine pain despite their regulatory status
[16]
Clinicians must stay informed about evolving FDA regulations, particularly for regenerative therapies, and should be aware of documented harms from unapproved products
1.
Journal of Pain Research. 2022. Sayed D, Grider J, Strand N, et al.Guideline
2.
Pain Physician. 2025. Manchikanti L, Navani R, Navani A, et al.
3.
JAMA Network Open. 2021. Hartnett KP, Powell KM, Rankin D, et al.
4.
Mesenchymal Stromal Cell Therapy: Progress to Date and Future Outlook.
Molecular Therapy : The Journal of the American Society of Gene Therapy. 2025. Lu W, Allickson J.New
5.
Pain Physician. 2020. Manchikanti L, Centeno CJ, Atluri S, et al.
6.
Intraocular Stem Cell Therapy - 2016.
American Academy of Ophthalmology. 2016. Guideline
7.
Intraocular Stem Cell Therapy.
American Academy of Ophthalmology (2016). 2016. Guideline
8.
Cell Stem Cell. 2021. Turner L.
9.
Arthroscopy : The Journal of Arthroscopic & Related Surgery : Official Publication of the Arthroscopy Association of North America and the International Arthroscopy Association. 2020. Fang WH, Vangsness CT.
10.
Regenerative Medicine: Pharmacological Considerations and Clinical Role in Pain Management.
Current Pain and Headache Reports. 2022. Kaye AD, Edinoff AN, Rosen YE, et al.
11.
BMC Musculoskeletal Disorders. 2023. Wongjarupong A, Pairuchvej S, Laohapornsvan P, et al.
12.
The American Journal of Sports Medicine. 2018. Chen X, Jones IA, Park C, Vangsness CT.
13.
Platelet-Rich Plasma: Fundamentals and Clinical Applications.
Arthroscopy : The Journal of Arthroscopic & Related Surgery : Official Publication of the Arthroscopy Association of North America and the International Arthroscopy Association. 2021. Sheean AJ, Anz AW, Bradley JP.
14.
Platelet-Rich Therapies for Musculoskeletal Soft Tissue Injuries.
The Cochrane Database of Systematic Reviews. 2014. Moraes VY, Lenza M, Tamaoki MJ, Faloppa F, Belloti JC.
15.
Pain Physician. 2018. Sanapati J, Manchikanti L, Atluri S, et al.
16.
Medicine. 2023. Peng B, Xu B, Wu W, et al.
Videos
Technical
https://www.youtube.com/watch?v=xLAa4FBuOF0
Medical
Blood Draw
Carestream PRP
https://www.youtube.com/watch?v=RcaMoXq2Al0
Level I – Strong evidence
Multiple high-quality randomized controlled trials (RCTs) and/or consistent meta-analyses with low bias.
Level II – Moderate evidence
At least one high-quality RCT or multiple moderate-quality RCTs with consistent findings.
Level III – Limited-moderate evidence
One moderate-quality RCT and/or multiple high-quality observational studies with consistent results.
Level IV – Limited evidence
Observational studies, single-arm studies, case series, or inconsistent RCT data.
Level V – Consensus / expert opinion
Expert opinion, narrative reviews, or mechanistic rationale without controlled clinical data.