Microneedling

Scientific Mechanisms of Microneedling

1. Controlled Micro-wounding & Wound Healing Cascade

   • The procedure uses tiny needles to create micro-injuries (microchannels) in the skin (both epidermis and dermis) without overly damaging the epidermal layer. NCBI+2Lippincott Journals+2

   • These micro-injuries trigger the skin’s innate wound-healing response: immediate hemostasis, then inflammation, proliferation, and finally remodeling. Lippincott Journals+3NCBI+3PubMed+3

2. Release of Growth Factors & Cellular Signaling

   • Platelets, neutrophils, and monocytes at the injury site release growth factors (e.g. transforming growth factor beta (TGF-β), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF)) that stimulate fibroblast activation. PMC+3Lippincott Journals+3NCBI+3

   • These signals stimulate keratinocyte proliferation and differentiation, and also help regulate inflammation. PubMed+2PMC+2

3. Collagen & Elastin Induction / Extracellular Matrix (ECM) Remodeling

   • Fibroblasts (dermal cells) are prompted to synthesize new collagen (especially types I, III and sometimes VII) and elastin. Over time, there is reorganization of collagen fibres (making them more aligned, thicker, better structured) which improves skin firmness and elasticity. Lippincott Journals+3dermatologypaper.com+3NCBI+3

   • The ECM also includes glycosaminoglycans (GAGs), proteoglycans, which help in hydration and structure. PubMed+2Lippincott Journals+2

4. Angiogenesis (New Blood Vessel Formation)

   • Microneedling stimulates neovascularization (formation of new capillaries) which improves blood flow to the treated area. Better blood supply helps deliver oxygen, nutrients, immune cells, and supports the repair and remodeling processes. Lippincott Journals+2PMC+2

5. Epidermal Regeneration & Barrier Improvement

   • The epidermis re-epithelialises (repairs itself) over a few days after treatment. Keratinocytes multiply and restore the outer skin layer. PubMed+2PMC+2

   • Microneedling also helps improve skin barrier function, reduces transepidermal water loss, and improves hydration by restoring lipid structures (in some studies via upregulation of genes related to ceramide production) PMC+1

6. Modulation of Inflammation

   • While the process starts with inflammation (which is necessary), microneedling tends to influence this in a way that doesn’t lead to chronic inflammation. Some inflammatory cytokines are downregulated in later stages.

 Supporting Studies & Evidence

Many studies confirms the main physiological effects as above: increased collagen and elastin, angiogenesis, improved barrier function. Clinical work shows repeated sessions lead to measurable increases in collagen types I, III and VII, and tropoelastin, with improvements in skin elasticity, reduction in wrinkles, shrinkage of enlarged pores, etc. Multiple treatments spaced over weeks are more effective than a single session. The remodeling of collagen and elastin continues over months after the treatments.

Medical Microneedling Affects Collagen and Elastin Gene Expression (Kenkel et al.) MedEsthetics

Human subjects (age ~44-65), four monthly treatments. Used high-res ultrasonography etc. Found big increases in dermal & epidermal density, facial elasticity. Also increases in collagen & elastin gene expression. MedEsthetics

Mechanism of Action from “Journal of Dermatology and Dermatologic Surgery” type reviews Lippincott Journals+2ejhm.journals.ekb.eg+2

Details the wound healing cascade: micro-wounds → release of growth factors (TGF, PDGF, etc.) → fibroblast activation → collagen/elastin/GAGs production → neovascularization → remodeling. Also shows how collagen type III transitions to type I over time. Lippincott Journals+1

El-Domyati M, Barakat M, Awad S, Medhat W, El-Fakahany H, Farag H. Multiple microneedling sessions for minimally invasive facial rejuvenation: an objective assessment. Int J Dermatol. 2015 Dec;54(12):1361-9. 

Exosomes

Autologous Exosome Therapy: Mechanisms, Applications.

Autologous exosome therapy represents an emerging frontier in regenerative and precision medicine. Exosomes—30–150 nm extracellular vesicles secreted by most cell types—serve as natural carriers of proteins, lipids, and nucleic acids that mediate intercellular communication and tissue homeostasis. In the autologous approach, exosomes are isolated from the patient’s own biological material, such as adipose-derived mesenchymal stem cells (ADSCs), bone-marrow stem cells, or platelet-rich plasma (PRP). When re-administered, these vesicles deliver regenerative and immunomodulatory signals without the risks associated with live-cell transplantation. Experimental studies have demonstrated that autologous exosomes modulate inflammation, inhibit apoptosis, and promote angiogenesis and extracellular matrix remodeling. Although early clinical observations in dermatology, orthopedics, and wound repair are promising, major challenges remain in standardization, large-scale production, potency quantification, and regulatory approval. This review outlines the biological mechanisms, current applications, and translational hurdles of autologous exosome therapy, emphasizing its potential as a safe, patient-specific, cell-free alternative to conventional stem-cell treatments.

1. What are exosomes?

Exosomes are nanosized extracellular vesicles enclosed by a lipid bilayer, secreted via the endosomal pathway, and found in virtually all body fluids. They carry a diverse molecular cargo—including mRNA, microRNA, cytokines, and bioactive lipids—that can reprogram recipient cells. Autologous exosome therapy utilizes these vesicles harvested from an individual’s own cells, thereby circumventing the immunogenicity and ethical concerns associated with allogeneic or embryonic products. The concept aligns with the modern shift toward cell-free regenerative medicine, in which secreted paracrine factors, rather than whole cells, drive tissue repair.

2. How do they work? 

Autologous exosomes mediate paracrine communication by transferring functional mRNAs and microRNAs that regulate gene expression in target cells. They also exert immunomodulatory effects by downregulating NF-κB signaling and reducing secretion of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), while enhancing IL-10 and TGF-β expression. Additionally, exosomal cargo such as VEGF, FGF2, IGF-1, and miR-21/miR-126 promotes angiogenesis, fibroblast proliferation, and inhibition of apoptosis.

3.  Autologous exosome production

Sample collection typically involves adipose tissue, bone marrow aspirate, or venous blood under sterile conditions. Cells are cultured ex vivo in exosome-depleted media, and exosomes are purified using ultracentrifugation, size-exclusion chromatography, or tangential-flow filtration. Characterization employs nanoparticle tracking analysis (NTA) and detection of CD9, CD63, CD81, and TSG101 markers. Purified exosomes are reintroduced via local injection, microneedling, or intravenous infusion.

4. Clinical applications

Applications span dermatology, orthopedics, neurology, cardiology, and immunology. In dermatology, exosomes enhance collagen synthesis and improve dermal density. In orthopedics, they promote cartilage regeneration and reduce pain and inflammation. In neurology, preclinical models show neuroprotection and reduced infarct size after stroke.

5. What are the advantages of the autologous approach?

Autologous exosomes provide immunological compatibility, ethical acceptability, reduced infection risk, and personalization reflective of the patient’s physiological state.

6. Limitations and Regulatory Considerations

Challenges include variable yield, lack of standardization in isolation and quantification, unclear mechanisms of action, and limited storage stability. Regulatory bodies such as EMA and MHRA currently classify exosome therapies as investigational biologics or ATMPs.

7. What are the future directions?

Research aims to develop bioengineered exosomes with targeted ligands or synthetic cargo, implement GMP-grade bioreactors for production, and apply AI for optimization. Large-scale clinical trials are essential for establishing safety and efficacy.

8. Conclusion

Autologous exosome therapy harnesses the body’s innate signaling network to stimulate regeneration and immunological balance. By offering a cell-free yet biologically active alternative to stem-cell transplantation, it holds potential as a next-generation personalized regenerative therapy.

References

1. Théry C. et al., Nat Rev Immunol (2022) 22: 77–95.
2. Mendt M. & Kalluri R., Cell (2019) 177: 225–229.
3. Lai R.C. et al., Stem Cell Research & Therapy (2018) 9: 63.
4. Bari E. et al., Front Bioeng Biotechnol (2020) 8: 557.
5. Phinney D.G., Stem Cells (2015) 33: 1501–1510.

Did you know? 

   🔬 10 Scientific Facts About Vitamin B12

1. Specific microorganisms make Vitamin B12

Neither animals nor plants can produce B12.
Only microorganisms (certain bacteria and archaea) can synthesize it.
Animals get B12 from bacteria in soil, water, or their gut, which is why meat contains it.

2. It’s one of the largest and most complex vitamins

B12 has a massive molecular structure, far bigger than other vitamins.
Because of this complexity, the body needs a special protein called intrinsic factor to absorb it

3. Humans store years’ worth of B12 in the liver

Unlike most vitamins, your liver can store 2–5 mg of B12 — enough for 2–5 years.
This is why deficiency can develop slowly but become serious when symptoms appear.

4. B12 is essential for DNA synthesis

Every time a cell divides, it needs B12.
Without it, red blood cells can’t form properly, leading to megaloblastic anemia.

5. Low B12 damages the nervous system — even if you’re not anemic

The brain and nerves need B12 to maintain myelin, the protective coating on nerve cells.
This is why deficiency can cause:

Tingling; Numbness; Difficulty walking; Memory issues and cognitive decline; Mood changes; Tiredness, etc.

And these can happen even if blood tests don’t show anemia.

6. Certain medications reduce B12 absorption

Scientific studies show that long-term use of:

●      Metformin (for diabetes)

●      Proton pump inhibitors (acid-reducing meds) can significantly lower B12 levels.

7. B12 deficiency may increase homocysteine, a cardiovascular risk factor

B12 helps break down homocysteine.
High homocysteine is linked to increased risk of: Stroke, Heart disease, Cognitive decline

B12 supplementation can lower homocysteine levels.

8. The body absorbs only a small fraction of oral B12

Even with high-dose pills (1000–2000 mcg), only about 1–2% is absorbed passively.
This is why injections are used when absorption is impaired.

9. B12 is critical for neurotransmitter production

It’s involved in making: Serotonin, Dopamine, Norepinephrine.

Low B12 can therefore influence mood, motivation, and mental clarity.

10. There is no plant-based natural B12 source

Some seaweeds and fermented foods contain B12 analogues (called Pseudovitamin B12) that do not work in humans. This is why vegans must supplement.

Restoring optimal B12 levels—particularly through intramuscular injections, support energy metabolism, cognitive clarity, and overall neurological health.