How Polynucleotides Work: The Cellular Mechanism Explained

In Part 1, we covered what polynucleotides actually are (purified DNA fragments derived from salmon sperm, not actual fish material on your face), their 40-year history in regenerative medicine, and why they're fundamentally different from fillers, Botox, and other injectables you've heard about.

Now in Part 2, we're diving into the fascinating part: how these DNA fragments actually communicate with your skin cells to produce collagen, repair damage, and regenerate tissue from within.

Read Part 1 first

TABLE OF CONTENTS

• Quick Answer: How Polynucleotides Work

• The Journey: From Injection to Cellular Activation

• The Adenosine Receptor Pathway (In Plain English)

• What Happens Inside Fibroblasts

• The Senescent Cell Problem

• Why This Is Different from Other Collagen Treatments

• The DNA Repair Mechanism

• Anti-Inflammatory and Antioxidant Effects

• What the Clinical Evidence Actually Shows

• The Timeline: Why Results Take 8-12 Weeks

• What Polynucleotides DON'T Do

• Key Takeaways

QUICK ANSWER: HOW POLYNUCLEOTIDES WORK

Polynucleotides work through cellular communication, not physical change. When injected into your dermis, they're broken down into smaller fragments that bind to adenosine receptors on fibroblast cell membranes. This triggers a cascade of cellular responses: increased collagen production (up to 47% in studies), DNA damage repair (particularly UV damage), activation of dormant "senescent" cells that had stopped functioning, and reduced inflammation throughout the tissue.

The mechanism in simple terms

DNA fragments get broken down by enzymes, then bind to cell receptors, which activate cellular repair signals. Your fibroblasts respond by producing more collagen, elastin, and hyaluronic acid. Improved skin quality emerges over 8-12 weeks.

Why it takes time

You're waiting for your body to respond to biological signals, produce new proteins, and rebuild tissue. That's a cellular process measured in weeks, not minutes.

Key difference from other treatments: Most aesthetic treatments add something (volume), block something (nerves), or irritate tissue to trigger repair. Polynucleotides communicate with cells through molecular signaling that your body already understands. They use adenosine pathways that your cells naturally employ during tissue repair.

Here's what still fascinates me after years in aesthetics: we can actually communicate with skin cells.

Not metaphorically. Not through vague "boosting" or "stimulating" that marketing teams love throwing around. I mean genuine molecular communication. Delivering biological instructions that cells recognize and respond to.

In my cardiac nursing days, I watched this principle save lives. We'd use medications that bound to specific cell receptors, triggering precise responses. Dilate this blood vessel. Slow that heart rate. Strengthen these contractions. The body has molecular keys and locks. Specific molecules (the keys) fit specific receptors (the locks) to activate particular cellular responses.

Polynucleotides use the exact same principle, just applied to skin regeneration instead of cardiac function.

When I first learned this mechanism, my cardiac nurse brain lit up. This wasn't beauty industry pseudoscience. This was legitimate cellular biology using established pathways that medical research had documented for decades.

Let me show you exactly how it works, step by step, without requiring a biology degree to understand.

THE JOURNEY: FROM INJECTION TO CELLULAR ACTIVATION

When I inject polynucleotides into your dermis (the deeper layer of skin where fibroblasts live), here's the precise sequence that unfolds over several weeks.

The First Hours: Dispersal Through Tissue

The clear gel spreads through the dermal tissue matrix. You'll see small raised bumps (blebs) at each injection point initially. That's the solution sitting in the dermis before it disperses. Over the next 6-12 hours, it spreads through the tissue planes.

Nothing dramatic is happening yet. The polynucleotides are just distributing through the area, waiting for the next phase.

Hours to Days: Enzymatic Breakdown Begins

Your body has enzymes called DNases. Think of them as molecular scissors specifically designed to cut DNA chains. These enzymes start breaking down the long polynucleotide chains into progressively smaller fragments.

The process looks like this: long chains (1,500 kDa) gradually break into medium fragments (500 kDa), then short chains (150 kDa), then very short fragments (50 kDa), and eventually individual building blocks called mononucleotides.

This breakdown process is gradual and controlled. That's why longer-chain products like Ameela provide sustained effects. They take weeks to fully break down, continuously releasing smaller active fragments.

Days to Weeks: Receptor Binding

Here's where the magic happens. Those DNA fragments, particularly the smaller ones, have a molecular shape that fits perfectly into adenosine receptors on fibroblast cell membranes.

Think of it like a key sliding into a lock. The DNA fragment (key) fits the adenosine receptor (lock). When the fit happens, the lock turns. The receptor activates and sends signals into the cell.

This isn't random. Your body uses adenosine signaling naturally for tissue repair, wound healing, and cellular communication. Polynucleotides are essentially borrowing an existing communication system to deliver regenerative instructions.

Weeks: Cellular Response Cascade

Once those receptors activate, a cascade of cellular responses begins inside the fibroblast.

Gene expression changes. Certain genes turn "on" that code for collagen production, elastin synthesis, and hyaluronic acid creation.

Protein synthesis increases. The cellular machinery starts producing more structural proteins at higher rates.

Cellular metabolism shifts. Energy production increases to support the heightened activity.

Growth factors release. The stimulated cells produce and release their own signaling molecules that amplify the effect.

This isn't instant. Gene expression takes hours to days. Protein synthesis takes days to weeks. Building significant amounts of new collagen takes weeks to months. That's why you don't see results immediately. You're waiting for biology to do its work.

Weeks to Months: Tissue Remodeling

As fibroblasts produce new collagen, elastin, and hyaluronic acid, the dermal structure gradually changes.

New collagen fibres form and organize into supportive networks. Elastin provides resilience and bounce. Hyaluronic acid holds moisture and creates volume at a cellular level. The extracellular matrix (the "scaffolding" between cells) becomes more robust. Tissue thickness increases measurably.

This remodeling continues for weeks after the polynucleotides themselves have been fully metabolized and cleared. You've triggered a repair process that continues under its own momentum.

Six to Eight Weeks: Complete Metabolism

By 6-8 weeks post-injection, all polynucleotide material has been completely broken down into individual nucleotides, absorbed, and either used by cells for their own DNA and RNA synthesis or metabolized for energy.

Nothing foreign remains in your tissue. Just the beneficial results of the cellular activation they triggered.

That's why maintenance treatments are needed. The stimulus is temporary, so the enhanced cellular activity gradually returns to baseline unless you provide another round of signaling.

THE ADENOSINE RECEPTOR PATHWAY

Let me explain the specific molecular mechanism without drowning you in biochemistry terminology.

Your body has four types of adenosine receptors on cell surfaces: A1, A2A, A2B, and A3. Each one triggers different cellular responses when activated. Polynucleotides primarily activate A2A receptors on fibroblasts.

Here's what happens when A2A receptors activate.

The receptor acts like a switch on the cell membrane. When polynucleotides bind to it, the switch flips "on." This activates an enzyme inside the cell called adenylyl cyclase. Adenylyl cyclase produces a molecule called cyclic AMP (cAMP). That cAMP acts as a "second messenger." It carries the signal deeper into the cell.

The cAMP activates protein kinases. These are enzymes that activate other proteins by adding phosphate groups to them. Those activated proteins enter the cell nucleus and bind to DNA. They turn on genes that code for collagen, elastin, and other extracellular matrix proteins. The cell starts producing these proteins at elevated rates.

I know that sounds complex, but here's the simple version: DNA fragments flip a switch. The switch activates a signaling cascade. The cascade turns on collagen-producing genes. The cell makes more collagen.

Why This Pathway Matters for Skin

This adenosine pathway isn't random. Your body uses it naturally during wound healing and tissue repair. When tissue gets damaged, cells release adenosine as a distress signal. Nearby cells detect it through these receptors and activate repair responses.

Polynucleotides essentially mimic that distress signal. They tell fibroblasts "repair mode needed" even though there's no actual injury. It's a controlled way to activate healing responses without creating real damage.

This is fundamentally different from treatments that work by causing actual tissue injury. RF microneedling, lasers, chemical peels all trigger repair through real trauma. Polynucleotides trigger repair through molecular signaling that mimics trauma signals without actual damage.

Less inflammation, less downtime, but still robust cellular activation. That's the advantage of working through receptor pathways rather than physical injury.

WHAT HAPPENS INSIDE FIBROBLASTS

Fibroblasts are the workhorses of your dermis. These cells produce collagen (structural support), elastin (resilience and bounce), and hyaluronic acid (hydration and volume). Everything that makes skin firm, plump, and youthful comes from fibroblast activity.

When you're young, fibroblasts are highly active. They're constantly producing fresh collagen, replacing damaged proteins, maintaining optimal extracellular matrix quality.

As you age, fibroblast activity declines. They produce less collagen (about 1% less per year after age 20). They respond more slowly to repair signals. Many become senescent. Essentially retired, no longer dividing or producing much of anything.

Polynucleotides Reactivate Fibroblast Function

When polynucleotides bind to those adenosine receptors on fibroblast membranes, here's specifically what changes inside the cell.

Collagen synthesis increases significantly. Gene expression for collagen ramps up. Studies document up to 47% increase in collagen production within 23 days of polynucleotide treatment.

The cell's ribosomes (protein-making machinery) work overtime producing collagen molecules. These get secreted outside the cell where they form long fibers that provide structural support.

Both Type I collagen (strength and structure) and Type III collagen (flexibility and early scar tissue formation) increase.

Elastin production follows similar patterns. The mechanisms activate elastin gene expression. Elastin provides the "spring" in skin. The ability to stretch and bounce back. As we age, elastin breaks down faster than it's replaced. Polynucleotides help shift that balance back toward production.

Hyaluronic acid synthesis increases too. Fibroblasts produce hyaluronic acid synthases. These are enzymes that create hyaluronic acid chains. This provides natural hydration and volume at the cellular level. Not from injected filler but from your own cellular production. The HA produced by your own cells integrates naturally into the extracellular matrix.

Growth factor release amplifies the effect. Activated fibroblasts produce and secrete growth factors like VEGF (vascular endothelial growth factor) and FGF (fibroblast growth factor). These create a positive feedback loop. Stimulated cells release signals that stimulate neighboring cells. This amplifies the effect beyond just the cells directly contacted by polynucleotides.

Cellular health improves overall. Mitochondria (cellular power plants) become more active, producing more ATP (cellular energy). Cellular repair mechanisms activate, fixing damaged proteins and clearing cellular debris. The cell essentially shifts from "maintenance mode" to "active production mode."

The Net Result

You have more fibroblasts actively working (as senescent ones reactivate), and the ones working are working more efficiently. More workers, all more productive. That's why the tissue quality improvements are so significant even though you're not adding volume or blocking anything.

THE SENESCENT CELL PROBLEM

This is one of the most fascinating aspects of how polynucleotides work, and it relates directly to why aging skin loses quality.

What Are Senescent Cells?

As fibroblasts age, many become senescent. Essentially retired. They stop dividing. They stop producing significant collagen, elastin, or hyaluronic acid. They just sit there, taking up space but not contributing to tissue health.

By middle age, approximately 30% of your dermal fibroblasts are senescent. That's nearly a third of your collagen-producing workforce essentially on permanent vacation.

These cells aren't dead. They're alive but non-functional. In some contexts, senescent cells serve purposes (tumour suppression, wound healing regulation). But in skin aging, they're a major problem. Fewer functional fibroblasts means less collagen production, declining tissue quality, and visible aging.

Can Senescent Fibroblasts Be Reactivated?

This was the big question in cellular biology for years. Once a cell becomes senescent, is it permanently retired? Or can it be coaxed back to productivity?

Research on polynucleotides suggests they can reactivate at least some senescent fibroblasts. The adenosine receptor signaling appears to wake up dormant cells, shifting them back toward productive function.

Not all senescent cells reactivate. Some are too far gone. But studies show measurable increases in active fibroblast populations after polynucleotide treatment.

This means you're not just making existing functional cells work harder. You're actually bringing retired cells back into the workforce. Increasing the total number of productive fibroblasts in your dermis.

Why This Matters Clinically

This explains why polynucleotide results are so sustained compared to treatments that just temporarily boost activity. You're fundamentally changing the cellular population in your dermis. More functional cells that continue producing collagen even after the polynucleotides are fully metabolized.

It's like the difference between giving workers a temporary energy drink (short-term productivity boost) versus hiring more workers and training the existing ones better (long-term capacity increase).

Other treatments provide the energy drink. Polynucleotides expand and train your workforce.

That's why results can last 6-9 months and why repeated treatments have cumulative benefits. You're progressively improving the functional cellular population in your skin.

WHY THIS IS DIFFERENT FROM OTHER COLLAGEN TREATMENTS

Most treatments that claim to "boost collagen" work through one of three main mechanisms. Let me show you how polynucleotides differ from all of them.

Physical Injury Leading to Wound Healing

RF microneedling, lasers, chemical peels, dermal needling all create controlled injury. Your body responds with wound healing, which includes collagen production. This works, but it's essentially tricking your body into repair mode by causing real damage. The collagen produced is scar tissue remodeling, not optimized structural collagen. Downtime is significant because there's actual injury. Inflammation is substantial because it's a true wound response.

Foreign Material Triggering Inflammatory Response

Sculptra (poly-L-lactic acid) works by injecting tiny particles that your body recognizes as foreign. This triggers an inflammatory response. As part of that inflammation, fibroblasts produce collagen to wall off the foreign material.

Again, this works. But you're leveraging inflammation. A blunt tool that comes with side effects, unpredictability, and the need to carefully manage the response.

Topical Stimulation

Retinoids, peptides, vitamin C all work by penetrating skin and providing signals or building blocks for collagen production.

These help, but penetration is limited. They can't reach the deeper dermis where significant collagen production happens. Effects are mild compared to injectable treatments.

Polynucleotides: Molecular Signaling Without Damage

Polynucleotides work through none of these mechanisms. There's no physical injury (beyond needle punctures, which are minimal). There's no foreign material triggering inflammation. There's no topical barrier limiting depth.

Instead, you're delivering molecular instructions through receptor pathways that cells use naturally during healing. You're activating repair without causing damage that needs repairing.

The collagen produced isn't scar tissue from wound healing. It's organized, structural collagen from optimized fibroblast function.

This distinction matters enormously. Less inflammation means less downtime and fewer complications. No injury means better tolerance for sensitive skin. Organized collagen production means more aesthetic outcomes rather than unpredictable healing. Receptor-mediated signaling is more controlled than injury-based responses.

From a nursing perspective, this is elegant medicine. Precise, controlled, working with the body's existing systems rather than forcing responses through crude mechanisms.

THE DNA REPAIR MECHANISM

Here's something that particularly excites me about polynucleotides: they help repair damaged DNA inside your skin cells.

Your skin accumulates DNA damage constantly, primarily from UV radiation. Every time you're in the sun, UV photons hit your skin cells and cause specific types of DNA damage. Particularly cyclobutene pyrimidine dimers (CPDs).

CPDs are lesions where two adjacent DNA bases abnormally bind together. These mutations interfere with normal cellular function. They can lead to cell dysfunction or death. They accumulate over years of sun exposure.

Your cells have repair mechanisms for CPDs, but they're imperfect. Some damage persists. Over decades, this accumulated damage contributes significantly to photoaging. The specific type of aging caused by sun exposure.

How Polynucleotides Help DNA Repair

Lee et al.'s 2024 research (published in the International Journal of Molecular Sciences, DOI: 10.3390/ijms25158224) documented something fascinating. They found that "PDRN promoted cyclobutene pyrimidine dimer (CPD) repair in UVB-exposed dermal fibroblasts."

In plain English, polynucleotides help cells fix UV damage to their DNA.

The mechanism isn't fully understood yet, but the working theory is that polynucleotides provide nucleotide building blocks that cells use to synthesize new DNA during repair. They may also activate DNA repair pathways through cellular signaling.

Either way, the result is measurable. Cells treated with polynucleotides show reduced CPD burden. Less accumulated UV damage in their DNA.

Why This Matters for Your Skin

This means polynucleotides aren't just stimulating collagen production in the present. They're helping reverse accumulated damage from the past. Specifically sun damage that's been accumulating for years.

Cells with less DNA damage function more efficiently. They're less likely to become senescent prematurely. They produce better quality proteins.

This contributes to the overall improvement in skin quality beyond just collagen quantity. You're improving cellular health at the most fundamental level.

For those of us with significant sun damage (and in the UK, that's most of us over 40), this DNA repair mechanism is particularly valuable. You're addressing photoaging at its root cause. Accumulated DNA damage in dermal cells.

ANTI-INFLAMMATORY AND ANTIOXIDANT EFFECTS

Beyond collagen stimulation and DNA repair, polynucleotides have documented anti-inflammatory and antioxidant properties. These contribute significantly to the overall skin quality improvements people experience.

The Anti-Inflammatory Mechanism

Inflammation accelerates skin aging. Chronic low-grade inflammation (sometimes called "inflammaging") damages collagen, impairs cellular function, and accelerates all aging processes.

Polynucleotides reduce inflammation through several pathways.

Adenosine receptor activation naturally has anti-inflammatory effects. The A2A receptor pathway that stimulates collagen production also suppresses inflammatory signaling.

They reduce pro-inflammatory cytokines. These are cellular signaling molecules that promote inflammation. Studies show decreased IL-6, TNF-alpha, and other inflammatory markers after polynucleotide treatment.

They increase anti-inflammatory mediators. Molecules that calm inflammation. Particularly IL-10, which is a powerful anti-inflammatory cytokine.

The result: treated tissue shows less redness, faster healing, reduced reactivity, and improved barrier function.

For those with sensitive skin, rosacea, or inflammatory conditions, this anti-inflammatory effect is often as valuable as the collagen stimulation.

Antioxidant Effects

Free radicals damage skin through oxidative stress. UV exposure, pollution, and normal metabolism all generate reactive oxygen species (ROS) that damage cellular components. Including DNA, proteins, and lipids.

Polynucleotides have antioxidant properties. They can neutralize some free radicals directly. They also activate cellular antioxidant defense systems.

Research shows reduced oxidative stress markers in treated tissue. Increased cellular antioxidant enzymes (superoxide dismutase, catalase). Better cellular protection against UV-induced oxidative damage.

This means polynucleotides both repair past damage and help protect against future damage. A rare combination in aesthetic treatments.

WHAT THE CLINICAL EVIDENCE ACTUALLY SHOWS

Let's look at what peer-reviewed research documents about polynucleotide mechanisms and outcomes. With appropriate scientific context.

Collagen Production Studies

Multiple studies document increased collagen synthesis after polynucleotide treatment. The numbers are impressive. A 47% increase in collagen production measured in cultured fibroblasts. A 52% increase in epidermal thickness in clinical trials. Histological analysis showing increased collagen density in treated skin biopsies.

These aren't manufacturer claims. These are published, peer-reviewed measurements.

Now here's the caveat. Laboratory studies with isolated cells usually show bigger effects than real-world human trials. That 47% figure comes from controlled laboratory conditions. Real results are typically more modest, though still clinically significant.

DNA Repair Documentation

Lee et al.'s study documented CPD repair promotion in UVB-exposed fibroblasts. This was laboratory research, not clinical trials on human patients. We can't yet say definitively how much this translates to actual photoaging reversal in clinical practice.

But the mechanism is biologically plausible and the laboratory evidence is solid. Clinical research is ongoing.

Elasticity and Hydration Improvements

Cavallini et al.'s 2020 consensus report (Journal of Cosmetic Dermatology, DOI: 10.1111/jocd.13679) analyzed multiple clinical studies. They found consistent improvements in skin elasticity (measured with cutometer devices), hydration levels (measured with corneometer), and overall skin quality (subjective assessment scales).

Results were maintained for 6 months in most studies. Some showed benefits up to 9 months.

Safety Profile

Lee et al.'s comprehensive review found something remarkable. "In all of the above studies, there were no serious adverse events reported."

This is remarkable consistency across multiple studies, different populations, and various treatment protocols.

Temporary side effects (swelling, bruising, discomfort) were common but resolved without intervention. No long-term complications. No serious reactions. No safety concerns that would preclude use.

Limitations of Current Research

Lee et al. note important caveats that honest practitioners should acknowledge.

Most studies are observational or small pilot trials, not large randomized controlled trials. Protocols vary significantly between studies, making direct comparisons difficult. Long-term effects beyond 12 months aren't well documented. Optimal dosing, frequency, and technique aren't definitively established. Mechanisms are understood in principle but not in complete molecular detail.

My Interpretation as a Nurse

The evidence supports polynucleotides as effective and safe for skin quality improvement. The mechanisms are biologically plausible and documented in laboratory research. Clinical outcomes are consistent across multiple studies.

However, we're not dealing with pharmaceutical-level evidence. More rigorous research would strengthen the case. Particularly long-term studies and head-to-head comparisons with other modalities.

That said, 40 years of medical use in wound healing provides substantial safety assurance. The consistency of reported outcomes across different practitioners provides reasonable efficacy confidence.

I'm comfortable recommending polynucleotides based on available evidence, while acknowledging that research is ongoing and our understanding continues to evolve.

THE TIMELINE: WHY RESULTS TAKE 8-12 WEEKS

People often ask: "If polynucleotides activate cells immediately, why do I wait weeks for results?"

Fair question. Let me break down the biological timeline so you understand what's happening during that seemingly empty waiting period.

Days One to Three: Dispersion and Initial Binding

Polynucleotides spread through tissue. Early fragments start binding to receptors. Cellular signaling begins. You see swelling and blebs, but no aesthetic change yet.

Week One: Receptor Activation and Gene Expression

Adenosine receptors fully activate. Gene expression changes begin. Cells ramp up protein synthesis machinery. Still no visible change. You're waiting for those proteins to be made.

Weeks Two to Four: Protein Production Begins

Fibroblasts start producing increased collagen, elastin, and hyaluronic acid. But producing proteins takes time. And you need significant quantities before visible tissue changes occur.

Some people notice very subtle improvements around week 3-4 (after their second treatment). Most don't see anything yet.

Weeks Four to Eight: Collagen Accumulation

New collagen accumulates in the dermis. Fibers organize into structural networks. The extracellular matrix becomes more robust. Tissue thickness increases measurably.

This is when you start noticing changes. Improved texture, better hydration, subtle firmness.

Weeks Eight to Twelve: Visible Results Emerge

By now, significant collagen remodeling has occurred. The cumulative effect of weeks of enhanced production becomes visible. Skin looks firmer. Texture improves. Fine lines soften.

This is also why you need the full 3-4 treatment course. Each treatment adds more stimulus. By treatment three, you have cumulative activation. Cells that were stimulated in treatment one are still producing while treatment three stimulates even more.

Months Three to Six: Peak Results

Results continue improving slightly even after treatments end because cellular activity remains elevated. Peak improvement typically occurs 4-6 weeks after the final treatment.

Months Six to Nine: Gradual Decline

As the stimulus fades, cellular activity gradually returns toward baseline. Results persist longer than the polynucleotides themselves (which are fully metabolized by 6-8 weeks) because you've created lasting changes in tissue structure.

But eventually, without maintenance, results fade as normal aging processes resume.

Why You Can't Speed This Up

Biology has its own timeline. You can't force cells to produce collagen faster without causing problems. The gradual timeline is actually a feature, not a bug. It means changes are natural, organized, and sustainable.

Treatments promising instant collagen "boost" are either not actually stimulating significant collagen production, or they're causing injury that produces scar tissue rapidly (which has its own downsides).

Patience is required because we're working with natural biological processes, not instant cosmetic changes.

WHAT POLYNUCLEOTIDES DON'T DO

As important as understanding what polynucleotides do is understanding what they don't do. This prevents disappointment from unrealistic expectations.

They Don't Add Volume

If you have significant volume loss (hollow cheeks, sunken temples, deflated lips), polynucleotides won't fill that. You need actual filler for volume replacement.

Polynucleotides improve tissue quality. They don't change tissue quantity or structure dramatically.

They Don't Tighten Significantly Lax Skin

If you have considerable sagging (jowls, significant neck laxity, descended facial structures), polynucleotides provide minimal improvement.

Some people see modest tightening from improved collagen networks, but it's subtle. Significant laxity requires mechanical tightening (threads, RF devices, or surgery).

They Don't Erase Deep Wrinkles

Deep expression lines, nasolabial folds, marionette lines that are etched into tissue. Polynucleotides soften these slightly but don't erase them.

For lines this significant, you need combination approaches. Toxins to prevent muscle movement creating the lines, plus fillers to fill the existing grooves, plus possibly polynucleotides to improve surrounding tissue quality.

They Don't Work Immediately

If you need results for an event in two weeks, polynucleotides are the wrong choice. The biological timeline is 8-12 weeks minimum.

For fast results, fillers and toxins are better options.

They Don't Work for Everyone Equally

Individual response varies based on age, genetics, lifestyle factors, skin condition baseline, and how well your particular cellular machinery responds to adenosine signaling.

Most people see meaningful improvement. Some see dramatic change. A few see minimal results despite proper treatment.

This variability is inherent to bio-stimulation treatments that work with your body's own responses rather than adding something external.

They Don't Replace Good Skincare

Polynucleotides optimize cellular function, but if you're simultaneously damaging skin with sun exposure, smoking, poor nutrition, or terrible skincare, you're working against yourself.

They're part of a comprehensive approach, not a standalone solution that overcomes all other factors.

KEY TAKEAWAYS FROM PART 2

What You've Learned About How Polynucleotides Work:

✓ Polynucleotides work through adenosine receptor activation on fibroblast cell membranes, triggering a cellular cascade that increases collagen production by up to 47% in studies.

✓ The mechanism is molecular communication through pathways your body uses naturally for tissue repair, not physical injury or foreign material inflammation like other collagen treatments.

✓ DNA fragments are broken down by natural enzymes into smaller pieces that bind to receptors, activate genes, and stimulate protein production over weeks, explaining the 8-12 week timeline for visible results.

✓ Fibroblasts (collagen-producing cells) increase their production of collagen, elastin, and hyaluronic acid while becoming more metabolically active and efficient.

✓ Senescent "retired" fibroblasts can be reactivated, effectively increasing the functional cell population in your dermis. This is why results are sustained even after polynucleotides are metabolized.

✓ DNA repair mechanisms help fix UV damage (CPDs) accumulated in skin cells, addressing photoaging at a fundamental level beyond just collagen stimulation.

✓ Anti-inflammatory and antioxidant effects reduce chronic inflammation and oxidative stress, contributing to overall skin quality improvements beyond structural changes.

✓ Clinical evidence shows consistent improvements in elasticity, hydration, and skin quality maintained for 6+ months, though more rigorous research would strengthen the evidence base.

✓ The gradual timeline (8-12 weeks) reflects genuine biological processes (gene expression, protein synthesis, tissue remodeling) that cannot be rushed without compromising quality.

✓ Polynucleotides don't add volume, tighten severely lax skin, erase deep wrinkles, or work immediately. Understanding limitations prevents disappointment from unrealistic expectations.

COMING IN PART 3: RESULTS, TIMELINE & WHAT TO REALISTICALLY EXPECT

Now you understand the cellular mechanisms. How polynucleotides communicate with fibroblasts, stimulate collagen, and repair DNA damage through adenosine receptor pathways.

But what does that actually translate to in terms of visible results? What will you see in the mirror? When will you see it? And what should you realistically expect for different concerns and treatment areas?

Part 3 will cover the practical outcomes:

• Week-by-week timeline of what happens (including the awkward "nothing visible yet" phase)

• Visible results you can expect: texture, tone, fine lines, hydration

• What polynucleotides do best (under-eyes, crepey skin, overall quality)

• Treatment areas: face, neck, décolletage, hands

• The actual treatment experience (what injections feel like, immediate aftermath)

• Downtime reality (swelling timeline, when you can return to normal activities)

• Individual variation: why some see dramatic results and others see modest improvement

• Honest expectations: the good, the limitations, and the "it depends" factors

We'll move from cellular science to real-world outcomes. What you'll actually experience if you decide polynucleotides are right for you.

Continue to Part 3: Results & Timeline

READY TO EXPLORE POLYNUCLEOTIDES FOR YOUR SKIN?

After understanding how polynucleotides work at cellular level (through adenosine receptor activation, fibroblast stimulation, and DNA repair mechanisms), you can see why results are gradual but sustained.

If you're interested in whether this cellular regeneration approach suits your skin concerns:

Book a consultation at Juvenology Clinic, 82 King Street, Maidstone, Kent.

Current Treatment Offers:

Polynucleotides 3 for 2: Three treatment areas for the price of two, £450 total (save £225)

Lumi Eyes 3 for 2: Buy 2 treatments, get 1 free, £300 total (save £150)

What Happens in Consultation:

✓ Comprehensive skin assessment (not just quick glance)

✓ Discussion of your specific concerns and realistic goals

✓ Honest evaluation of whether polynucleotides are appropriate or if alternatives suit you better

✓ Treatment protocol explanation with evidence-based timelines

✓ Complete pricing transparency with all costs outlined

✓ Opportunity for all your questions without pressure

✓ No obligation to book treatment immediately (take time to decide)

Easily accessible from London (30-40 minutes by train from various London stations) Free parking available nearby Flexible appointment times including evenings

Book Free Consultation: https://juvenology-clinic.book.app/book-now

Prefer to call? 07413 138825 Have questions first? Email: office@juvenology.co.uk

ABOUT THE AUTHOR

Nurse Marina is an aesthetic nurse specialist with 8 years of experience leading Juvenology Clinic in Maidstone, Kent. Her background includes 6 years as a cardiac nurse at KIMS Hospital (where she developed expertise in vascular anatomy and precision injection technique) and 2 years as an aesthetic nurse specialist at Spencer Private Hospitals.

She holds NMC registration and is a member of BACN (British Association of Cosmetic Nurses), JCCP (Joint Council for Cosmetic Practitioners), ACE Group, and the Royal College of Nursing. She's also registered with the ICO (Information Commissioner's Office) and verified by the Professional Standards Authority.

Her approach combines rigorous medical expertise with warm, maternal care. Bringing cardiac nursing precision and anatomical knowledge to aesthetic practice. She's passionate about evidence-based treatments over trend-chasing, patient education over sales pressure, and honest conversations about realistic outcomes.