Skip to main content

Microfat & Nanofat Grafting (GSM / Vulvar Atrophy / Lichen Sclerosus)

Microfat and nanofat grafting is an autologous regenerative-medicine approach using mechanically processed adipose tissue to treat genitourinary syndrome of menopause (GSM), vulvovaginal atrophy, and vulvar dystrophies including lichen sclerosus (VLS). The technique exploits both the volumizing properties of microfat and the regenerative / trophic properties of nanofat (rich in adipose-derived stem cells and growth factors) to attempt reversal of atrophic changes — distinct from filler-style HA, which is volumizing but not regenerative, and distinct from topical estrogen, which palliates without reversing atrophy.[1][2][3] For positioning vs other female cosmetic options see Cosmetic Genital Surgery — Female.

Therapeutic vs cosmetic context. Microfat / nanofat grafting for GSM, vulvovaginal atrophy, or lichen sclerosus refractory to topical steroids is a therapeutic indication with a small but maturing evidence base — distinct from purely cosmetic applications. ACOG 2020 Committee Opinion No. 795 classifies cosmetic genital procedures as not medically indicated, with safety and effectiveness not established; FIGO 2025 echoes this for cosmetic indications. The therapeutic indications above are not what those positions target. Counsel patients clearly on the therapeutic-vs-cosmetic distinction and document the indication.[4]

Critical safety: rare but reported case of severe pulmonary fat embolism after vaginal fat grafting (Wang 2020) — anatomical knowledge and careful technique are mandatory.[5]

Background — GSM and the limits of standard therapy​

GSM affects the majority of peri- and postmenopausal women and includes vaginal dryness, burning, itching, dyspareunia, urinary urgency / frequency, and recurrent UTIs — driven by estrogen deficiency and progressive vulvovaginal atrophy.[1][6] Standard treatments (topical estrogen, DHEA, ospemifene, moisturizers) are effective but require ongoing therapy to maintain benefit and cannot reverse the underlying atrophic process.[6][7] This limitation has driven interest in regenerative approaches that may provide longer-lasting tissue restoration.[7]

Definitions — macrofat vs microfat vs nanofat​

Fat typeParticle sizeHarvestingProcessingPrimary function
Macrofat> 2 mmStandard liposuction cannulaMinimalVolume restoration (large defects)[1][2]
Microfat~ 100–120 µmSmall multiport cannula (1–2 mm holes)Centrifugation or decantingVolume restoration + moderate regeneration[1][3][8]
NanofatSubmicron (no viable adipocytes)Derived from microfatMechanical emulsification + filtrationTissue regeneration (no volumizing)[1][9]

Microfat uses a multiport cannula with small (0.8–1 mm) side holes, retaining intact adipocytes and providing both volume and regenerative capacity.[8][9]

Nanofat was first described by Tonnard et al. 2013 — produced by mechanical emulsification (vigorous back-and-forth between two syringes via a Luer-lock connector, typically 30 passes) followed by filtration through a nylon mesh. The process destroys all viable adipocytes but preserves abundant adipose-derived stem cells (ADSCs), stromal vascular fraction (SVF) cells, growth factors, and extracellular matrix components. The resulting fluid emulsion can be delivered through fine needles (up to 27-gauge).[9]

Biological rationale and mechanism​

The therapeutic effects extend beyond simple volume replacement:

  • ADSCs. Nanofat contains abundant ADSCs with proliferation and differentiation capacity equivalent to unprocessed fat; multilineage differentiation (adipocyte / osteocyte / chondrocyte) plus highly pluripotent MUSE cells.[9][10]
  • Proteomic profile. Mechanical emulsification of microfat into nanofat upregulates pathways involved in innate immunity, coagulation, wound healing, and antimicrobial defense.[11]
  • Lipidomic profile. Nanofat is enriched in anti-inflammatory, antifibrotic, and antimelanogenic lipid mediators (prostacyclin, coumaric acids) vs microfat.[12]

Histologic effects in vulvovaginal tissue (Lai 2023; Casarotti 2018):[13][3]

  • Neocollagenesis — increased collagen production
  • Neoangiogenesis — new blood-vessel formation
  • Increased estrogen-receptor expression — enhanced local hormonal responsiveness
  • Decreased PGP 9.5 (neuropathic-pain marker)
  • Glycogen production, epithelial regeneration, and restoration of lactobacilli colonization with normalization of vaginal pH (sustained at 36 mo)

Surgical technique​

1. Fat harvesting​

  • Donor sites: abdomen, medial thighs, flanks. No significant difference in fat-cell viability between sites.[1][14]
  • Multiport cannula with small side holes for microfat.[1][14]
  • Local or general anesthesia.

2. Fat processing​

StepDetail
MicrofatCentrifugation typically 3 min at 3,000 rpm, or decanting, to separate fat from aqueous and oil fractions.[14][8]
NanofatMicrofat is mechanically emulsified by passing between two syringes (~ 30 times) and then filtered through nylon mesh. The result is a homogeneous, fluid emulsion.[9]
PRP enrichmentSome protocols add PRP to nanofat to enhance regenerative effects.[14][15]

3. Injection​

Menkes 2021 protocol (the landmark vulvovaginal series):[1]

  • Microfat → labia majora (volume restoration of atrophic / deflated labia majora).
  • Nanofat → vaginal mucosa (submucosal) (tissue regeneration).

Lai 2023 MAFT technique injected an average of 21.9 mL into the vagina and 20.8 mL into the vulva and mons pubis.[13]

Procedure performed under local anesthesia ± sedation as an outpatient procedure.

Clinical evidence​

GSM / vulvovaginal atrophy​

StudynTechniqueFollow-upKey outcomes
Menkes 2021[1]50Microfat (labia) + nanofat (vagina)18 moVHI + FSD significantly improved (p < 0.0001); 80% normalized at 6 mo; stable at 18 mo; particular benefit for dryness and dyspareunia
Casarotti & Tremolada 2020[16]35MFAT (vulvar injection)36 mo99% complete symptom resolution at 9–12 mo; no relapse at 3 years; single injection
Casarotti 2018[3]3MFAT (Lipogems®)36 moComplete symptom resolution at 9 mo; histology — glycogen production, vascular hyperplasia, epithelial regeneration, lactobacilli restoration
Lai 2023 MAFT[13]20MAFT (vulvovaginal)6 moFSFI 43.8 → 68.6 (p < 0.001); histologic neocollagenesis + neoangiogenesis + ER expression
Mantovani 2022[17]12MFAT (SEFFIGYN™)5 moAll symptoms significantly improved (p = 0.001–0.008); all patients resumed sexual life

The Moccia 2023 SR of injection treatments for VVA found that microfat + nanofat + PRP led to significant improvement on VHI and FSDS-R, but MFAT alone did not reach significance on validated questionnaires in the studies assessed.[18]

Positioning vs standard GSM therapies​

TherapyMechanismDurabilityKey advantageKey limitation
Low-dose vaginal estrogenRestores ER signalingContinuous useMost robust evidence; AUA/SUFU/AUGS 2025 first-choice pharmacotherapy[40]Continuous therapy; counseled cautiously in HR+ breast cancer survivors on AIs
Vaginal DHEA (prasterone)Local androgen → estrogen conversionContinuousFDA-approved; improves dryness and dyspareuniaDaily application
OspemifeneOral SERM with vaginal estrogenic effectContinuousOral; non-vaginal routeLimited cancer-safety data
CO₂ / Er:YAG laserMicroablation → collagen remodelingMultiple sessionsNon-hormonal, office-basedInsufficient placebo-controlled data; FDA has not cleared for GSM
Microfat / nanofat / MFATVolumetric + ADSC-mediated regeneration + ER upregulationSingle treatment; up to 36 mo without relapse[16]Autologous; durable single-session; addresses root pathologyNo RCTs; not in any GSM guideline; requires liposuction

The 2025 AUA / SUFU / AUGS guideline retains low-dose vaginal estrogen as the pharmacotherapy with the most robust evidence and frames treatment as individualized shared decision-making.[40] Fat grafting is not yet incorporated into any GSM guideline.

The estrogen paradox in postmenopausal fat grafting​

Treating GSM with fat grafting means transferring autologous adipose between two hypoestrogenic compartments, and the preclinical signals point in opposing directions:

  • Low E2 paradoxically favors volumetric retention. In ovariectomized mice, fat-graft retention was 79% vs 35% in controls — driven by enhanced early macrophage infiltration and adipocyte hypertrophy.[41] Clinically mirrored: elderly low-E2 cohorts retain grafted fat better than young women (AQP-7-mediated adipocyte hypertrophy).[42]
  • But E2 supports ADSC regenerative function. Estradiol-treated ADSCs increased VEGF output and graft survival (77% vs 56%) in nude-mouse models.[43]
  • Postmenopausal ASCs are transcriptomically distinct. RNA-seq shows ~2,299 differentially expressed genes vs premenopausal ASCs, with altered immunoregulation (M1 polarization).[44]
  • Estrogen effects are donor-depot-specific (femoral vs abdominal) and more critical at donor than recipient site.[45]

Net implication: volumetric retention is favored, but the regenerative ceiling may be lower — consistent with the gradual 9–12 month time course to peak symptom resolution observed by Casarotti.[16]

GSM in breast cancer survivors — the highest-unmet-need population​

GSM affects up to 60% of breast cancer survivors and is typically worsened by aromatase-inhibitor (AI) estrogen depletion. NCCN Survivorship and the 2024 Lancet "Managing menopause after cancer" consensus recommend non-hormonal therapies first-line, reserving local estrogen for persistent symptoms after oncology discussion.[46] Fat grafting is mechanistically attractive (autologous, non-hormonal) but two caveats apply:

  • No published study has specifically evaluated fat grafting for GSM in breast cancer survivors.
  • Fat grafting upregulates vaginal-tissue ER expression (Lai 2023) — desired for GSM physiology, but a theoretical safety question for HR+ disease that has not been formally addressed.[13]
  • A pilot of PRP for GSM in breast cancer survivors (n = 20, 65% on AIs) demonstrated 6-mo safety and significant symptom improvement, providing proof of concept for autologous regenerative therapy in this population.[47]

FDA regulatory positioning​

  • Autologous microfat / MFAT (mechanical processing only, no enzymatic digestion): minimally manipulated autologous tissue; falls under the practice of medicine; no FDA premarket approval required.[48]
  • Enzymatically isolated SVF (collagenase digestion): classified by the FDA as more than minimally manipulated; regulated as a 351 HCT/P biological product.[48]
  • Mechanically isolated SVF / nanofat: regulatory gray area — mechanical processing without enzymatic digestion is generally considered minimal manipulation, but the determination is product- and indication-specific.

Vulvar lichen sclerosus (VLS) — refractory to topical steroids​

Rationale​

VLS is a chronic relapsing inflammatory dermatosis with progressive atrophy, stromal hyalinization, decreased microvessel density, and architectural distortion (clitoral burying, labial fusion, introital stenosis, dyspareunia). First-line ultrapotent topical corticosteroids (clobetasol propionate 0.05%) per ACOG 2020 and the 2026 German S3 guideline fail to achieve adequate symptom control in 30–40% of patients, and even responders frequently have persistent scarring, atrophy, and sexual dysfunction.[25][26][27] Adipose-derived stem/stromal cells (ADSCs) directly target the three core pathological processes of VLS — chronic T-cell inflammation, decreased angiogenesis, and excessive fibrogenesis — making fat grafting a mechanistically rational regenerative second-line therapy.[28] For the disease context, see Lichen Sclerosus.

Three-pillar mechanism in VLS​

PillarADSC effectHistologic confirmation in VLS
Anti-fibroticDownregulation of Col-1, Col-3, α-SMA, IL-17, p38/MAPK; mechanical rigottomy disrupts fibrotic bands[28]Reduced stromal hyalinization at 12 mo (Lichen-SVF, p = 0.0036)[19]
Immunomodulatory↓ IL-6, TNF-α, STAT3/STAT6; ↑ IL-10; M1 → M2 macrophage polarization[28]Reduced CD3+ T-cell infiltration (Lichen-SVF, p = 0.0068); decrease in all inflammatory cell types on biopsy in the only RCT[15][19]
Pro-angiogenic↑ VEGF, HGF, bFGF; ADSC → pericyte differentiation[28]Increased microvascular density at 12 mo (Lichen-SVF, p = 0.0121)[19]

Why combine PRP with fat grafting?​

Three of the five VLS series (Tedesco 2020, Gutierrez-Ontalvilla 2022 RCT, Casabona 2023 — totaling 132 of the 166 published patients) used PRP + fat-graft / SVF combinations, on the rationale that platelet α-granule growth factors (PDGF, TGF-β1, VEGF, EGF, IGF-1, FGF) amplify ADSC paracrine activity rather than merely sum with it.[34][35] Preclinical data support a true synergy:

  • Amplified angiogenic output — MSCs cultured with PRP secrete > 4× more VEGF plus increased uPA and ET-1 vs MSCs alone.[36]
  • Enhanced ADSC proliferation and pluripotency — platelet-rich-fibrin extract upregulates NANOG, SOX2, and proliferation markers in ADSCs.[37]
  • Platelet → ADSC mitochondrial transfer restores mitochondrial function, reduces ROS, and improves graft survival under oxidative stress — directly relevant to the chronically inflamed VLS bed.[38]
  • i-PRF directly attenuates VLS fibrosis via TGF-β / SMAD3 pathway inhibition (↓ fibronectin, Col-1) and NF-κB inhibition (↓ IL-17, IFN-γ), with concurrent ↑ CD31 / VEGF expression — providing a stand-alone fibroreductive mechanism that complements the ADSC effects above.[39]

Combination therapy is most beneficial in early-stage disease (Tedesco); in late-stage / heavily hyalinized disease the regenerative ceiling appears lower regardless of PRP enrichment.[20]

Published clinical evidence (~166 patients across 5 series)​

StudyYearDesignnInterventionFollow-upKey outcomes
Boero[29]2015Prospective cohort36Microfat (Coleman)NR94% improved trophism; 75% improved introital caliber; 50% reduced clitoral burying; 95% stopped routine TCS; DLQI / FSFI significantly improved (p < 0.001)
Tedesco[20]2020RCT 1:140AD-SVF vs AD-SVF + PRP6 moBoth arms improved DLQI; combination superior in early-stage; combination discouraged in late-stage disease
Gutierrez-Ontalvilla[15]2022RCT (pilot)20Nanofat + PRP ×2 (q3mo) vs topical clobetasol12 moSignificant improvement in itching, pain, burning, dyspareunia, erosions, fissures, stenosis, leukoderma; biopsy ↓ inflammatory cells; no improvement in skin elasticity; only RCT vs TCS
Casabona[30]2023Retrospective cohort72PRP + fat graftingNRSkindex-29 −31.8; FSFI +7.6; DLQI −9; CSS −24; IGA −4 (all p < 0.001); largest published cohort
Gutierrez-Ontalvilla (Lichen-SVF)[19]2025Prospective open-label18Nanofat 40 mL + mechanically isolated SVF 2–3 mL, single treatment12 moCSS Symptoms 20.1 → 4.7 (p = 0.003); CSS Signs 5.8 → 2.0 (p = 0.001); 5D Itch 6.8 → 2.4 (p = 0.014); Skindex-29 42.9 → 24.8 (p = 0.031); FSFI non-significant; histologic reversal of hyalinization, T-cell infiltration, microvascular density

Comparison with other approaches for refractory VLS​

ApproachInvasivenessLargest nKey advantageKey limitation
Fat grafting ± PRP / SVFMinimal72Targets inflammation and fibrosis directly; repeatable; favorable safetyDoes not improve skin elasticity; limited long-term data; less effective late-stage[15][20]
PRP monotherapyMinimal50Reduces TCS need ~42%; improves elasticity / colorNo volume restoration; limited durability[31]
Nd:YAG / Er:YAG laserMinimal44Superior clinical-score improvement vs TCS at 6 mo (RCT)No long-term data; multiple sessions; does not address tissue loss[32]
Perineoplasty / de-adhesionModerateVariableAddresses introital stenosis, labial adhesionsDoes not treat underlying disease; variable durability
aOAP flap (O'Dey)High61Definitive tissue replacement; significant dyspareunia reductionMajor surgery; higher complication risk in LS tissue[33]

See also Vulvar Reconstruction and the aOAP Flap atlas page.

Positioning and unanswered questions​

  • Not yet in formal guidelines. ACOG 2020 and the 2026 German S3 guideline keep ultrapotent TCS first-line and topical calcineurin inhibitors second-line; fat grafting remains investigational for refractory disease.[25][26]
  • Complementary, not curative. The Lichen-SVF protocol maintained low-dose TCS throughout follow-up; positioning is adjunctive rather than replacement.[19]
  • Therapeutic window. Combination SVF + PRP was less effective in late-stage disease (Tedesco) and elasticity did not improve in the only RCT (Gutierrez-Ontalvilla 2022) — suggesting established structural fibrosis is not fully reversible and earlier intervention may yield better results.[15][20]
  • Malignancy surveillance unchanged. VLS carries a 4–7% lifetime SCC risk; whether fat grafting modifies this is unknown. Continued biopsy of suspicious lesions remains essential regardless of regenerative therapy.[25]
  • Open questions. Standardized protocol (microfat vs nanofat vs SVF; volumes; sessions); durability beyond 12 mo; head-to-head trials vs PRP monotherapy and vs laser.

Duration of effect — a defining advantage​

The most striking feature compared to other vaginal-injection treatments is durability:

  • 18 mo — stable in all patients with further FSD improvement between 12 and 18 mo (Menkes 2021).[1]
  • 36 mo — 99% maintained complete symptom resolution with no relapse after a single injection (Casarotti 2020). Histology at 36 mo confirmed sustained tissue regeneration.[16][3]

This long-lasting effect is attributed to the regenerative mechanism (tissue remodeling, neovascularization, stem-cell engraftment) rather than a simple filler effect, distinguishing it from HA-based approaches that require repeat injections every 9–12 mo.[16][3]

Comparison with other vaginal-injection treatments for GSM​

AgentMechanismVolume effectRegenerative effectDurationSessions
Microfat + nanofatVolume + ADSC-mediated regenerationYes (microfat)Strong (nanofat)Up to 36 moUsually single[1][16]
Cross-linked HAVolume + mild tissue stimulationYesModerate (collagen mRNA upregulation)9–12 moRepeat[18]
PRPGrowth-factor-mediated regenerationNoModerateVariableMultiple[18]
MFAT (Lipogems®)Volume + regenerationModerateStrongUp to 36 moSingle[16][3]
CollagenVolume + analgesicMildMild3–6 moMultiple[21]

Complications and safety​

Generally favorable. No major side effects in the published GSM / VLS series.[1][13][19]

Minor complications (common)​

  • Ecchymosis at donor and recipient sites
  • Transient tenderness and swelling
  • Mild pain at injection sites[22]

Potential serious complications (rare but consequential)​

  • Fat embolism (most serious). Wang 2020 case report of severe pulmonary fat embolism after vaginal fat grafting — fat presumably injected directly into perivaginal vessels. The most critical safety concern; underscores the importance of anatomical knowledge and careful injection technique.[5]
  • GRAFT registry (n = 7,052 fat-grafting procedures across all body sites): overall complication rate 5.01%; rates of palpable mass, infection, granuloma, oil cyst all low.[23]
  • Vascular embolism is the principal serious risk of vaginal-wall injection and must be actively prevented.[24]
  • No infections, fat cysts, granulomas, or lipoma formation reported in the nanofat-specific vulvovaginal series.[1][13][9]

Advantages and limitations​

Advantages

  • Autologous material — no allergic / foreign-body reactions.
  • Dual mechanism: volume restoration (microfat) + tissue regeneration (nanofat).
  • Long-lasting results (up to 3 years documented) with a single treatment session.
  • Histologically confirmed reversal of atrophic changes — not just symptom palliation.
  • Applicable to both GSM and refractory VLS.

Limitations

  • Requires a donor-site procedure (liposuction) — additional surgical complexity and morbidity.
  • Not suitable for patients with very low body fat.
  • Evidence base is observational studies and small case series (Level III–IV); no large RCTs specifically for GSM.
  • Variable fat-graft survival; unpredictable resorption.
  • Risk of fat embolism, although extremely rare.[5]
  • Lack of standardized protocols — volumes, processing methods, and injection sites vary across studies.
  • ACOG 2020 and FIGO 2025 classify cosmetic genital procedures as not medically indicated. The GSM / VLS-refractory therapeutic context is distinct, but counseling must clearly distinguish.[4]

Emerging directions​

  • SVF-enriched nanofat (Lichen-SVF protocol) for VLS with histologically confirmed anti-inflammatory and regenerative effects.[19]
  • Nanofat + PRP combinations for early-stage VLS.[15][20]
  • Proteomic and lipidomic profiling of nanofat to identify specific bioactive mediators responsible for regenerative effects.[11][12]
  • ADSC-enriched nanofat with higher pluripotent (MUSE) stem-cell content.[10]

Key takeaways​

  • Microfat / nanofat grafting may reverse the underlying atrophic process in GSM, vulvovaginal atrophy, and refractory VLS — a fundamentally different mechanism from HA / topical estrogen / topical steroids.[1][3][19]
  • Longest follow-up data (36 mo) suggest durable single-session results with histologic evidence of tissue regeneration including neocollagenesis, neoangiogenesis, and restoration of vaginal flora.[16][3]
  • Therapeutic vs cosmetic distinction matters — the strongest evidence is for GSM and VLS-refractory disease, not for cosmetic enhancement in healthy women. Document indication accordingly.
  • Evidence remains small observational studies; fat embolism is the dominant safety concern despite its rarity.[5]
  • Larger RCTs are needed to standardize protocols and confirm long-term safety.

Postoperative management​

  • Activity restriction. Avoid intercourse, tampon use, and strenuous exercise for 2–4 weeks; protect donor site per general lipofilling protocol.
  • Donor-site care. Compression at donor site; avoid pressure on recipient site so as not to compress the graft.
  • Wound care. Ice 48–72 h; loose-fitting clothing; antibiotic ointment to donor incisions.
  • Follow-up. 1 week, 6 weeks, 6 months, 12 months, with VHI / FSFI / FSD as relevant; some series have extended to 18–36 months.
  • Counseling on durability. Counsel that regenerative effects may continue to emerge between 6 and 18 months — early follow-up does not capture the full effect.

See Also​

References​

1. Menkes S, SidAhmed-Mezi M, Meningaud JP, et al. Microfat and nanofat grafting in genital rejuvenation. Aesthet Surg J. 2021;41(9):1060–1067. doi:10.1093/asj/sjaa118

2. Ding P, Lu E, Li G, et al. Research progress on preparation, mechanism, and clinical application of nanofat. J Burn Care Res. 2022;43(5):1140–1144. doi:10.1093/jbcr/irab250

3. Casarotti GA, Chiodera P, Tremolada C. Menopause: new frontiers in the treatment of urogenital atrophy. Eur Rev Med Pharmacol Sci. 2018;22(2):567–574. doi:10.26355/eurrev_201801_14211

4. Committee on Gynecologic Practice, American College of Obstetricians and Gynecologists. Elective female genital cosmetic surgery: ACOG Committee Opinion No. 795. Obstet Gynecol. 2020;135(1):e36–e42. doi:10.1097/AOG.0000000000003616

5. Wang C, Wang X, Huang J, Yu N, Long X. Severe fat embolism after autologous fat grafting in vaginal tightening and breast augmentation surgery. J Int Med Res. 2020;48(8):300060520949109. doi:10.1177/0300060520949109

6. Capito L, Antsaklis A, Gupte S. FIGO Statement: cosmetic genital surgery. Int J Gynaecol Obstet. 2025;170(1):11–14. doi:10.1002/ijgo.70203

7. Kamat P, Frueh FS, McLuckie M, et al. Adipose tissue and the vascularization of biomaterials: stem cells, microvascular fragments and nanofat — a review. Cytotherapy. 2020;22(8):400–411. doi:10.1016/j.jcyt.2020.03.433

8. Yang Z, Jin S, He Y, et al. Comparison of microfat, nanofat, and extracellular matrix/stromal vascular fraction gel for skin rejuvenation: basic research and clinical applications. Aesthet Surg J. 2021;41(11):NP1557–NP1570. doi:10.1093/asj/sjab033

9. Tonnard P, Verpaele A, Peeters G, et al. Nanofat grafting: basic research and clinical applications. Plast Reconstr Surg. 2013;132(4):1017–1026. doi:10.1097/PRS.0b013e31829fe1b0

10. Quintero Sierra LA, Biswas R, Conti A, et al. Highly pluripotent adipose-derived stem cell-enriched nanofat: a novel translational system in stem cell therapy. Cell Transplant. 2023;32:9636897231175968. doi:10.1177/09636897231175968

11. Sanchez-Macedo N, McLuckie M, Grünherz L, Lindenblatt N. Protein profiling of mechanically processed lipoaspirates: discovering wound healing and antifibrotic biomarkers in nanofat. Plast Reconstr Surg. 2022;150(2):341e–354e. doi:10.1097/PRS.0000000000009345

12. Grünherz L, Kollarik S, Sanchez-Macedo N, McLuckie M, Lindenblatt N. Lipidomic analysis of microfat and nanofat reveals different lipid mediator compositions. Plast Reconstr Surg. 2024;154(5):895e–905e. doi:10.1097/PRS.0000000000011335

13. Lai YW, Wu SH, Chou PR, et al. Autologous fat grafting in female genital area improves sexual function by increasing collagenesis, angiogenesis, and estrogen receptors. Aesthet Surg J. 2023;43(8):872–884. doi:10.1093/asj/sjad040

14. Strong AL, Cederna PS, Rubin JP, Coleman SR, Levi B. The current state of fat grafting: a review of harvesting, processing, and injection techniques. Plast Reconstr Surg. 2015;136(4):897–912. doi:10.1097/PRS.0000000000001590

15. Gutierrez-Ontalvilla P, Giner F, Vidal L, Iborra M. The effect of lipofilling and platelet-rich plasma on patients with moderate-severe vulvar lichen sclerosus who were non-responders to topical clobetasol propionate: a randomized pilot study. Aesthet Plast Surg. 2022;46(5):2469–2479. doi:10.1007/s00266-021-02718-1

16. Casarotti G, Tremolada C. A new treatment of genito-urinary post-menopausal atrophy with autologous micro-fragmented fat tissue: a thirty-six months follow-up case series. Eur Rev Med Pharmacol Sci. 2020;24(13):7420–7426. doi:10.26355/eurrev_202007_21910

17. Mantovani M, Gennai A, Russo PR. A new approach to regenerative medicine in gynecology. Int J Gynaecol Obstet. 2022;157(3):536–543. doi:10.1002/ijgo.13906

18. Moccia F, Pentangelo P, Ceccaroni A, et al. Injection treatments for vulvovaginal atrophy of menopause: a systematic review. Aesthet Plast Surg. 2023;47(6):2788–2799. doi:10.1007/s00266-023-03550-5

19. Gutierrez-Ontalvilla P, Gomez Rojas A, Iborra Colomino M, et al. Clinical and histopathological investigation of stromal vascular fraction and nanofat in vulvar lichen sclerosus. Aesthet Surg J. 2025;sjaf148. doi:10.1093/asj/sjaf148

20. Tedesco M, Bellei B, Garelli V, et al. Adipose tissue stromal vascular fraction and adipose tissue stromal vascular fraction plus platelet-rich plasma grafting: new regenerative perspectives in genital lichen sclerosus. Dermatol Ther. 2020;33(6):e14277. doi:10.1111/dth.14277

21. Borobia Pérez AI, Estévez Espejo JJ, Jiménez-González M, García López RD. Vulvovaginal collagen injection as a regenerative strategy in genitourinary syndrome of menopause: results of a pilot study. J Clin Med. 2026;15(4):1408. doi:10.3390/jcm15041408

22. Cihantimur B, Aglamis O, Ozsular Y. 360 genital fat transfer. Aesthet Plast Surg. 2021;45(6):2996–3002. doi:10.1007/s00266-021-02488-w

23. Kaur S, Rubin JP, Gusenoff J, et al. The General Registry of Autologous Fat Transfer: concept, design, and analysis of fat grafting complications. Plast Reconstr Surg. 2022;149(6):1118e–1129e. doi:10.1097/PRS.0000000000009162

24. Zheng Z, Yin J, Cheng B, Huang W. Materials selection for the injection into vaginal wall for treatment of vaginal atrophy. Aesthet Plast Surg. 2021;45(3):1231–1241. doi:10.1007/s00266-020-02054-w

25. Committee on Practice Bulletins–Gynecology. Diagnosis and management of vulvar skin disorders: ACOG Practice Bulletin No. 224. Obstet Gynecol. 2020;136(1):e1–e14. doi:10.1097/AOG.0000000000003944

26. Kirtschig G, Woelber L, Günthert A, et al. Evidence- and consensus-based guideline on lichen sclerosus. J Dtsch Dermatol Ges. 2026;24(4):566–584. doi:10.1111/ddg.70000

27. Brodrick B, Belkin ZR, Goldstein AT. Influence of treatments on prognosis for vulvar lichen sclerosus: facts and controversies. Clin Dermatol. 2013;31(6):780–786. doi:10.1016/j.clindermatol.2013.05.017

28. van der Sluis N, Scheers ECAH, Krenning G, et al. Autologous lipoaspirate as a new treatment of vulvar lichen sclerosus: a review of the literature. Exp Dermatol. 2022;31(5):689–699. doi:10.1111/exd.14561

29. Boero V, Brambilla M, Sipio E, et al. Vulvar lichen sclerosus: a new regenerative approach through fat grafting. Gynecol Oncol. 2015;139(3):471–475. doi:10.1016/j.ygyno.2015.10.014

30. Casabona F, Gasparini G, Cozzani E, et al. Improvement in quality of life and sexual function in patients affected by vulvar lichen sclerosus treated with combined autologous platelet-rich plasma and fat grafting. Eur J Dermatol. 2023;33(3):249–254. doi:10.1684/ejd.2023.4480

31. Boero V, Cetera GE, Caia C, et al. Is there a role for platelet-rich plasma injection in vulvar lichen sclerosus? A self-controlled pilot study. Arch Gynecol Obstet. 2024;309(6):2719–2726. doi:10.1007/s00404-024-07424-2

32. Zivanovic I, Gamper M, Fesslmeier D, et al. Nd:YAG/Er:YAG dual laser compared with topical steroid to treat vulvar lichen sclerosus: a randomised controlled trial. BJOG. 2024;131(6):740–749. doi:10.1111/1471-0528.17737

33. O'Dey DM, Rosendahl M, Mordehay D, Kameh Khosh M. Anterior obturator artery perforator (aOAP) flap: a last-resort treatment option for sexual dysfunction in lichen sclerosus et atrophicus. J Plast Reconstr Aesthet Surg. 2024;95:331–339. doi:10.1016/j.bjps.2024.05.046

34. Tobita M, Tajima S, Mizuno H. Adipose tissue-derived mesenchymal stem cells and platelet-rich plasma: stem cell transplantation methods that enhance stemness. Stem Cell Res Ther. 2015;6:215. doi:10.1186/s13287-015-0217-8

35. Tatsis D, Vasalou V, Kotidis E, et al. The combined use of platelet-rich plasma and adipose-derived mesenchymal stem cells promotes healing: a review of experimental models and future perspectives. Biomolecules. 2021;11(10):1403. doi:10.3390/biom11101403

36. Myung H, Jang H, Myung JK, et al. Platelet-rich plasma improves the therapeutic efficacy of mesenchymal stem cells by enhancing their secretion of angiogenic factors in a combined radiation and wound injury model. Exp Dermatol. 2020;29(2):158–167. doi:10.1111/exd.14042

37. Wachtel N, Weber L, Moellhoff N, et al. Platelet-rich fibrin mediates beneficial effects on adipose-derived stem cells via increased levels of key cytokines. Wound Repair Regen. 2025;33(3):e70040. doi:10.1111/wrr.70040

38. Ke C, Liu K, Chen W, et al. Platelets facilitate fat grafting by mitochondrial transfer and reducing oxidative stress in adipose-derived stem cells. Stem Cells Transl Med. 2025;14(11):szaf059. doi:10.1093/stcltm/szaf059

39. Sun SH, Fan HH, Wang XW, Bing BD, Hu YJ. Platelet-rich fibrin attenuates inflammation and fibrosis in vulvar lichen sclerosus via the TGF-β/SMAD3 pathway. Arch Dermatol Res. 2025;317(1):360. doi:10.1007/s00403-025-03811-0

40. Kaufman MR, Ackerman AL, Amin KA, et al. The AUA/SUFU/AUGS guideline on genitourinary syndrome of menopause. J Urol. 2025;214(3):361–371. doi:10.1097/JU.0000000000004589

41. Mok H, Feng J, Hu W, et al. Decreased serum estrogen improves fat graft retention by enhancing early macrophage infiltration and inducing adipocyte hypertrophy. Biochem Biophys Res Commun. 2018;501(1):266–272. doi:10.1016/j.bbrc.2018.04.232

42. Xie W, Li F, Zhang Y, et al. Elderly women have a higher survival rate of grafted donor fat than do young women under the influence of low-estrogen conditions. Aesthet Plast Surg. 2024;48(15):2879–2886. doi:10.1007/s00266-024-04095-x

43. Luo S, Hao L, Li X, et al. Adipose tissue-derived stem cells treated with estradiol enhance survival of autologous fat transplants. Tohoku J Exp Med. 2013;231(2):101–110. doi:10.1620/tjem.231.101

44. Xie Y, Fang B, Liu W, et al. Transcriptome differences in adipose stromal cells derived from pre- and postmenopausal women. Stem Cell Res Ther. 2020;11(1):92. doi:10.1186/s13287-020-01613-x

45. Bills JD, Derderian C, Barker J, et al. The role of estrogen in the modulation of autologous fat graft outcomes. Plast Reconstr Surg. 2015;135(1):103e–113e. doi:10.1097/PRS.0000000000000792

46. Hickey M, Basu P, Sassarini J, et al. Managing menopause after cancer. Lancet. 2024;403(10430):984–996. doi:10.1016/S0140-6736(23)02802-7

47. Chen AH, Trabuco EC, Chumsri S, et al. Platelet-rich plasma for genitourinary syndrome of menopause in breast cancer survivors. Obstet Gynecol. 2025;Online ahead of print. doi:10.1097/AOG.0000000000006081

48. Rohrich RJ, Wan D. Making sense of stem cells and fat grafting in plastic surgery: the hype, evidence, and evolving U.S. Food and Drug Administration regulations. Plast Reconstr Surg. 2019;143(2):417e–424e. doi:10.1097/PRS.0000000000005207