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Nasolabial fold

The nasolabial fold is a bilateral skin crease extending from the side of the nose, near the alar base, to the corner of the mouth, forming a natural contour that becomes visible during facial expressions like smiling and more permanent with age.^[1] This fold is defined anatomically by underlying structures that support the buccal fat pad, including muscle insertions and connective tissues, which create a demarcation between the malar and nasolabial fat compartments.^[2] Anatomically, the nasolabial fold arises from the insertion points of several mimetic muscles into the dermis along its course, including the levator labii superioris alaeque nasi medially, the levator labii superioris and zygomaticus minor in the middle third, and the zygomaticus major and levator anguli oris laterally, with the orbicularis oris blending at the oral margin.^[3] These muscles, originating from the zygomatic bone and maxilla, elevate the upper lip and modulate the fold's depth during expressions, while ligaments such as the lateral and medial maxillary ligaments anchor the skin and superficial musculoaponeurotic system (SMAS) to the underlying bone, contributing to structural integrity.^[4] The fold's formation is further influenced by compartmentalized facial fat pads: the nasolabial fat compartment above the fold tends to hypertrophy with age, contrasting with the atrophy of the buccal fat below, which accentuates the crease through volume differential and gravitational descent.^[2] Nasolabial folds are ubiquitous across all races and genders, initially appearing as dynamic lines during youth but progressing to static wrinkles due to progressive loss of collagen and elastin, flattening of cheekbones, and cumulative effects of sun exposure or smoking that degrade skin elasticity.^[1] Three primary morphological types are recognized based on etiology: type 1 involving paranasal volume deficiency, type 2 characterized by sagging nasolabial fat laxity, and type 3 resulting from muscular hyperkinesis.^[4] This structure not only serves as a key element in the smiling mechanism but also represents a critical boundary in facial aesthetics and reconstructive surgery, highlighting its role in both physiological expression and age-related changes.^[3]

Anatomy

Structure and location

The nasolabial fold is defined as the oblique cutaneous groove extending bilaterally from the ala of the nose to the corner of the mouth on each side of the face.^[2] This natural feature demarcates the boundary between the cheek and the upper lip, serving as a visible landmark in facial anatomy.^[5] At the surface level, the nasolabial fold manifests as a crease formed by the folding of the skin over underlying connective tissues and muscle attachments, with a typical length of approximately 4–5 cm in adults.^[6] Its composition primarily involves the dermis and epidermis, influenced by the tethering of superficial musculoaponeurotic system (SMAS) layers to deeper structures.^[2] Prominence of the nasolabial fold varies across ethnic groups, often appearing more pronounced in individuals of Caucasian descent compared to those of African or Asian ancestry, attributable to differences in dermal thickness, subcutaneous fat distribution, and collagen density.^[7] For instance, Caucasian skin tends to exhibit greater fold depth and visibility due to relatively thinner dermal layers and reduced protective pigmentation.^[8]

Associated structures

The nasolabial fold is primarily accentuated by the actions of several key mimetic muscles that insert into the overlying skin and superficial musculoaponeurotic system (SMAS). The levator labii superioris alaeque nasi originates from the frontal process of the maxilla and nasal bone, inserting into the skin of the upper lip near the fold, where it elevates the upper lip and ala of the nose during smiling, thereby deepening the fold by creating a relative concavity below the muscle insertion.^[2] The zygomaticus minor arises from the zygomatic bone and inserts into the upper lip lateral to the fold, contributing to the elevation of the upper lip and accentuation of the fold's contour during smiling through its musculocutaneous attachments.^[9] Similarly, the zygomaticus major, originating from the zygomatic bone, inserts into the modiolus at the corner of the mouth but influences the fold by pulling the overlying skin laterally and superiorly during smiling, enhancing fold visibility via integration with the SMAS.^[2] The soft tissue layers supporting the nasolabial fold include distinct superficial fat compartments that contribute to its contour. The malar fat pad, a triangular structure with its base along the fold and apex at the zygoma, overlies the zygomaticus major and levator labii superioris muscles, providing volume to the cheek and influencing fold prominence through its attachments.^[10] The nasolabial fat compartment, located lateral to the nasolabial crease, forms a bulging pad that directly contributes to the fold's raised appearance, separated from deeper layers by fibrous septa within the SMAS.^[11] Retaining ligaments, such as the zygomatic ligaments anchoring the malar fat to the periosteum and the mandibular ligament securing lower facial tissues, stabilize these compartments and limit soft tissue descent, with dermis attachment points occurring via dense fibrous connections from the SMAS to the undersurface of the skin along the fold.^[11] The vascular supply to the nasolabial fold region arises from branches of the facial artery and vein, including the superior labial artery and vein, which provide perfusion to the upper lip and adjacent fold, as well as the infraorbital artery and vein emerging from the infraorbital foramen to nourish the cheek and midface.^[12] Innervation is primarily sensory via the infraorbital nerve, a terminal branch of the maxillary division of the trigeminal nerve, which exits the infraorbital foramen and supplies sensation to the skin, mucosa, and muscles around the fold.^[12] In cosmetic procedures such as dermal fillers or thread lifts targeting the fold, risks include injury to these vessels, potentially leading to vascular occlusion, tissue necrosis, or embolism if injectables enter arterial branches like the infraorbital or facial artery.^[13] Histologically, the dermis underlying the nasolabial fold consists of dense collagen bundles oriented perpendicular to the fold's axis, forming a supportive framework that integrates with the SMAS through fibrous septa, while elastin fibers form a loose network in the papillary dermis that provides baseline elasticity but decreases with age.^[14] This composition, including type I collagen predominant in the reticular dermis and interwoven elastic fibers, anchors the skin to deeper structures and defines the fold's structural integrity at rest.^[14]

Causes and development

Primary factors

The formation of nasolabial folds begins primarily through repetitive facial expressions, such as smiling, laughing, and chewing, which repeatedly crease the skin between the nose and mouth, leading to the development of dynamic lines that can evolve into more permanent grooves starting in the 20s and 30s. During these expressions, muscles like the levator labii superioris contract, pulling the skin and creating tissue expansion pressure that accentuates the fold's concavity below and fat prominence above. Over time with consistent repetition, these movements leave imprints on the skin, making the lines visible even at rest.^[2]^[15]^[4] Genetic predisposition plays a significant role in the initial visibility and depth of nasolabial folds by influencing inherited traits such as skin elasticity and subcutaneous fat distribution patterns. Genome-wide association studies in populations like Japanese women have identified specific genetic variants associated with nasolabial wrinkle morphology, suggesting that certain individuals are prone to earlier or more pronounced fold development due to these hereditary factors. More recent genome-wide association studies, including one in 2025, have identified additional genetic variants associated with nasolabial fold morphology, further supporting hereditary influences.^[16]^[17]^[18]^[19] Environmental influences, particularly ultraviolet (UV) exposure and smoking, accelerate the early breakdown of skin components, enhancing nasolabial fold visibility through mechanisms like collagen degradation and impaired dermal support. Chronic UV exposure from sun damage induces photodamage that thins the epidermis, reduces elasticity, and directly breaks down collagen fibers in the dermis, leading to increased wrinkling in areas like the nasolabial groove as observed in comparative studies across skin types. Similarly, smoking compromises dermal blood flow via vasoconstriction and oxidative stress, altering skin thickness, density, and surface characteristics to promote fold formation, with biophysical assessments showing measurable impacts on nasolabial areas in smokers.^[20]^[21]^[22] Anatomical variations further contribute to the baseline prominence of nasolabial folds, with factors such as thinner skin in certain facial types or midface hypoplasia creating inherent structural vulnerabilities. Individuals with thinner superficial musculoaponeurotic system (SMAS) layers around the nose, cheeks, and jawline experience less resilient tissue support, allowing folds to appear more defined even without external stressors. Midface hypoplasia, characterized by paranasal volume deficiency or underdeveloped maxillary structures, results in hollowing and shadowing that accentuates the fold's depth, as seen in classifications of fold types driven by differential tissue laxity or volume discrepancies.^[2]^[4]

Role in aging

The nasolabial fold, initially a dynamic crease formed by the contraction of facial muscles during smiling, undergoes progressive deepening with chronological aging, transitioning into a more permanent static feature due to cumulative structural changes in the skin, fat, muscle, and bone of the midface.^[1] This evolution typically becomes noticeable in the third decade of life and intensifies by midlife, contributing to a perceptibly aged facial appearance as the fold loses its transient nature and persists at rest.^[15] A primary driver of nasolabial fold deepening is the degradation of collagen and elastin in the dermal layer, which compromises skin elasticity and support. After age 20, collagen production declines by approximately 1% annually, accompanied by increased enzymatic breakdown, resulting in skin thinning, laxity, and enhanced fold prominence by the fourth or fifth decade.^[23] Elastin synthesis similarly decreases sharply after age 40, leading to fragmented elastic fibers that fail to recoil the skin effectively, exacerbating the gravitational pull on the nasolabial region.^[15] These changes collectively reduce the skin's ability to resist deformation, transforming subtle expression lines into etched creases.^[24] Midface volume loss further accentuates the nasolabial fold through the descent of malar fat pads and resorption of underlying maxillary bone. Beginning in the 30s, deflation of the deep medial cheek and buccal fat compartments diminishes structural support, allowing soft tissues to migrate inferiorly and deepen the fold under gravity.^[15] Concurrently, maxillary bone resorption, which accelerates after age 40, reduces midface projection and creates a pseudojowl effect, pulling overlying skin into sharper nasolabial contours.^[25] This volumetric and skeletal attrition shifts the fold from a superficial expression line to a pronounced trough by midlife.^[26] Weakening of the mimetic muscles, including the levator labii superioris and zygomaticus major, contributes to reduced tensile support around the nasolabial fold as aging progresses. Muscle atrophy and diminished contractility, evident by the fifth decade, allow the skin envelope to sag without adequate counteraction, rendering the fold increasingly static rather than responsive to facial expressions.^[15] This loss of muscular tone compounds the effects of dermal and volumetric changes, promoting persistent fold visibility even in repose.^[27] In women, hormonal influences during menopause around age 50 amplify these processes through estrogen decline, which accelerates dermal thinning and collagen fragmentation. Postmenopausal hypoestrogenism reduces skin collagen content by up to 30% in the first five years, heightening nasolabial fold depth via diminished hydration and elasticity.^[28] This estrogen-mediated exacerbation interacts with baseline genetic predispositions to modulate the rate of fold progression in aging.^[15]

Clinical significance

Appearance and perception

Nasolabial folds typically manifest as shallow, dynamic lines in younger individuals, becoming visible primarily during facial expressions like smiling due to contractions of the levator labii superioris muscle. As people age, these lines evolve into deeper, static creases that persist at rest, often etching into the skin by the 30s and becoming more pronounced through the 50s owing to reduced skin elasticity, fat redistribution, and repetitive muscle activity. Upper nasolabial fold changes initiate in the thirties and progress until the fifties, while lower fold alterations peak between the forties and sixties.^[18] These folds frequently exhibit asymmetry, influenced by habitual behaviors such as preferential chewing or sleeping on one side, which can accentuate one fold over the other. In terms of gender differences, nasolabial folds appear more noticeable and severe in men, attributed to thicker dermal layers and earlier volumetric changes starting around age 35, compared to women who experience later intensification in color depth and area after the mid-40s.^[29]^[18] Culturally, nasolabial folds are commonly viewed as indicators of aging and maturity in Western societies, where they contribute to perceptions of reduced attractiveness and health. Across diverse ethnic groups, wrinkles including nasolabial folds serve as the primary predictors of estimated age, though acceptance varies; for instance, differential emphasis on facial aging signs exists in Asian populations, where other features like periorbital changes may garner more attention. The psychological ramifications include an association with perceived older age, which studies link to diminished self-esteem, particularly among women over 40, as deeper folds heighten negative trait inferences in social evaluations.^[30]^[7]^[31]

Associated conditions

In conditions involving facial volume loss, such as HIV-associated lipodystrophy syndrome, subcutaneous fat atrophy leads to a skeletal appearance with prominent and deepened nasolabial folds, often accompanied by concave cheeks and visible musculature.^[32] This syndrome, linked to antiretroviral therapy, exacerbates fold depth through midface ptosis and perioral rhytids, contributing to a hollowed facial contour.^[33] Neurological disorders can alter nasolabial fold appearance through muscle dysfunction. In Bell's palsy, unilateral facial nerve paralysis results in deepened folds on the affected side due to unopposed muscle pull and subsequent synkinesis, where aberrant reinnervation causes increased resting tone and fold prominence during recovery.^[34] Conversely, systemic sclerosis (scleroderma) causes skin tightening and fibrosis, leading to a taut, mask-like facies with smoothing or obliteration of nasolabial folds as normal expression lines diminish.^[35] Dental factors, including malocclusion and tooth loss, can produce asymmetric nasolabial folds by altering the pull of facial muscles like the zygomaticus major and levator labii superioris, resulting in uneven soft tissue support and fold depth.^[36] For instance, unilateral tooth loss or Class III malocclusion may shift midline structures, accentuating fold asymmetry through compensatory muscle hyperactivity.^[37] Rare connective tissue disorders, such as the musculocontractural type of Ehlers-Danlos syndrome, feature deepened nasolabial folds due to inherent skin and collagen fragility, often presenting with prominent folds alongside hypertelorism and thin vermilion borders on clinical examination.^[38]

Diagnosis and classification

Assessment techniques

Assessment of the nasolabial fold in clinical settings begins with a thorough physical examination, which involves visual observation of the fold at rest and during facial animation, such as smiling, to evaluate its depth, length, and dynamic changes.^[39] Palpation is performed to assess the fold's depth and tissue firmness, allowing clinicians to differentiate between superficial skin laxity and deeper structural changes.^[40] Standardized grading scales, such as the Merz Nasolabial Fold Scale—a validated 5-point photonumeric scale ranging from 0 (no wrinkle) to 4 (deeply furrowed)—are commonly applied to quantify severity objectively and reproducibly.^[41] Patient history plays a crucial role in contextualizing the assessment, with clinicians querying factors like smoking history, which accelerates collagen degradation and deepens folds, chronic sun exposure that promotes photoaging and elastin loss, and family traits indicative of genetic predisposition to early fold prominence.^[22]^[42]^[43] These elements help identify modifiable risk factors and inherent susceptibilities without altering the direct evaluation of the fold itself. Photographic documentation is essential for baseline and longitudinal tracking, utilizing standardized protocols with consistent lighting (e.g., diffuse frontal illumination at 45-degree angles), patient positioning (neutral expression, Frankfort horizontal plane alignment), and camera settings to ensure reproducible images that capture fold contours accurately.^[44] This method facilitates comparison over time and supports grading scale application by minimizing variability from shadows or poses.^[45] Advanced imaging modalities, such as high-frequency ultrasound, are occasionally employed to visualize subcutaneous fat pads and dermal thickness in the nasolabial region, providing quantitative data on tissue layers without radiation exposure.^[46] Magnetic resonance imaging (MRI) can assess deeper structures like ligament integrity and dynamic fold movement, though its use is limited to research or complex cases due to high cost and limited accessibility in routine practice.^[47] These techniques complement but do not replace standard clinical evaluation.

Types of nasolabial folds

Nasolabial folds are classified into three primary types based on their underlying etiology and anatomical features, enabling a structured approach to understanding their development and implications. This categorization—skeletal, ligamentous, and cutaneous/muscular—highlights distinct mechanisms, from structural deficiencies to soft tissue dynamics.^[2] Type 1 (skeletal) arises from maxillary retrusion or midface skeletal deficiency, often congenital and resulting in paranasal volume loss that accentuates the fold through recession of the maxillary canine fossa or overall midface hypoplasia. These folds manifest as persistent depressions due to inadequate bony support, independent of soft tissue changes. Assessment relies on cephalometric analysis to quantify skeletal parameters, such as the nasolabial angle, which reflects maxillary positioning.^[48]^[49]^[50] Type 2 (ligamentous) develops from weakening or attenuation of facial retaining ligaments, particularly McGregor's patch (the zygomatic ligament complex) and mandibular ligaments, which anchor midface soft tissues to the underlying skeleton. This laxity permits descent of the malar fat pad and overlying skin, creating a sagging contour that deepens the fold, typically emerging in early aging as ligamentous integrity declines. It often presents as a hybrid with skin sagging elements.^[51]^[52] Type 3 (cutaneous/muscular) stems primarily from skin laxity due to collagen and elastin degradation or hyperdynamic activity of perioral muscles, such as the levator labii superioris alaeque nasi, which insert into the dermis and create creasing through repetitive motion like smiling. These folds emphasize superficial tissue changes, appearing as fine lines that may progress to static grooves with cumulative use.^[2]^[53] Clinical differentiation involves dynamic evaluation (observing fold prominence during facial animation) versus static assessment (at rest), with Type 1 and Type 2 typically static and ligament- or bone-driven, while Type 3 shows pronounced dynamism; this aids precise etiological identification without overlapping with broader causative factors.^[2]^[52]

Management and treatment

Non-surgical options

Non-surgical options for addressing prominent nasolabial folds primarily involve minimally invasive procedures and topical therapies aimed at restoring volume, stimulating collagen production, and improving skin texture without requiring incisions. These treatments are typically performed in outpatient settings and offer reversible results with lower risks compared to surgical interventions.^[54] Dermal fillers, particularly hyaluronic acid-based products such as Juvederm, are commonly used to restore lost volume in the nasolabial folds by injecting the gel-like substance into the mid-to-deep dermis. This approach plumps the area, softening the fold's appearance, with clinical studies demonstrating significant improvement in fold severity for up to 18-21 months following optimal repeat treatments. Injection techniques, including fanning—where the filler is distributed in a fan-like pattern from multiple entry points—allow for even coverage and natural-looking augmentation while minimizing lumps.^[55]^[56]^[57] Botulinum toxin injections, such as Botox, target dynamic nasolabial folds caused by muscular hyperkinesis by relaxing the underlying mimetic muscles like the levator labii superioris. Administered in small doses along the fold, they reduce muscle pull and smooth expression lines, with effects lasting 3-6 months and requiring repeat treatments for maintenance. This is particularly effective for type 3 folds and can be combined with fillers for enhanced results.^[58] Topical agents like retinoids and peptides target collagen stimulation to gradually reduce fold depth over time. Retinoids, such as tretinoin, promote keratinocyte proliferation and new collagen synthesis in the dermis, leading to improved skin firmness when applied daily for several months. Peptides, often incorporated in serums, enhance extracellular matrix production, with evidence showing wrinkle reduction, including in nasolabial areas, after consistent use over 2-16 weeks. These treatments yield subtle, progressive enhancements rather than immediate volume correction.^[59]^[60]^[61] Energy-based devices, including radiofrequency (RF) microneedling and ultrasound therapy (e.g., Ultherapy), deliver heat to deeper skin layers to stimulate collagen remodeling and tighten tissue. RF microneedling combines microneedles with RF energy for improved texture and fold reduction, typically requiring 3-4 sessions spaced 4-6 weeks apart, with 1-3 days of mild redness. Ultrasound treatments focus on SMAS layer lifting, offering results lasting 1-2 years after 1-2 sessions, with minimal downtime of 1-2 days. These are suitable for mild to moderate folds and complement other therapies.^[62] Laser resurfacing with fractional CO2 or erbium lasers works by creating microthermal zones in the skin to tighten tissue and remodel collagen, thereby reducing nasolabial fold prominence. Fractional CO2 lasers effectively improve wrinkle depth and skin texture, often requiring 1-3 sessions spaced 4-6 weeks apart, with a typical downtime of 3-7 days involving redness and peeling. Erbium lasers offer similar efficacy for skin tightening but with potentially milder thermal effects and shorter recovery, around 5-7 days, making them suitable for patients seeking less disruption. Multiple sessions enhance cumulative benefits without excessive risk.^[63]^[64]^[65]^[66] Chemical peels using medium-depth trichloroacetic acid (TCA) at concentrations of 20-35% penetrate to the dermal layers, promoting epidermal renewal and collagen remodeling to enhance skin texture around nasolabial folds. These peels improve fine lines and surface irregularities, with studies showing significant gains in hydration and elasticity after 1-3 sessions, though they do not address underlying volume loss. Recovery involves 3-7 days of peeling and erythema, emphasizing their role in texture refinement over structural support.^[67]^[68]^[69]

Surgical approaches

Surgical approaches to nasolabial folds target severe or persistent cases through tissue repositioning, volume augmentation, or suspension techniques, often requiring general anesthesia and incisions for long-lasting results. These methods are selected based on preoperative assessment of fold depth and facial structure, providing more durable outcomes compared to non-operative interventions. Facelift procedures, including variants such as SMAS plication, involve tightening the superficial musculoaponeurotic system (SMAS) layer to elevate and reposition descending midfacial tissues, thereby reducing the prominence of nasolabial folds and improving jawline definition.^[70] Midface lifts, a specialized facelift extension, focus on elevating the malar fat pads and cheek tissues to directly address midfacial ptosis contributing to fold formation.^[71] Hematoma remains the most common complication in these surgeries, occurring at rates under 5%, with studies reporting incidences as low as 1.1% in large cohorts.^[72] Autologous fat grafting restores volume to the nasolabial region by harvesting fat from donor sites such as the abdomen via liposuction, purifying it through centrifugation, and injecting microdroplets into the subcutaneous plane for natural contouring.^[73] This technique achieves volume augmentation with retention rates of up to 50% at one year, though variability depends on graft processing and patient factors.^[74] Thread lifts utilize polydioxanone (PDO) barbed threads inserted via small punctures to anchor and suspend facial ligaments, providing mechanical lift to the midface and shallowing nasolabial folds in a minimally invasive manner.^[75] These absorbable threads stimulate collagen production for gradual tightening, with clinical effects typically lasting 1-2 years before gradual resorption and relaxation.^[76] Subperiosteal dissection represents an advanced endoscopic technique for patients with pronounced skeletal nasolabial folds, involving elevation of periosteal attachments along the zygomatic and maxillary bones to release and reposition the entire midfacial envelope.^[77] Accessed through intraoral or temporal incisions, this method achieves powerful malar augmentation and fold effacement by restoring youthful skeletal support, often combined with suspension sutures for enhanced stability.^[78]

Prevention

Lifestyle strategies

Adopting certain lifestyle strategies can help mitigate the progression of nasolabial folds by addressing environmental and behavioral factors that contribute to skin aging. Consistent sun protection is essential, as ultraviolet radiation accelerates photoaging, which deepens these folds through collagen degradation. Daily application of a broad-spectrum sunscreen with at least SPF 30, reapplied every two hours during outdoor exposure, has been shown to significantly reduce signs of photoaging, including wrinkle formation around the nasolabial area.^[79] Additionally, avoiding peak UV hours between 10 a.m. and 4 p.m. minimizes cumulative damage, preserving skin elasticity and delaying fold prominence.^[1] Quitting smoking represents another critical behavioral change, as tobacco use induces oxidative stress that impairs skin repair and exacerbates nasolabial fold depth by breaking down collagen and elastin. Cessation reduces this oxidative damage, allowing for improved blood flow and nutrient delivery to the skin, which can lead to visible enhancements in wrinkle appearance, including nasolabial folds, within several months to a year.^[80]^[81] Studies indicate that skin tone and texture begin to improve as early as 4-12 weeks post-cessation, with continued benefits over time as collagen production rebounds.^[81] A nutrient-dense diet and adequate hydration further support skin health by enhancing elasticity and combating free radical damage that contributes to fold formation. Consuming antioxidant-rich foods, such as berries and sources of omega-3 fatty acids like fatty fish, helps neutralize oxidative stress and promotes collagen synthesis, thereby maintaining firmer skin in the nasolabial region.^[82] Drinking 2-3 liters of water daily ensures optimal skin hydration, which is vital for plumpness and resilience, reducing the visibility of folds.^[83] Modifying facial habits can prevent uneven deepening of nasolabial folds, particularly unilateral asymmetry. Minimizing repetitive expressions like squinting, which contracts muscles around the eyes and mouth, limits the etching of lines over time, as repeated facial movements contribute to wrinkle permanence.^[83] Similarly, sleeping on the back rather than the side avoids prolonged pressure on one cheek, which can compress facial tissues and accentuate the fold on the dependent side, leading to asymmetry.^[84]

Skincare practices

Skincare practices play a crucial role in preventing the deepening of nasolabial folds by maintaining skin hydration, promoting collagen production, and protecting against environmental damage that accelerates aging. A consistent routine focused on gentle cleansing, moisturization, and sun protection can help preserve skin elasticity and minimize the appearance of these folds over time.^[1] Daily cleansing with a gentle, non-irritating cleanser twice a day removes impurities without stripping the skin's natural oils, which is essential for preventing dryness that can exacerbate fold visibility. Following cleansing, applying a moisturizer formulated for the face helps restore the skin barrier and lock in hydration, reducing the prominence of fine lines in the nasolabial area. Dermatologists recommend selecting moisturizers containing humectants like glycerin to support overall skin health.^[1] Broad-spectrum sunscreen with at least SPF 30 applied every morning, and reapplied every two hours during outdoor exposure, is a cornerstone of anti-aging skincare. Ultraviolet radiation breaks down collagen and elastin, contributing to the formation and deepening of nasolabial folds; regular sunscreen use has been shown to retard skin aging by up to 24% in randomized trials. Opt for water-resistant formulas if sweating or swimming to ensure consistent protection.^[1]^[85] Incorporating topical retinoids, such as retinol or tretinoin, into a nighttime routine can stimulate collagen synthesis and improve skin texture, leading to a reduction in wrinkle depth including nasolabial folds after consistent use over several months. Start with lower concentrations to minimize irritation, applying 2-3 times per week initially. Retinoids are among the most evidence-based topical agents for anti-aging, with clinical studies demonstrating enhanced epidermal thickness and decreased fold severity.^[59]^[86] Hyaluronic acid (HA) in serum or cream form provides immediate plumping effects by drawing moisture into the skin, which can temporarily soften the appearance of nasolabial folds while supporting long-term hydration. Clinical evaluations show topical HA increases skin hydration by over 100% upon application and improves elasticity with regular use, making it suitable for daily morning or evening application under moisturizer. Low-molecular-weight HA penetrates deeper for better efficacy.^[87]^[88] Antioxidants like vitamin C, applied as a stable serum in concentrations of 10-20%, neutralize free radicals and boost collagen production, helping to fade hyperpigmentation and refine nasolabial fold contours. Systematic reviews confirm topical vitamin C reduces wrinkle appearance and improves skin firmness after 12 weeks of use, particularly when combined with sunscreen during the day.^[89] Peptides, short chains of amino acids found in targeted serums, signal skin cells to produce more collagen and elastin, offering a gentler alternative to retinoids for addressing nasolabial folds. Studies on peptide complexes demonstrate significant wrinkle reduction and improved skin basement membrane integrity after 4-12 weeks, with examples like palmitoyl pentapeptide-4 showing up to 20% decrease in fold depth in clinical trials. Apply peptide products nightly for optimal results.^[60]^[90]

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