Over the past decade, regenerative aesthetic medicine has evolved rapidly, with expanding therapeutic options including biostimulatory injectables, autologous therapies and energy-based technologies. These developments have shifted aesthetic medicine from a reactive approach towards a more biologically oriented, preventative and reparative model focused on tissue regeneration and restoration.  

Despite these advances, treatment planning within aesthetic practice often remains protocol-driven or product-led, rather than grounded in a structured analysis of the biological mechanisms underlying facial ageing. 

Traditional treatment approaches may overlook the significant variability in how ageing manifests across individuals. Facial ageing is not a singular process but rather a complex interaction between skeletal remodelling, soft tissue redistribution, dermal matrix degradation and systemic factors such as hormonal changes. When these mechanisms are not adequately differentiated, interventions may be misdirected, resulting in suboptimal outcomes, over-treatment or progressive compromise of tissue integrity. 

One approach which may improve long-term patient outcomes is a phenotype-based assessment model that classifies ageing according to dominant anatomical and biological drivers. The term “phenotype” is used here in a descriptive clinical sense, referring to the observable pattern of dominant ageing mechanism, rather than implying a validated taxonomic system. The framework proposed below should be regarded as a working clinical model requiring prospective validation rather than an established classification system. Such frameworks could support more precise and personalised treatment planning and may reduce the tendency toward repetitive or trend-driven interventions. 

This article proposes a clinically practical classification framework based on four dominant facial ageing phenotypes. The rationale for four categories reflects the four principal anatomical domains most frequently implicated as dominant drivers in the clinical literature: the bony skeleton, the soft tissue suspension system, the dermal extracellular matrix and systemic hormonal physiology. These categories are not mutually exclusive and most patients will exhibit features of more than one. The objective is to support regenerative treatment planning that prioritises anatomical precision, safety and long-term tissue harmonisation through mechanism-led, individualised care. 

While mixed phenotypes are common in clinical practice, treatment planning may still benefit from identifying the dominant biological driver responsible for the greatest proportion of visible ageing change. In practical terms, phenotype assignment should be regarded as a weighted clinical judgement based on the relative contribution of skeletal, soft tissue, dermal and systemic factors rather than a rigid categorical diagnosis. A semi-structured assessment model incorporating static analysis, dynamic assessment, palpation findings, photographic comparison and systemic history may improve reproducibility and reduce purely subjective interpretation. 

The four dominant facial ageing phenotypes 

While most individuals exhibit a combination of ageing mechanisms, clinical assessment often reveals one dominant driver that shapes the overall facial phenotype. Recognising this primary pattern can guide treatment priorities and reduce unnecessary intervention. 

Structural-dominant ageing 

Structural-dominant ageing is characterised primarily by skeletal remodelling and deep volumetric loss. Progressive bone resorption occurs across multiple facial regions, including the orbital rim, maxilla, piriform aperture and mandibular angle.1 These changes alter facial proportions and reduce structural support for overlying soft tissues. 

From an anatomical perspective, skeletal changes are accompanied by deflation of deep fat compartments such as the deep medial cheek fat and sub-orbicularis oculi fat. As these deep supports diminish, superficial soft tissues lose projection and appear flattened or recessed.2 The midface may appear shortened, with increased prominence of nasolabial folds secondary to structural deterioration rather than primary gravitational soft tissue displacement.3  

Key clinical indicators include flattening of the midface, widening of the orbital aperture, loss of anterior cheek projection and reduced definition of the jawline due to diminished skeletal support.4,5 Patients may present with a “tired” appearance despite relatively preserved skin quality. A common assessment pitfall is misinterpreting structural deficiency as superficial soft-tissue laxity. In such cases, attempts to correct the appearance through superficial volumisation or skin tightening alone may produce unnatural contouring without restoring foundational support. Recognition of skeletal contributions is therefore critical, as the primary therapeutic objective is restoration of structural integrity rather than surface correction. 

Soft tissue descent-dominant ageing 

Soft tissue descent-dominant ageing arises primarily from progressive changes within the facial soft tissue suspension system and the redistribution of superficial fat compartments. Understanding the mechanism of this phenotype requires careful consideration of the anatomical evidence, which is more nuanced than a simple model of ligamentous laxity. 

The facial retaining ligaments are a structurally heterogeneous group. The true osteocutaneous ligaments, including the zygomatic known as McGregor’s patch,6 orbital, buccomaxillary and mandibular ligaments, demonstrate relative structural stability with advancing age. Biomechanical cadaveric studies have found no statistically significant relationship between biophysical properties of these structures and donor age.7 

More recent experimental animal data suggest that the zygomatic ligament may increase in stiffness and rigidity with age rather than becoming lax, though human studies are needed to confirm this finding.8 This evidence could challenge the widespread clinical assumption that soft tissue descent is primarily explained by weakening of the primary osteocutaneous ligaments. 

The descent process is better understood as the product of two converging mechanisms. First, the finer retinacular branches running superficially from the SMAS through the subcutaneous layer to the dermis are susceptible to cumulative mechanical fatigue through repetitive facial animation.  It is this superficial retinacular layer, rather than the deeper osteocutaneous ligaments, that undergoes the most clinically relevant age-related weakening.9,10  

Second and critically, progressive resorption of the facial skeleton displaces the bony origin of the retaining ligaments posteriorly. This posterior repositioning of ligament anchors alters the mechanical geometry of soft tissue support even when the ligaments themselves retain structural integrity.11,12 The result is a system in which the suspension framework remains structurally present but is no longer mechanically positioned to resist gravitational forces on the overlying tissue. 

In patients with this phenotype, skeletal support may remain relatively preserved while soft tissue displacement is clinically prominent. Superficial fat compartments shift inferiorly, contributing to the development of nasolabial folds, marionette lines and jowl formation. The distinction between true laxity of the suspension system and positional displacement secondary to skeletal remodelling has meaningful implications for treatment selection. 

Clinically, patients with this phenotype typically demonstrate preserved midface volume but clear signs of soft tissue displacement. The lateral cheek may appear flattened, the jawline loses continuity and the mandibular border becomes obscured by jowl formation.13,14 Dynamic assessment often reveals increased tissue mobility during facial animation. Palpation may demonstrate reduced ligamentous resistance and altered soft-tissue biomechanics. 

A frequent diagnostic error is attributing these changes to simple volume loss. Repeated volumisation without addressing the underlying structural context may exacerbate heaviness and further distort natural contours. In such cases, the underlying issue is not deficiency of volume but redistribution of existing tissue within a compromised support environment. Careful differentiation between descent and deflation is therefore essential to avoid over-correction and to maintain facial harmony. 

Skin quality-dominant ageing 

Skin quality-dominant ageing is primarily driven by degeneration of the dermal extracellular matrix. Progressive decline in collagen, elastin and glycosaminoglycans results in reduced dermal thickness, impaired elasticity and increased susceptibility to environmental damage. 

Intrinsic ageing mechanisms are compounded by extrinsic factors including ultraviolet radiation, pollution and oxidative stress. These influences accelerate matrix metalloproteinase activity, further degrading structural proteins within the dermis.15 Age-related impairment of TGF-beta/Smad signalling, driven by ROS-mediated downregulation of TGF-beta type II receptor, reduces collagen synthesis while concurrent AP-1 activation upregulates MMP expression, creating a self-reinforcing catabolic shift within the dermal matrix.16,17  

Patients with this phenotype may exhibit relatively preserved facial volume and structural support but demonstrate prominent textural changes. Clinical indicators include fine lines, dermal crepiness, dryness, enlarged pores, dyschromia and overall loss of skin luminosity.18 In early stages, these changes may be most evident in high-movement areas such as the periorbital and perioral regions. With progression, dermal thinning may also contribute to visible vascularity and reduced barrier function.19 

One of the most common assessment pitfalls is focusing on volumetric correction in patients whose primary concern relates to skin quality deterioration. In such individuals, repeated volumisation may fail to address the underlying dermal pathology and can create unnecessary tissue expansion. Recognition of dermal-dominant ageing therefore supports a biostimulatory approach centred on improving skin health, function and resilience rather than prioritising structural augmentation. 

Hormonal-decline dominant ageing 

Hormonal decline represents a frequently under-recognised driver of facial ageing, particularly in midlife female patients. The reduction in oestrogen associated with menopause has profound effects on skin physiology, collagen metabolism and fat distribution. Hormone production declines with age, affecting cell metabolism, gene expression and protein synthesis.20 Reductions in sex hormones alongside changes in melatonin, cortisol, growth hormone, vitamin D and related receptors contribute to accelerated ageing.21  

Oestrogen plays a key role in maintaining skin integrity by supporting DNA repair, collagen production and hydration. Its decline, particularly post-menopause, is associated with skin thinning and dryness.22 While therapies such as topical oestrogens or phytoestrogens may improve skin health, their use requires careful timing to balance potential benefits against associated risks.23 

Studies suggest a 30% decrease in types I and III collagen in the 5 years around menopause24 and a further collagen decline of between 1-2% per year after the menopause.25 Reduced oestrogen levels impair fibroblast activity, diminish dermal hydration and contribute to progressive skin thinning.26 In addition, hormonal shifts influence facial fat compartment behaviour, often resulting in accelerated volume loss in the midface.26 

Clinically, hormonal-decline dominant ageing often presents with a combination of dermal fragility, sudden onset volume reduction and increased skin laxity. Patients may report relatively rapid changes in facial appearance over a short time period.27 Other indicators may include dull skin tone, increased fine wrinkling and decreased wound-healing capacity. In some cases, systemic symptoms of hormonal transition may also be present.27 

Importantly, hormonal-decline dominant ageing may coexist with structural or dermal-dominant phenotypes but may alter tissue responsiveness to regenerative intervention. Reduced fibroblast activity, impaired wound healing and diminished collagen turnover may influence both treatment selection and expected regenerative capacity, however evidence to support this is limited.  

A key diagnostic pitfall is assuming that accelerated ageing in this group reflects purely anatomical factors. Without consideration of underlying hormonal influences, treatment may address symptoms rather than root causes. While aesthetic clinicians do not generally manage systemic endocrine health directly, awareness of hormonal influences allows more realistic treatment planning and may prompt appropriate multidisciplinary involvement where relevant. 
 

Semi-quantitative phenotype weighting 

Given that most patients demonstrate overlapping ageing mechanisms, phenotype identification should not be approached as a binary classification process. Instead, clinicians may benefit from assigning relative weighting to each anatomical domain based on the predominance of observed ageing features. 

One potential clinical approach would involve semi-quantitative scoring across four domains: skeletal support, soft tissue descent, dermal quality and hormonal/systemic influence. Each category could be graded according to severity and contribution to the presenting phenotype. The dominant phenotype would therefore reflect the highest weighted mechanism rather than the exclusive presence of one ageing pathway. 

For example, a patient demonstrating moderate skeletal resorption with severe dermal deterioration and relatively preserved ligamentous support may be more appropriately classified as skin quality-dominant despite measurable structural ageing changes. Conversely, a patient with relatively preserved skin quality but marked jowl formation and tissue mobility may demonstrate a soft tissue descent-dominant phenotype despite concurrent dermal ageing. 

Although such an approach remains conceptual, structured weighting may improve consistency between practitioners and facilitate future validation studies examining interrater reliability and treatment response correlation. 

Structured clinical assessment framework 

Effective phenotype-based planning requires a reproducible clinical assessment strategy. A systematic approach helps minimise subjective bias and ensures that underlying anatomical drivers are accurately identified. 

Layer-by-layer anatomical analysis 

Assessment should proceed sequentially through the anatomical layers of the face consistent with established frameworks for layer-specific facial evaluation.11,28 

Bone structure: Evaluation begins with skeletal projection, symmetry and structural proportions. Particular attention should be paid to the maxilla, zygomatic arch, mandibular angle and chin position, as these regions strongly influence overall facial support and determine the bony origin of the retaining ligament system. 

Deep and superficial fat compartments: The distribution and volume of facial fat compartments should be assessed visually and through palpation. Distinguishing between deep compartment deflation and superficial compartment descent is essential for accurate phenotype classification.  

Retaining ligaments: Assessment of the soft tissue suspension system should consider both the retinacular layer, which is subject to fatigue-related weakening and the mechanical geometry of the system as a whole, which is influenced by the position of skeletal ligament origins. Increased mobility of superficial fat pads during facial animation may reflect compromise of the retinacular layer rather than laxity of the primary osteocutaneous ligaments. 

Dermis and epidermis: Skin thickness, elasticity, pigmentation and surface texture should be evaluated under natural light. These observations help determine the extent of dermal matrix deterioration.  

Static and dynamic assessment 

Static assessment provides an overview of resting facial proportions, but dynamic observation often reveals additional diagnostic information. Facial animation highlights areas of muscular dominance, soft-tissue displacement and structural imbalance. Observing patients during natural expressions such as smiling, speaking and frowning can reveal patterns of tissue movement that may not be visible in static photographs. 

Soft tissue biomechanics 

Palpation provides valuable information regarding tissue density, elasticity and resilience. Differences in tissue resistance can help distinguish between volume depletion, laxity and dermal thinning. Biomechanical evaluation also assists in determining how tissues may respond to regenerative therapies and whether structural support is adequate to maintain treatment outcomes. 

Hormonal and systemic considerations 

A comprehensive consultation should include discussion of systemic factors that may influence tissue health. Age, menopausal status, lifestyle factors and medical history may all contribute to the ageing phenotype. While aesthetic practitioners do not diagnose endocrine disorders, awareness of systemic influences supports realistic treatment planning and long-term patient management. 

Documentation and photographic analysis 

Standardised photography remains a critical component of assessment. Images should be obtained in consistent lighting conditions and include frontal, oblique and lateral views at rest and during animation. 

As well as their requirement for optimal medical record keeping, photographic comparison over time allows clinicians to track subtle changes in tissue position, skin quality and facial proportions, supporting more objective treatment planning. 

Treatment mapping: aligning intervention with mechanism 

Once the dominant ageing phenotype has been identified, regenerative interventions can be mapped according to the underlying mechanism. The table below summarises the alignment between phenotype, dominant mechanism and primary treatment priority as a clinical reference.