Age’s Impact on The Aesthetic Units of the Face
What morphological changes occurwith ageing? During youthful years, the face manifests as one single dynamic unit with smooth facial contours and little shadowing between different facial features. However, as we age the face gradually morphs into
What morphological changes occurwith ageing?
During youthful years, the face manifests as one single dynamic unit with smooth facial contours and little shadowing between different facial features. However, as we age the face gradually morphs into distinct separate facial units. This process may result from changes in the thickness of skin, subcutaneous tissue composition, facial skeleton contours and the location of facial ligaments. The combination of superficial visual changes to the skin and the deeper compartmentalisation of facial features, leads to the overall appearance of an aged face.
The ageing of a face is a gradual yet constant process that involves evolving of the bony facial structure and overlying soft tissues. This natural and uncontrollable ageing process is called internal or intrinsic ageing, whereby soft tissue maturation, the effects of gravity and the constant activity of facial muscles (combined with their eventual reduction in strength), changes the appearance of the face. Skeletally, bone movement, growth, deformations and stomatognathic system changes all affect facial structure over time
Visual differences as the soft tissue matures, include a change in the colour and texture of the skin and the formation of lines and wrinkles.
This intrinsic ageing process is affected by hereditary factors to a degree and is largely beyond our control. In comparison, extrinsic ageing is the result of our lifestyles. Factors such as smoking, sun exposure and dietary choices all influence how we age.
Changes in the skin:
The most visually prominent age-related changes in the skin result form chronic exposure to the sun; changes in colour (hyperpigmentation), tone (age spots) and texture (lines and wrinkles) are a result of photo-ageing.
Anatomically as skin ages:
- Collagen production slows down (collagen contributes to the firmness of skin)
- Production of elastin decreases (elastin contributes to elasticity of skin)
- Fat cells start to diminish (resulting in sagging skin)
- The skin’s ability to retain moisture decreases
- Frown lines appear due to repetitive contraction of small muscles
- The shedding of superficial dead skin cells slows down (leading to a dull appearance)
- The turnover of new skin cells reduces
Microscopically, it is possible to see cellular age-related changes. Epidermal thinning, collagen loss and dermal-epidermal junction flattening can be seen. The skin loses its natural elasticity and increased transepidermal water loss occurs.
Dry skin is a consequence of both reduced water-binding capacity and decreased activity of sebaceous gland. This loss of skin elasticity and volume, along with repeated activity of muscles, contributes to the formation of rhytides over the habitual muscle contraction regions such as the orbicularis oculi and oris, risorius, frontalis, and corrugators, etc.
In intrinsic ageing, the papillary organisation of subcutaneous vasculature is lost and the interface of epidermis and dermis flattens resulting in atrophy of the dermis and subcutaneous tissue. The organisation of elastin and collagen is lost with a reduction in their relative amount, and they exhibit histologic signs of degeneration. The production of TypesI and III collagen by fibroblasts is decreased. Fibroblasts, particularly those located within the papillary dermis, exhibit a selective decline in function and number as compared to those located in the reticular dermis.
Smoking, photodamage and the effects of other environmental factors contribute to the increase in intracellular reactive oxidative species resulting in multiple skin changes that lead to characteristics that are consistent with skin ageing. This is accompanied by age or dark spots and hyperpigmentation on skin’s surface, caused by increased production of melanin due to excessive sun exposure.
Changes in Volume
A youthful face is characterised by appropriately filled facial fat compartments in their anatomically correct places. Due to progressive ageing, the subcutaneous fullness of the forehead region, brows, temple and upper eyelid region is lost. This makes the bony structure of the skull, supra-orbital rims, brow muscles and the temporal blood vessels more pronounced. Fat redistribution, accumulation and atrophy cause loss of facial volume11].
- Some facial areas lose fat such as the forehead and cheeks
- Other facial areas gain fat such as the mouth and jaw
- These changes in fat pads cause contour deficiencies.
The zygomatic-cutaneous, orbitomalar, and mandibular retaining facial ligaments attenuate, which gives a drooping appearance to the soft facial tissues. These act as a hammock for the atrophied compartments of facial fat and soft tissues, which contribute to the appearance of tear trough, malar bags and jowling. The deflation, as well as the decrease in the normal anatomical subcutaneous fat compartments of the face, contributes to an increase in skin laxity and distinct folds that appear around the nasolabial region, periorbital region, and jowl.
The illustrations above demonstrate that as ageing occurs, the fat compartments become increasingly spaced apart, visually appearing as separate entities rather than a smooth nearly continuous layer
Changes in shape
The shape of the face is determined by the underlying anatomy of the muscles and their supporting ligaments. Ligaments are the fundamental supporting structures of the face. The relationship that exists between ligaments, the SMAS, lower eyelid and lateral canthus has been extensively described in various studies. The orbicularis oculi muscle gets support through adhesion to the temporalis, and zygomaticomalar ligaments suspend the cheeks. The infraorbital area has superficial and the deep fat pads that are suspended by a ligament which originates at the arcus marginalis, called the “orbicularis retaining ligament” or the “orbitomalar ligament”.
Mendelson has provided extensive details about ligaments, septae, brow adhesion zones, the periocular region, and midface. He suggested that the laxity of ligaments might be a primary reason for facial ageing. Mendelson hypothesised that the ligaments stabilise the youthful face, but constant activity of facial muscles combined with intrinsic ageing changes, cause ligamentous support weakness. This progressive lack of structural support for the face, combined with the pull of gravity leads to ptosis of the soft facial tissues and the “drooping” aged appearance.
The combination of visibly apparent skin changes as well as underlying structural disparities, involving bone, muscles, fat and ligaments is responsible for the ageing appearance of the face.
1- Coleman SR, Grover R. The anatomy of the aging face: volume loss and changes in 3-dimensional topography. AesthetSurg J. 2006;26(1S):S4-S9.
Rzany B, Carruthers A, Carruthers J, et al. Validated composite assessment scales for the global face. Dermatol Surg. 2012;38(special issue 2):294-308
González-UlloaM. Regional aesthetic units of the face.PlastReconstr Surg. 1987;79(3):489-490.
2 – Tan SL, et al. The Aesthetic Unit Principle of Facial Aging.JAMA Facial Plast Surg. 2015 Jan-Feb.
3 – Zimbler, M., M. Kokoska, and J. Thomas, ‘Anatomy and pathophysiology of facial aging’. Facial plastic surgery clinics of North America, 2001. 9(2): p. 179-87, vii.
4 – Desai, S., M. Upadhyay, and R. Nanda, ‘Dynamic smile analysis: changes with age’. American Journal of Orthodontics and DentofacialOrthopedics, 2009. 136(3): p. 310. e1-310. e10.
5 – Uitto J. The role of elastin and collagen in cutaneous aging: intrinsic aging versus photoexposure. J Drugs Dermatol. 2008;7(2 Suppl):s12–6
6 – Varani J, Dame MK, Rittie L, et al. Decreased collagen production in chronologically aged skin: roles of age-dependent alteration in fi broblast function and defective mechanical stimulation. Am J Pathol. 2006;168(6):1861–
7 – Mine S, Fortunel NO, Pageon H, Asselineau D. Aging alters functionally human dermal papillary fibroblasts but not reticular fibroblasts: a new view of skin morphogenesis and aging. PLoS One. 2008;3(12):e4066.
8 – Hinderer UT. Correction of weakness of the lower eyelid and lateral canthus. Personal techniques. ClinPlast Surg. 1993;20:331–349.
9 – Schlessinger J, Kenkel J, Werschler P. Further enhancement of facial appearance with a hydroquinone skin care system plus tretinoin in patients previously treated with botulinum toxin Type A. AesthetSurg J. 2011;31:529–539.
10 – Zimbler MS, Kokoska MS, Thomas JR. Anatomy and pathophysiology of facial aging. Facial PlastSurgClin North Am. 2001;9:179-187.
Donofrio LM. Fat distribution: a morphologic study of the aging face. Dermatol Surg. 2000;26:1107-1112.
11 – Vleggaar D, Fitzgerald R. Dermatological implications of skeletal aging: a focus on supraperiostealvolumization for perioral rejuvenation. J Drugs Dermatol. 2008;7:209-220.
12 – Vleggaar D, Fitzgerald R. Dermatological implications of skeletal aging: a focus on supraperiostealvolumization for perioral rejuvenation. J Drugs Dermatol. 2008;7:209-220.
Donofrio LM. Fat distribution: a morphologic study of the aging face. Dermatol Surg. 2000;26:1107-1112.
13 – Stuzin JM, Baker TJ, Gordon HL. The relationship of the superficial and deep facial fascias: relevance to rhytidectomy and aging. PlastReconstr Surg. 1992;89:441
14 – Reece EM, Pessa JE, Rohrich RJ. The mandibular septum: anatomical observations of the jowls in aging-implications for facial rejuvenation. PlastReconstr Surg. 2008;121:1414–1420.
15 – Furnas DW. The retaining ligaments of the cheek.PlastReconstr Surg. 1989;83:11–16.
16 – Barton FE.,Jr The SMAS and the nasolabial fold. PlastReconstr Surg. 1992;89:1054.
17 – Gonzalez-Ulloa M, Flores ES. Senility of the face—basic study to understand its causes and effects. PlastReconstr Surg. 1965;36:239–246.
18 – Rohrich RJ. Ethical approval of clinical studies, informed consent, and the Declaration of Helsinki: what you need to know. PlastReconstr Surg. 2007;119:2307–2309.
19 – Rohrich RJ, Pessa JE, Ristow B. The youthful cheek and the deep medial fat compartment.PlastReconstr Surg. 2008:2107–2112.
20 – Vieggaar D, Fitzgerald R. Dermatological implications of skeletal aging: a focus on supraperiostealvolumization for perioral rejuvenation. J Drugs Dermatol. 2008;7:209-220.
21 – Muzaffar AR, Mendelson BC, Adams Jr WP. Surgical anatomy of the ligamentous attachments of the lower lid and lateral canthus.PlastReconstr Surg. 2002;110(3):873–84.
Ghavami A, Pessa JE, Janis J, et al. The orbicularis retaining ligament of the medial orbit: closing the circle. PlastReconstr Surg. 2008;121(3):994–1001.
Kikkawa DO, Lemke BN, Dortzbach RK. Relations of the superficialmusculoaponeurotic system to the orbit and characterization of the orbitomalar ligament.OphthalPlastReconstr Surg. 1996;12(2):77–88.
Mendelson BC, Jacobson SR. Surgical anatomy of the midcheek: facial layers, spaces, and the midcheek segments. ClinPlast Surg. 2008;35(3):395–404.
22 – Mendelson BC, Muzaffar AR, Adams Jr WP. Surgical anatomy of the midcheek and malar mounds.PlastReconstr Surg. 2002;110(3):885–96.
23 – Mendelson BC. Surgery of the superficialmusculoaponeurotic system: principles of release, vectors, and fixation. PlastReconstr Surg. 2001;107(6):1545–52.
24 – Mendelson BC. Surgery of the superficial musculoaponeurotic system: principles of release, vectors, and fixation. PlastReconstr Surg. 2001;107(6):1545–52.