Keywords volume loss - face-lift - rhytidectomy - aging face - facial rejuvenation
It has been clearly stated in the literature for almost 50 years that changes in all
four structural tissue types—skin, fat, muscle, and bone—contribute to facial aging.[1 ] However, the extent to which changes in each of these tissues contribute to aging
continue to be debated. The debate is complicated by the fact that proportional relationships
can be deceiving as separate structures age and influence the perception of adjacent
structures. Thus, an illusion can be created of a change in one tissue type where
the change is actually in a different type ([Fig. 1 ]).
Fig. 1 Which center circle is larger? Both are the same. The illusion that the left center
circle is larger is created by our brain's ability generalize relationships of adjacent
structures from past experience.
As early as 1911, volume restoration was advocated as a technique for facial rejuvenation.[2 ]
[3 ] However, for most of the 20th century, the “surgical model” stated that the majority
of facial aging was because of the gravity's effects on the facial soft tissue; therefore,
lifting, repositioning, and excising excess soft tissue was the optimal solution to
restore the face to its prior form. There were however, limitations and inadequacies
in the esthetic outcomes, especially, when associated with techniques requiring skin
tension, which lead to questioning of the “surgical model.” The apparent inability
of the “surgical model” to consistently address facial aging led to the recent popularity
of the “volume model.” This model emphasizes deflation and touts the resultant folds
and hollows seen in the aging face as evidence of facial fat loss causing the majority
of aging changes. Advances in soft tissue fillers and fat transfer techniques, as
well as the ease, cost, and consumer demand for the “volume model” has fueled growth
of this approach, despite similar evidence of limitations and inadequacies in esthetic
outcomes.
Recently, several studies have documented the neglected contribution of the facial
skeleton in understanding the aging process.[4 ]
[5 ]
[6 ]
[7 ] By understanding the complex three-dimensional bony changes associated with the
aging process, both the limitations of the surgical model and the successes of the
volume model can be better understood.
It is our view, that facial aging is not because of significant facial fat loss, but
is an illusion of loss produced by several factors. First, the normal physiology of
soft tissue is to stretch secondary to intrinsic force, such as weight gain or pregnancy,
and explains the success of tissue expansion techniques where extrinsic force is used
to create soft tissue redundancy to repair soft tissue deficits.[8 ] The extrinsic force of gravity on facial soft tissue also produces soft tissue redundancy,
and differs in appearance from true cases of volume loss, such as HIV wasting syndrome,
where the soft tissue retracts, resulting in an ill appearing rather than aged face.
Second, the anatomical limitations restricting the ptotic, redundant facial soft tissue's
movement produces similar hollows, folds, and signs of deflation in the face, mimicking
volume depletion. Third, skeletal changes occur in the exact regions that volume enhancement
have their greatest success: the medial cheek and periorbital region. In addition,
the facial bone loss also explains the limitations in the “surgical model” approach
to the aging face. We will present evidence to support these contributing factors
that create the volume illusion and challenge the esthetic community to produce contradictory
evidence of facial fat loss as the major contributor to the aged face.
Relevant Anatomy
The diagnosis and treatment of volume loss has mainly pertained to the periorbital
and midface. For the purpose of our discussion, we will review midface anatomy. Viewing
the structure of the face by layer ([Fig. 2 ]), we first encounter the superficial soft tissue envelope which is bounded by the
skin superficially and deeply by the submuscular aponeurotic system (SMAS) layer.
This embryologic boundary is contiguous from the platysma in the neck to the galea
in the forehead ([Fig. 3 ]). The fibrous septae which span the vertical thickness of this layer, are pathways
for the vascular supply, coalesce into the facial retaining ligaments (zygomatic and
mandibular), and compartmentalize what appears otherwise to be homogeneously distributed
fat.[9 ] The majority of the facial fat is distributed in the superficial soft tissue envelope.[10 ]
Fig. 2 Layers of the face. The superficial muscular aponeurotic system (SMAS) is the deep
layer of the superficial soft tissue containing most of the facial fat distributed
homogeneously superficial to the SMAS. (Adapted with permission from Mendelson BC,
Jacobson SR. Surgical anatomy of the midcheek: facial layers, spaces, and midcheek
segments. Clin Plast Surg 2008;35(3):398).
Fig. 3 The superficial soft tissue envelope bound superiorly by the skin and deeply by the
superficial muscular aponeurotic system is an embryonic boundary contiguous from the
platysma in the neck to the galea in the forehead. (Adapted with permission from Zoumalan
RA, Larrabee WF. Anatomic considerations in the aging face. Facial Plast Surg 2011;27(1):18).
Below this layer is the superficial layer of the deep cervical fascia. The potential
space located between these layers represents the embryologic cleavage plane of the
midface and defines the deep plane. The three layers of the deep cervical fascia cover
and envelope all the deeper structural elements of the face ([Fig. 4 ]) including the masseter muscle, facial nerve, major vasculature, and the deep facial
fat pads. The anatomical description of the deep fat compartments vary according how
the anatomy is defined. While Rohrich and Pessa[9 ] describe the midface fat pads as nasolabial, medial, middle, and lateral cheek,
as well as separate nasolabial and orbital compartments, the distinction between the
compartments in the superficial soft tissue envelope versus the deep subfacial layer
are not well defined. In Raskin and La Trenta's cadaver study,[10 ] the layers of the face are better appreciated; the deep fat compartments are described
as lacking uniformity with globules of cheek fat sparsely contained by fascia strands
but also including defined structures such as the buccal fat and deep temporal pad.
Fig. 4 Retaining ligaments of the face, with the superficial muscular aponeurotic system
elevated. Both the zygomatic ligament (McGregor patch) superiorly, and the mandibular
ligament inferiorly, are strong ligaments with periosteal attachments (wide arrows ). Deep cervical fascia envelopes the underlying structural layers. (Adapted with
permission from Zoumalan RA, Larrabee WF. Anatomic considerations in the aging face.
Facial Plast Surg 2011;27(1):20).
These soft tissue layers rest on the periosteum encasing the facial skeleton.
Aging
Clinical and research evidence show that the facial aging involves complex, multidimensional
interactions between all the different tissue types.[11 ] By understanding these relationships, we can better understand the degree of change
in each tissue, and how changes in one tissue type can create the illusion of changes
in a different tissue type. In addition, the success of certain clinical treatments,
and failures or limitations of others, will also influence our current opinion of
the predominant etiology of facial aging.
There is clear evidence that the soft tissues of our body were designed to respond
to tensile force by stretching.[8 ] The predominant factor in facial aging is caused by the slow insidious force of
gravity and facial movement combining to create soft tissue redundancy in response
to the stress.[3 ]
[12 ] As the superficial soft tissue envelope of the face contains the majority of the
facial fat and is poorly anchored to the underlying anatomy by two facial ligaments
in the midface, the most significant effects of tensile force will be evident in this
layer[10 ] ([Fig. 4 ]). However, as this layer is not free to descend in all the directions, as it is
limited by the anatomical boundaries such as the nasolabial fold and the mandibular
septum, as well as being influenced by other tissue layers, the soft tissue redundancy
can “pile up” at these anatomical restriction areas creating folds and hollows mimicking
volume depletion.
In HIV wasting syndrome, both lipodystrophy and lipoatrophy occur. Lipoatrophy specifically
affects the midface creating medial hollows, prominent nasolabial folds, and skeletonized
musculature. This creates an accurate appearance of the volume loss in the midface
because of lipoatrophy. In true facial fat atrophy, hollows and folds are created
without the evidence of soft tissue redundancy as would occur with aging. The look
of HIV wasting syndrome is not of an aged individual, but of a sick, malnourished
person ([Fig. 5 ]).
Fig. 5 Lipodystrophy in HIV wasting syndrome demonstrating true volume loss. (Image reprinted
with permission from Medscape Reference [http://emedicine.medscape.com/ ] 2014. Available at: http://emedicine.medscape.com/article/1082199-overview .)
To our knowledge, there has been no objective study defining facial fat loss because
of aging, but cadaveric studies have been done that better define the anatomical relationships
of facial fat compartments. These studies expose the difficulty in interpreting the
relationships and influence that one tissue type has to an adjacent type.
Rohrich et al illustrated improvement of the “deflated midface” by the injection of
50 cc of saline into the deep medial cheek pad and noted this as evidence of lipoatrophy
as a cause of midface facial aging.[13 ] As we will show, the tissue being replaced is not necessarily fat and the behavior
of a cadaver's noncompliant soft tissue is not an accurate model to compare with the
compliant soft tissue of the living.
In another cadaver study, Rohrich and Pessa demonstrated that although the superficial
soft tissue envelope contains the majority of facial fat, it is not homogeneous but
separated into units or compartments by fibrous septal bands.[9 ] This, combined with the clinical observation of certain subunits, such as the medial
cheek fat compartment preferentially appearing hollow, led to the conclusion that
the fat compartments lose facial fat independent of one another.
If we view the superficial soft tissue envelope as a thick, quilted blanket, we can
gain a better understanding of the illusion created by this study. If a blanket is
lying on a flat, regular surface then the blanket will appear smooth or homogeneous.
If something that is supporting the blanket is removed in only one area underneath,
the contour of the blanket will change, but the true change in surface contour is
not because of the blanket, but it is in the underlying support. We feel that the
more logical answers as to why these illusions are created lies in understanding the
changes in the bony facial skeleton that occur with aging.
In the last 15 years, a growing body of evidence has focused attention on facial skeletal
remodeling and its effects on the aging face. Selective bone deposition and resorption
is well documented in the facial skeleton and occurs regardless of the state of dentition,
although loss of dentition significantly accelerates bone resorption of the maxilla
and mandible.[14 ]
[15 ] Using computed tomographic (CT) scans and other radiograph data, multiple authors
have quantified the specific sites and relationship changes that occur because of
bone resorption.[4 ]
[5 ]
[6 ]
[7 ]
[16 ] By understanding these changes, the secondary effects on adjacent tissue types become
evident.
In the periorbital region, the orbital aperture increases with age, mainly because
of bone resorption in the superior/medial and inferior/lateral orbit. Retrusion is
also evident in the inferior/lateral region[7 ] ([Figs. 6 ] and [7 ]).
Fig. 6 Arrows indicate the areas of the facial skeleton susceptible to resorption with aging. The
size of the arrow correlates with the amount of resorption. (Adapted with permission
from Mendelson B, Wong C-H. Changes in the facial skeleton with aging: implications
and clinical applications in facial rejuvenation. Aesth Plast Surg. 2012/08/01 2012;36(4):753–760).
Fig. 7 Changes in bony orbit with age. (Adapted with permission from Shaw RB, Katzel EB,
Koltz PF, Yaremchuk MJ, et al. Aging of the facial skeleton: aesthetic implications
and rejuvenation strategies. Plast Reconstruct Surg. 2011;127(1):374–383).
In the midface, evidence reveals that the maxilla both resorbs, causing the base of
the pyriform aperture to increase in width, as well as retrudes with age causing loss
of projection, regardless of dentition[5 ] ([Figs. 6 ] and [8 ]).
Fig. 8 The piriform (piriform angle) and the maxilla (maxillary angle) significantly recede
with aging, from youth (left ) to old age (right ). (Adapted with permission from Shaw RBJ, Kahn DM. Aging of the midface bony elements:
A three-dimensional computed tomographic study. Plast Reconstruct Surg. 2007;119(2):675–681).
In the lower face, the height of the mandibular ramus and body decreases with age,
especially with loss of dentition. In addition, retrusion occurs at the prejowl area[6 ] ([Figs. 6 ] and [9 ]).
Fig. 9 Changes in bony mandible with age. (Adapted with permission from Shaw RB, Katzel
EB, Koltz PF, Yaremchuk MJ, et al. Aging of the facial skeleton: aesthetic implications
and rejuvenation strategies. Plast Reconstruct Surg. 2011;127(1):374–383).
When viewing the facial skeleton from the lateral view, aging can be observed to cause
remodeling with clockwise, inward rotation of the midface, decreasing projection in
relation to the cranial skull base, confirming Lambros' theory of skeletal remodeling
in the aging face[17 ] ([Figs. 6 ] and [8 ]). The consequences of the combined facial bone remodeling changes are significant
and help explain both the limitations of the “surgical model” and the success of the
“volume model.”
Correlating These Bony Changes to Aging
Correlating These Bony Changes to Aging
In the upper orbit, the superior medial bone loss explains the aging changes in the
glabella as well as its resistance to treatment by brow lifting, especially in the
elderly when skeletal changes are more advanced. In addition, this leads to a loss
of fascial support and contributes to upper eyelid medial fat pseudoherniation. In
the lower orbit, the inferior/lateral bone resorption and retrusion can cause pseudo
fat herniation in the lower eyelid because of a posterior displacement of the orbital
rim. It additionally explains the development of malar mounds or festoons, which are
because of the loss of bony support for the orbicularis oculi muscle.
In the midface, generalized retrusion of the maxilla causes a loss of maxillary projection
explaining the prominence of nasolabial folds and the tear trough deformity. In addition,
the loss of fascial support causes buccal fat pseudoherniation, contributing to jowl
formation. Combined with bone loss in the medial maxilla, the base of the pyriform
aperture widens creating the appearance of the senile nose where a lack of support
for the attachment of the lower lateral cartilages and nasal base leads to loss of
projection and inferior rotation.
In the lower face, loss of mandibular height contributes to loss of support of the
submandibular gland/digastric muscle triangle and exacerbates the ptotic, redundant
neck soft-tissue by reducing the bony infrastructure. Retrusion at the prejowl region
of the mandible also contributes to the appearance of jowls in the aging face.
Discussion
Lambros observed that the aged face when lifted in front of the mirror improved by
layering out the excesses of soft tissue.[3 ] This led to his generalization of all techniques of the “surgical model” in which
soft tissue excesses were removed by traction. He questioned the validity of the “surgical
model” because surgical outcomes did not approach the results of the “mirror lift.”
His dissatisfaction with the unnatural signs of “traction” on the skin and variability
in cosmetic outcome led him to look at facial fat loss as the main etiology in facial
aging, and emphasized volume enhancement as a priority in aging face treatment.[3 ]
A better understanding of the influence of procedure technique helps explain some
of the perceived “surgical model” inadequacy. In SMAS rhytidectomy, the dissection
is accomplished in the subcutaneous plane, disrupting the septal barriers between
the fat compartments that directly connect the SMAS fascia to the skin, preventing
the superficial soft tissue envelope from behaving as a unit. This disruption of normal
anatomy limits soft tissue mobilization and repositioning, creating the necessity
for skin traction as well as other inadequacies which lead Lambros to question the
“surgical model.”
In deep-plane rhytidectomy, the entire superficial soft tissue envelope is kept intact
preserving the important structural anatomy. By keeping the fibrous septum connecting,
the SMAS/platysma to the dermis intact, the superficial soft tissue envelope behaves
as one unit ([Fig. 10 ]). Significant traction needs only to be applied to the deep SMAS/platysma layer,
as it is connected to the dermis by these fibrous septae, causing the entire superficial
soft tissue envelope to mobilize without any tension necessary at the skin level.
This eliminates the unnatural surface changes and other inadequacies of the “surgical
model” defined by Lambros.[3 ] The entire superficial soft tissue envelope is mobilized by creating greater fat
repositioning which “volumizes” the midface and maximizes the amount of soft tissue
reduction necessary in reversing aging changes, creating outcomes that better duplicate
the “mirror lift” ([Figs. 11 ] and [12 ]).
Fig. 10 A deep plan dissection schematically representing a fully degloved midface in the
deep plane. The superficial soft tissue envelope contains the majority of the facial
fat and behaves as a unit. (Adapted with permission from Gordon NA, Adam, SI. The
deep plane approach to neck rejuvenation. Facial plastic surgery clinics of North
America. 2014;22(2):269–284.)
Fig. 11 Preoperative (A ) and postoperative (B ) photos of a 59-year-old woman who was treated with a deep plane facelift, browlift,
upper and lower blepharoplasty, and periocular Er:YAG laser skin resurfacing. Note
the recreation of her facial shape at both the midface and jawline with revolumization
of the midface without the addition of extrinsic volume.
Fig. 12 Preoperative (A ) and postoperative (B ) photos of a 59-year-old woman who was treated with a deep-plane facelift, browlift,
upper and lower blepharoplasty, and periocular and perioral Er:YAG laser skin resurfacing.
Note the significance of gravity reversal, soft tissue reduction procedures in creating
this outcome.
Using intraoperative evidence from deep-plane rhytidectomies as the method to define
the proportional contribution of gravity's effects to the facial aging process, we
can see very significant amounts of soft tissue redundancy created both in obvious
cases in the older patients, but also, surprisingly, in younger patients ([Fig. 13 ]). The amount of soft tissue excess created by surgical facial degloving in the subfascial
“deep” plane reveals gravity's significant effect in creating aging. The fact that
younger patients also can exhibit large amounts of soft tissue redundancy points to
soft-tissue compliance being a significant predictor of the rate of facial aging.
Fig. 13 Intraoperative photos demonstrating the excessive soft-tissue redundancy created
after deep-plane dissection and mobilization of the facial soft tissues, even in the
younger patient. This redundancy supports gravity's effects on facial soft tissue
as the etiology in facial aging. (A ) A 43-year-old woman undergoing deep plane facelift. (B ) A 59-year-old woman undergoing deep plane facelift.
As soft-tissue redundancy cannot descend uninhibited because of the anatomical barriers
such as the nasolabial fold, mandibular ligament, and the mandibular septum, the redundant
soft tissue will “pile up” resulting in hollows and folds which mimic the appearance
of facial fat loss. The illusion of fat loss is better understood by viewing in [Fig. 14 ]. In the figure, there are two containers which each contain the same volume, the
first figure is a smaller container (young face) and appears full. The same volume
in a larger container (gravity-affected face) appears half empty or volume depleted.
If we view the superficial soft tissue envelope as a container that holds the facial
fat, the volume of fat can stay the same, but if the container increases in size because
of the gravity's effects, an illusion of facial fat loss will occur.
Fig. 14 Same volume but different size containers creates the illusion of greater volume
in the smaller cylinder and less volume in the larger cylinder.
Our recent understanding of facial skeletal changes provides the final piece of the
puzzle. Loss of overall bony volume enhances the overall appearance of soft tissue
redundancy by shrinking the infrastructure over which the superficial soft tissue
envelope rests, explaining the progression of neck changes in the advanced age. Specifically,
the illusion of independent fat compartments aging in an otherwise homogeneous superficial
soft tissue unit is better explained by understanding the changes in the structure
that the soft tissue “blanket” rests on. Evidence from skeletal research shows one
of the major areas of bone resorption and retrusion associated with aging is the medial
maxilla. This is where clinical observation suggests the most obvious region of facial
fat loss occurs. The bone resorption directly causes a loss of medial maxillary projection
and increases the pyriform aperture both of which contribute to the illusion of independent
fat compartment atrophy. The production of nasolabial folds and hollows, not fully
reversible by the “surgical model,” is more likely, in our opinion, proportional because
of the skeletal loss rather than actual fat loss. In further support, the area also
recalcitrant to the “surgical model,” and simultaneously responsive to the “volume
model,” is the periorbital region. Here again, evidence points to significant skeletal
resorption and loss of support structures as the predominant etiology.
While the proportion of aging changes because of the gravity's effects on the superficial
soft-tissue envelope, which appear to be the predominant factor in aging, changes
in the facial skeleton are significant and become more pronounced with advancing age.
This helps explain the limitations in outcomes in certain older patients even with
subfascial, soft-tissue reduction procedures.
Volume enhancement is an essential part of facial rejuvenation. Its success as a treatment
modality is best seen in younger patients where gravity changes are subtle and in
areas of greatest facial bone resorption. The addition of volume is most likely camouflaging
early gravity's effects on the soft tissues in younger patients, while restoring skeletal
volume in advancing age. The use of volume enhancement is also successful in camouflaging
certain inadequacies of soft tissue reduction procedures. Facial fat loss clearly
can occur because of aging, but currently there is no study to our knowledge that
documents these changes. As stated by Lambros, volume used as the sole treatment for
the aging face just produces a “fat face.”[3 ]
Conclusion
Research and clinical evidence combine to reveal that gravity's effects on the superficial
soft-tissue envelope of the face are the most significant effect in explaining the
aged face. Skeletal remodeling and bone loss both enhance the appearance of gravity's
effects, provide limitations to the surgical model of facial rejuvenation, and are
likely being successfully treated by volume enhancement modalities. These effects
combine to produce an illusion of facial fat loss as a major etiology in the aging
face.
Key Points
Debate exists as to the etiology of facial aging with the “surgical model” emphasizing
gravity's effects causing soft-tissue descent and ptosis while the “volume model”
emphasizes deflation and fat loss.
The platysma muscle/SMAS/galea are the continuous superficial cervical fascia encompassing
the majority of facial fat within the superficial soft tissue envelope, is poorly
anchored to the face and most susceptible to gravity's stretching effects.
Research shows that the facial fat is compartmentalized but there is no direct evidence
of facial fat loss because of aging.
Substantial evidence supports facial skeletal remodeling with bone loss in critical
areas such as the orbit and maxilla explaining many aging changes.
Anatomical barriers impede the descent of soft tissue redundancy, creating hollows
and folds, mimicking volume loss in the face.
Facial bone loss is greatest in regions most successfully treated with volume enhancement.
Facial aging is mainly because of gravity's long-term effects on the superficial soft
tissue envelope, with increasing effects because of skeletal remodeling, especially
with advanced age.
The visual effects of redundant soft tissue and selective bone loss create an illusion
of facial fat loss being the significant contributor to the facial aging.
