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Video 12.1 Mandible angle augmentation. This video demonstrates the placement of a
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porous polyethylene mandible angle implant immobilized with titanium screws.
178.e1
Chapter 13
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Rejuvenation of the aging face
and skeleton with implants
In his article “Anatomy and pathophysiology of facial aging”, Zimbler states,
“Facial aesthetics begin with the marriage of hard and soft tissue integration;
however, it is the changing balance of these elements that is the hallmark of the
aging process … A youthful face therefore represents a point in time when a
particular set of skeletal proportions are ideal for their soft tissue envelope.”
SOFT TISSUE AGING
Soft tissue ptosis secondary to gravity has long been considered the major
mechanism responsible for facial aging. There is no doubt that gravity and
ptosis are the main factors leading to facial aging.2 Lambros and others have
concluded that changes in volume of cheek fat, both loss and gain, rather than
ptosis account for an aged appearance.
ever, show that there are also many changes to the craniofacial skeleton as
patients age that contribute to the aging process.
The aging face typically shows the following changes: descent of the brow,
changes in contour of the upper eyelid, medialization of the lateral canthus,
lower eyelid descent, deflated infraorbital skin envelope, increased visibility of
the lid–cheek junction and nasojugal crease, increased prominence and depth
of the nasolabial fold, and increased prominence of the labiomandibular crease.
These signs of aging have been related to changes in skin and soft tissue.
In addressing soft tissue ptosis and volume changes, many facelifting techniques involve the removal of excess skin and also fat grafting and sculpturing. The main purpose of this chapter is to address the skeletal changes in the
face that contribute to aging. Other chapters discuss the techniques available to
address and reconstruct the facial skeleton for a more youthful appearance as a
sole procedure or in addition to other techniques.
3,4
Numerous anatomical studies, how-
1
FACIAL SKELETON AGING
In addition to soft tissue changes, it has been demonstrated that there is remodeling of the craniofacial skeleton with age,
the orbit.
which is the process of skeletal remodeling due to mechanical forces of soft tissue on bone.
factors and processes are the prior, proximate, extrinsic, and primary cause
of all adaptive, secondary responses of skeletal tissues and organs.”10 This
8,9
These will be discussed separately in the remainder of this chapter.
One of the theories behind the skeletal changes is mechanotransduction,
10
The functional matrix hypothesis states that “epigenetic, extra skeletal
5–7
for example, bony remodeling in
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Chapter 13 Rejuvenation of the aging face and skeleton with implants
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is, in essence, a restatement of Wolff’s Law, which is the observation that a
long bone changes its external shape and internal architecture in response
to stresses acting on it. A recent revision of the functional matrix hypothesis
stresses the importance of mechanotransduction, which is defined as the process of intercellular transaction of mechanical information into osteoblastic
changes.
10
Several studies have shown craniofacial changes as a result of facial muscle
and nerve ablation. Sinsel et al. in a laboratory study on rabbits demonstrated
misdirection of bony growth and changes in bony shape after ablating the buccal branches of the facial nerve and the muscles innervated by these branches.11
Matic et al. also demonstrated a decrease in bone volume of the mandible and
zygoma in rabbits after paralyzing the masseter muscle unilaterally with botulinum toxin.
12
A study conducted on patients with Moebius syndrome by Instrum et al.
exemplifies the relationship between musculature and bony changes. In this
neuromuscular syndrome, patients suffer congenital facial paralysis that is usually bilateral and involves cranial nerves VI and VIII. In some patients, cranial
nerve V is also involved, causing paralysis of the muscles of mastication. Skeletal changes are evident on cephalograms of patients with Moebius syndrome
and research has shown that these changes are more apparent in the cephalograms of patients with cranial nerve V involvement. These patients were found
to exhibit an “extreme pattern of vertical growth, clockwise rotation of the mandible, and an anterior open bite.”
13
Craniofacial skeletal changes, including significant lengthening of the face
and an anterior flare of the upper incisors, has been found to occur in patients
with spinal muscular atrophy and myotonic dystrophy, both syndromes that
cause weakening of the muscles of mastication.
14
The above studies indicate that muscle functionality is important to the
development of the bones on which they insert. When comparing the craniofacial skeletal changes that occur in aging with the changes that occur with
neuromuscular syndromes, it becomes apparent that the two are quite similar.
Therefore, we can conclude that normal facial muscle strength is important in
maintaining a youthful craniofacial skeleton.
THE AGING ORBITAL SKELETON
The notion of orbital aging has been the focus of several strands of research.
Pessa analyzed the changes to the orbital rims in 30 male skulls in three age
categories at the Smithsonian Institute. It was found that there was no change
in orbit width or height with increasing age. However, there was curve distortion of the superomedial upper orbit and inferolateral orbit, which led Pessa to
believe that the orbital rims receded in only these regions, without an overall
change in orbit height or length.
In a more comprehensive study by Kahn and Shaw, 60 white patients (30
female, 30 male), underwent facial bone computed tomography (CT) scans to
demonstrate how specific bony aspects of the orbit change with age. The study
population included 10 male and 10 female patients from each of the three age
categories: young (25–44 years), middle (45–64 years), and old (65+ years). CT
scans underwent three-dimensional reconstruction with volume rendering.9
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The results, illustrated in Fig. 13.1, concluded that, with age, bony changes and
soft tissue consequences occur. These include the following:
8
Young Female Old Female
Youth Age
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• A significant increase in orbital aperture width and area.
• A significant increase in height of the superior orbital rim medially, suggesting that the superior orbital rim recedes with age in this region. The
superomedial rim reshaping may cause exposure of the medial upper lid
fat, a change currently attributed to weakening of the orbital septum.
• The glabellar angle becoming more acute leads to the perceived descent of
the medial brow and the formation of glabella skin creases.
• The inferiolateral rim remodeling and increase in orbital aperture width
may contribute to the formation of crow’s feet and lower lid lag.
• The mediolateral rim remodeling found in the male study population may
contribute to the formation of the nasojugal groove and lower lid lag.
• The changes seen in the upper half of the orbit may result in the soft tissues
rolling into the orbital aperture and thus, the appearance of brow descent
and lateral orbital hooding.
• In the lower half of the orbit, the tissues may roll over the recessed
bony ledge leading to lag of the lower lid, appearance of descent of the
lid–cheek junction, and a deepening of the nasojugal groove as disproportionate tissue piles up against the orbicularis origin along the medial
rim.
This study expanded on previous literature, as it accounted for bony change
trends in males and females separately. It also provided a more accurate threedimensional representation, with the CT scans measured at 1.25-mm slice
widths, as opposed to 3-mm CT slices in previous studies. It therefore provides
convincing evidence that bony elements of the orbit undergo dramatic changes
with age and, along with soft tissue changes, lead to the appearance of the aged
eye and orbit.
The more extensive aging of the inferior orbital rim in male subjects than
in female subjects in this study correlates with the findings of Van den Bosch
in 1999.15 His study of 320 male and female subjects, aged between 10 and 89
years, found that after the age of 35, both genders experienced lower lid droop,
but the extent of this droop was twice as much in the male subjects. These two
studies draw a correlation between the recession of bone and soft tissue drooping in the lower lid lag.
The aging orbital skeleton
Fig. 13.1 Upper panel: Illustrations showing the typical appearance
of orbital tissues in youth (left) and old age (right). Lower panel:
Three-dimensional CT scans showing typical contours of the orbital
skeleton in a young female (left) and old female (right). These
illustrations and images correlate the aging changes that take place
in periorbital appearance with changes to the underlying skeleton as
described in detail in the body of this chapter.
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Chapter 13 Rejuvenation of the aging face and skeleton with implants
Youthful Orbits Aged Orbits Rejuvenated Orbits
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A B C
Fig. 13.2 Alloplastic augmentation of the infraorbital rim can restore youthful contour in an aged skeleton. (A) Youthful orbit. (B) Aged orbit.
(C) Implant augmenting aged orbit to simulate contour of youthful orbit.
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A B
Fig. 13.3 Clinical example of a 45-year-old man who underwent infraorbital rim skeletal augmentation together with subperiosteal
midface elevation to rejuvenate the aged orbit. Note postoperative elevation of lower lid and cheek, lengthening and narrowing of
palpebral ssure, as well as lateralization of lateral canthus. (A) Preoperative appearance. (B) Postoperative appearance at 1 year after
surgery.
Alloplastic augmentation of the infraorbital rim can restore youthful contour
in an aged skeleton as demonstrated in Fig. 13.2. Together with midface elevation, the stigmata of skeletal and soft tissue periorbital aging demonstrated in
Fig. 13.1 can be ameliorated with implant elevation and subperiosteal midface
soft tissue elevation (Fig. 13.3).
THE AGING MIDFACIAL SKELETON
The midfacial skeleton, consisting of the inferior orbital rim, the maxilla
(including the pyriform aperture), and the zygoma, are also subject to the
process of facial aging and bony changes. Literature by Pessa,
and others
of the midface as the aging process unfolds (Fig. 13.4). These changes can be
10,11,20,21
has shown a number of changes that occur to the bones
16,17
defined as:
• retrusion of the lower maxilla, resulting in the development of nasolabial
folds18;
• retrusion of the orbital rim and anterior cheek mass in relation to the cor-
neal surface17 (Fig. 13.5).
The above bony changes may result in the appearance of a midface concavity,
which gives the appearance of being tired due to the presence of long lower
eyelids, loss of cheek prominence, rounding of the lateral canthal angle, and
increased vertical height of the palpebral fissure.
22
Shaw,
18,19
The aging midfacial skeleton
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A
B
angles. (A) Young female skeleton. (B) Aged female skeleton. From Shaw and Kahn,18 with permission.
Fig. 13.5 Artist’s depiction of the changes on the
Aging faceYouthful face
midface and periorbita that occur with aging as
described by Pessa etal.17 He showed that in the
youthful face, the cheek fat lies anterior to the
cornea and the orbital fat lies slightly anterior to
the orbital rim (A). With aging, the cheek mass
tends to lie posterior to the anterior surface of the
cornea, the orbital fat moves slightly anterior, and
the infraorbital rim has a signicant movement
posteriorly (B). Hence, retrusion of the infraorbital
rim with aging makes the eyes appear more
Orbital fat
Infraorbital rim
Cheek mass
A
Cornea Cornea
B
Orbital fat
Cheek fat
prominent by changing globe–rim relations, and it
signicantly impacts the appearance of the lower
lid bags, particularly in those who tend toward
maxillary hypoplasia.
It is believed that the decrease in bony projection that occurs with aging
speeds the effect of gravity on the descent of an unsupported soft tissue envelope.22 An alternate hypothesis is put forward by Levine, who suggests that soft
tissue descent is the “engine” driving the aging process, with bone relocation
and reshaping determined by the pull of surrounding tissues.20 Regardless of
the pathophysiologic mechanism, skeletal augmentation provides an effective
method to restore facial convexity and to rebuild a platform that supports the
soft tissues of the face.
23
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Chapter 13 Rejuvenation of the aging face and skeleton with implants
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The potential for implants to restore youthful midface contours is illustrated
in Fig. 13.6 and demonstrated clinically in Fig. 13.7.
A B
C D E
Fig. 13.6 The potential for implants to restore youthful midface contours is illustrated. (A) Young skeleton. (B) Aged skeleton. Illustrations
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demonstrating the potential of implants to restore a youthful (more projecting and convex) midface skeletal contour. (C) Infraorbital rim
implant, (D) malar implant, and (E) pyriform aperture implant.
The aging lower facial skeleton
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A B
Fig. 13.7 An example of the projecting and rejuvenating eect of pyriform aperture augmentation on the lower midface: (A)
preoperative and (B) postoperative appearance.
THE AGING LOWER FACIAL SKELETON
The mandible is the foundation of the lower face. Normal mandibular proportions, including ramus height and length of the mandibular body, provide excellent support for the soft tissue repositioning that occurs with aging. However,
patients with a short ramus, rounded mandibular angle, and decreased mandibular projection are less skeletally equipped to gracefully support middle and
lower face soft tissue repositioning with age.
What exactly happens to the mandible as it ages? Which proportions are affected
by the aging process? In a study by Shaw et al.,21 facial bone CT scans were obtained
from 120 white subjects, of which 60 were female and 60 were male. The population
was further organized into three different age groups (20–40 years, 41–64 years, 65+
years), with 20 females and 20 males in each age category. The patients were measured for: bigonial width, ramus breadth, ramus height, mandibular body height,
mandibular body length, and mandibular angle. Fig. 13.8 demonstrates the morphology of a young and aged female mandible. The results revealed the following:
• Mandibular width did not significantly change with increasing age, which
implies that skeletal width of the lower face does not impact the aged appearance of the lower face.
• Mandibular angle increased with age and became more blunted, which
results in less jawline definition and a softer, more oval appearance of the
lower face.
• Mandibular height and mandibular length (projection) significantly de-
creased with age. Interestingly, the mandible projection decreases before
there is a decrease in mandible length. These changes may cause the appearance of a receding chin, and the overall loss of mandibular volume
21
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Chapter 13 Rejuvenation of the aging face and skeleton with implants
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A B
188
Fig. 13.8 Morphologic changes that occur with age in the mandible. (A) Young skeleton. (B) Aged skeleton.
may weaken the support of the buccal fat pad, allowing it to descend and
cause the appearance of jowls. Loss of mandibular volume also affects
the aging process of the neck by contributing to the increased laxity of the
platysma and soft tissues of the neck.
• The male study subjects had greater values for ramus height and mandibular body length as compared to the female subjects.
• The only measurement that was larger for female subjects compared to
male subjects was the mandibular angle. This explains why males tend to
exhibit stronger, more prominent jawlines than females, as the male mandibular angle is more acute.
The mandible changes dramatically with age, and the bony aging process is
primarily that of contraction and morphologic change. Effective rejuvenation of
the mandibular area should thereby account for both soft tissue treatments and
bony loss compensation. This approach is demonstrated in Fig. 13.9 where a
53-year-old woman underwent chin and mandible augmentation together with
rhytidectomy.
A limitation in the above-referenced human studies is that they are cohort
studies, not longitudinal, meaning they involved different groups of patients
at different age intervals, rather than observing the same patients over time. In
2017, the first longitudinal study of human facial skeletal aging was published
by Paskhover et al.24 It documents patterns of change in the facial skeleton
of 14 patients who underwent CT scans at least 8 years apart, with the initial
CT measurements documented between 40–55 years. The study revealed that,
with aging, the maxillary and piriform angles significantly decrease, as do
the glabellar and maxillary angles, whereas the piriform width significantly
increases. The study also notes some differences in these patterns between
sexes.24
PEARL
Facial skeletal convexity and
projection identify facial youth.
References
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Fig. 13.9 The rejuvenative eect of combined skeletal augmentation
and soft tissue manipulation. (A) Preoperative appearance of
a 53-year-old woman. (B) Postoperative appearance 1 year
after rhytidectomy combined with chin and mandible angle
augmentation. (C) Illustration of implant augmentation.
A
C
B
DELAYING SKELETAL SENESCENCE
Shaw et al.25 have suggested that skeletal bone mineral density of the face
changes with age similar to the axial skeleton. Their pilot study attempts to
pinpoint the time when these skeletal changes occur, which can allow objective
testing of specific treatments aimed at slowing or reversing these bony aging
changes. Pharmaceuticals and mechanical devices may delay, treat, or even
prevent these facial skeletal changes from occurring, opening up a whole new
paradigm in facial aging prevention.24 In the meantime, the aging process can
be masked and rejuvenated using facial implants in combination with soft tissue manipulations.
REFERENCES
1. Zimbler MS, Kokoska MS, Thomas JR. Anatomy and pathophysiology of facial aging. Facial
Plast Surg Clin North Am 2001;9(2):179–87, vii.
2. Tonnard PL, Verpaele A, Gaia S. Optimising results from minimal access cranial suspension
lifting (MACS-lift). Aesthetic Plast Surg 2005;29(4):213–20; discussion 221.
3. Lambros V. Observations on periorbital and midface aging. Plast Reconstr Surg
4. Coleman SR. Facial recontouring with lipostructure. Clin Plast Surg 1997;24(2):347–67.
5. Israel H. Recent knowledge concerning craniofacial aging. Angle Orthod 1973;43(2):176–84.
6. Behrents RG. Growth in the aging craniofacial skeleton. Monograph 17. Craniofacial Growth
Series. Ann Arbor: Center for Human Growth and Development, University of Michigan;
1985.
7. Bartlett SP, Grossman R, Whitaker LA. Age-related changes of the craniofacial skeleton: an
anthropometric and histologic analysis. Plast Reconstr Surg 1992;90(4):592–600.
8. Pessa JE, Chen Y. Curve analysis of the aging orbital aperture. Plast Reconstr Surg
2002;109(2):751–5; discussion 756–760.
9. Kahn DM, Shaw RB. Aging of the bony orbit: a three-dimensional computed tomography
study. Aesthetic Surg J 2008;28(3):258–64.
10. Moss ML. The functional matrix hypothesis revisited. 1. The role of mechanotransduction. Am
J Orthod Dentofac Orthop 1997;112(1):8–11.
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