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. Lambros and others have concluded that changes in volume of cheek fat, both loss and gain, rather than ptosis account for an aged appearance. Numerous anatomical studies, however, 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.
Facial Skeleton Aging
In addition to soft tissue changes, it has been demonstrated that there is remodeling of the craniofacial skeleton with age, for example, bony remodeling in the orbit. These will be discussed separately in the remainder of this chapter.
One of the theories behind the skeletal changes is mechanotransduction, which is the process of skeletal remodeling due to mechanical forces of soft tissue on bone.
The functional matrix hypothesis states that “epigenetic, extra skeletal factors and processes are the prior, proximate, extrinsic, and primary cause of all adaptive, secondary responses of skeletal tissues and organs.” This 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.
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. 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.
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.”
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.
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. The results, illustrated in Fig. 13.1 , concluded that, with age, bony changes and soft tissue consequences occur. These include the following:
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 three-dimensional 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. 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.
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 ).