Facial bone loss

Bone is a living tissue that undergoes remodeling throughout life, which involves the alternating processes of resorption carried out by osteoclasts and the formation of new bone by osteoblasts. In youth, both processes remain relatively balanced. With age, depending on the anatomical region, bone metabolism can shift toward a predominance of resorption or lead to changes in bone geometry without a uniform reduction in all of its dimensions.

Aging of the facial skeleton is a multifactorial process. It is influenced by:

• genetic predispositions, biological sex, and craniofacial structure;
• hormonal changes, especially estrogen deficiency after menopause;
• osteopenia and osteoporosis;
• tooth loss, periodontal diseases, and atrophy of the alveolar processes;
• changes in mechanical loading associated with chewing and muscle function;
• nutritional deficiencies, low physical activity, tobacco smoking, and excessive alcohol consumption;
• chronic diseases and certain medications, including long-term use of glucocorticosteroids.

Facial bone loss is not synonymous with osteoporosis. Physiological remodeling of the craniofacial skeleton can occur in a person with normal skeletal mineral density. Osteoporosis, however, can exacerbate the loss of bone quality, especially in postmenopausal women. The assessment of bone changes should also take into account the dentition, periodontium, occlusion, and the condition of the maxilla and mandible.

Remodeling does not occur uniformly. Imaging studies indicate several areas that are particularly susceptible to resorption and changes in projection:

• Orbits: the most pronounced changes are usually observed in the superomedial and inferolateral aspects of the orbital rim. The orbital aperture gradually increases in surface area, and its shape becomes less regular.
• Maxilla: the anterior surface of the maxilla may recede, especially in the infraorbital region and the medial cheek. The bony support of the midface is reduced.
• Piriform aperture region: the margins of the bony nasal aperture may widen and recede. This alters the support for the nasal base, alae, and upper lip.
• Alveolar processes: following tooth loss, particularly intensive resorption takes place. Atrophy can reduce the height and width of the bone, affecting the profile of the lips and the lower face.
• Mandible: remodeling involves the body, ramus, mandibular angle, chin, and the area anterior to the jowl, referred to as the prejowl. The mandibular angle may become more obtuse, and its anterior contour less defined.
• Zygomatic bones: their central part is relatively more stable than the maxilla; however, changes in the adjacent zygomaticomaxillary region limit cheek support.

The extent of remodeling depends on baseline anatomy, sex, population origin, dental status, and mechanical loads. Therefore, a single pattern of aging should not be considered universal for every face.

Physiological craniofacial remodeling cannot be completely stopped. However, modifiable risk factors can be limited, and diseases that accelerate bone loss can be treated. Adequate intake of protein, calcium, and vitamin D, resistance training, not smoking tobacco, limiting alcohol, treating periodontal diseases, and replacing missing teeth as quickly as possible are of fundamental importance. If osteoporosis is suspected, a medical consultation, risk factor assessment, and, if indicated, a DXA bone density scan are recommended. Osteoporosis medications are used for medical reasons, not as an aesthetic procedure.

The procedures available at Ambasada Urody can correct the external consequences of the loss of bone support function, but they do not rebuild or stop the physiological atrophy of the facial skeleton:

• volumetric lifting and V-lifting using cross-linked hyaluronic acid, calcium hydroxyapatite, or hybrid preparations can restore the projection of the cheeks, temples, and selected support points;
• cheek and chin modeling and Texas jawline lifting can improve the contour of the lower face;
• tear trough filling can reduce the hollow at the junction of the eyelid and cheek, but requires particularly careful qualification;
• autologous fillers, including CGF Harmony, can replenish selected soft tissue deficits;
• collagen stimulators, such as Sculptra, Radiesse, and Lenisna, improve the tissue scaffold and skin quality, but do not create new bone;
• Nefertiti Lift using botulinum toxin reduces the activity of the platysma muscle and selected depressor muscles of the lower face. It can thereby improve the jawline contour, but it does not restore lost volume and does not affect bone structure.
• lifting threads mechanically lift and stabilize sagging soft tissues. They do not rebuild lost bone support, so their suitability depends on the degree of skin laxity, tissue distribution, and facial anatomy.
• firming treatments, using radiofrequency or ultrasound energy, among others, aim to improve skin tension and collagen remodeling. They can reduce some external signs of aging, but they do not inhibit craniofacial bone resorption.

These procedures can be considered as part of a multi-level facial aging correction if, in addition to the loss of bone support, there is excessive activity of depressor muscles, tissue displacement, or skin laxity. However, they are not methods for treating facial bone atrophy.

A correction plan should be developed following an analysis of the entire face. Excessive or superficial administration of the product does not restore skeletal anatomy and can lead to an unnatural increase in volume. Fillers are also associated with a risk of vascular complications, which is why the procedure should be performed by a physician with an in-depth knowledge of facial anatomy.