Why Do Men’s Faces Get Wider With Age?

As men age, their facial structure changes, including a noticeable widening. This transformation results from biological and physiological processes affecting bones, muscles, fat distribution, and skin integrity.

Various factors contribute to this shift, from hormonal fluctuations to structural remodeling of facial tissues. Understanding these mechanisms explains how aging shapes the male face and why some individuals experience more pronounced changes than others.

Hormonal Factors

Hormones significantly influence facial structure throughout life, continuing into adulthood. As men age, shifts in hormone levels affect bone density, muscle mass, and fat distribution, altering facial width. Three key hormones—testosterone, growth hormone, and cortisol—play central roles in this process.

Testosterone

Testosterone, the primary male sex hormone, shapes facial bone structure, particularly during puberty, when it drives jawline development and broader features. However, its influence persists beyond adolescence. Research indicates testosterone levels decline about 1% per year after age 30 (Matsumoto, 2002, Journal of Clinical Endocrinology & Metabolism). This decline reduces bone density, contributing to changes in the lower jaw through resorption and remodeling. Lower testosterone also affects fat distribution, leading to increased fat deposition in the cheeks and jawline, further altering facial proportions. Additionally, reduced testosterone weakens the masseter and temporalis muscles, impacting facial contours and making the face appear broader due to soft tissue laxity.

Growth Hormone

Growth hormone (GH) is crucial for bone remodeling and soft tissue maintenance. While highest during puberty, GH continues influencing facial structure into adulthood. It stimulates osteoblast activity, affecting bone density and shape. As GH levels decline with age—a phenomenon known as somatopause—bone resorption can outpace formation, leading to subtle but cumulative changes in facial width. A study in Aging Cell (2017) found that decreased GH contributes to mandibular widening due to differential bone resorption and deposition. GH also regulates collagen synthesis, supporting skin and connective tissue integrity. As levels drop, collagen production declines, increasing skin laxity and soft tissue redistribution, further emphasizing facial broadening. In cases of GH dysregulation, such as acromegaly, excessive GH leads to exaggerated jaw and facial bone growth, highlighting its role in facial morphology.

Cortisol

Cortisol, the primary stress hormone, influences facial structure through its effects on fat distribution, muscle composition, and bone metabolism. Chronically elevated cortisol—linked to prolonged stress and aging—can increase fat accumulation in the cheeks and jawline, contributing to a wider appearance. This is well-documented in conditions like Cushing’s syndrome, where excessive cortisol causes a characteristic “moon face” due to abnormal fat deposition (New England Journal of Medicine, 2015). Even without pathological cortisol excess, age-related increases in cortisol levels promote changes in facial fat storage. Additionally, cortisol’s catabolic effects weaken facial musculature, reducing support for the overlying skin and contributing to a broader, more rounded facial shape over time.

Facial Bone Remodeling

Facial widening with age is not solely due to soft tissue changes but also structural remodeling of the facial skeleton. Unlike long bones, which stop growing after adolescence, craniofacial bones undergo subtle but significant changes throughout life. This remodeling is influenced by mechanical forces, hormonal shifts, and the balance between bone resorption and deposition.

One of the most noticeable skeletal changes occurs in the lower jaw. Longitudinal cephalometric studies show the mandibular angle becomes more obtuse with age, broadening the lower face (Behrents, 1985, American Journal of Orthodontics). This results from bone resorption at the gonial angle and periosteal apposition along the mandible’s inferior border. Additionally, remodeling in the condylar region increases transverse dimensions over time. Declining bone mineral density further alters the facial skeleton’s structural integrity, exaggerating the perception of widening.

Changes also occur in the midface, particularly in the maxilla and zygomatic bones. Three-dimensional CT scans reveal that the midfacial skeleton gradually shifts posteriorly and inferiorly with age (Pessa et al., 1999, Plastic and Reconstructive Surgery). This affects the orientation of the zygomatic arches, contributing to increased facial width. Bone resorption in the maxilla reduces anterior projection, subtly flattening the midface and emphasizing lateral expansion.

Mechanical forces from surrounding musculature also influence facial bone remodeling. The masseter and temporalis muscles exert continuous pressure on the underlying structures, leading to adaptive changes over decades. A study in the Journal of Anatomy (2013) found that individuals with stronger masticatory function exhibited more pronounced mandibular flaring, demonstrating the role of muscle activity in shaping facial width. As muscle tone diminishes with age, the balance between muscle-induced remodeling and bone resorption shifts, potentially contributing to a broader and less defined mandibular contour.

Cartilage And Soft Tissue Changes

As men age, cartilage and soft tissue undergo gradual transformations that contribute to increased facial width. Unlike bone, which remodels through resorption and deposition, cartilage continues to grow and change in composition. This is particularly noticeable in areas such as the nasal septum and ear cartilage, which influence facial proportions. The nasal cartilage weakens and elongates over time, subtly widening the bridge and base. Combined with gravitational forces acting on the nasal tip, this can create a broader midface appearance.

Supporting soft tissues, including ligaments and fascia, also change with age. Over time, the retaining ligaments anchoring facial fat pads lose elasticity and tensile strength. This allows soft tissue to shift laterally, particularly in the lower face and jawline. Additionally, degradation of elastin and glycosaminoglycans in the extracellular matrix diminishes the skin’s ability to maintain its original contours, further accentuating these changes.

Skin And Collagen Dynamics

Collagen, a fibrous protein providing tensile strength and resilience, is essential for skin integrity. In early adulthood, collagen production remains stable, maintaining skin firmness. However, as men age, collagen synthesis declines by about 1% per year, leading to progressive changes in skin texture and elasticity (Varani et al., 2006, Journal of Investigative Dermatology). This reduction affects how skin drapes over bones and soft tissue, contributing to facial broadening as it becomes less taut and more susceptible to gravitational shifts.

Beyond collagen depletion, the organization of collagen fibers within the dermis deteriorates. Younger skin features a dense, structured network that resists mechanical stress, but aging fragments and disorganizes these fibers. This leads to decreased skin thickness and increased sagging, particularly in the lower face, exacerbating the widening effect.

Facial Musculature

Facial muscles, particularly those involved in mastication and expression, change in tone, strength, and distribution with age, affecting facial width. The masseter muscles, responsible for jaw movement and chewing, may hypertrophy in individuals who grind their teeth or engage in excessive jaw movement, widening the jawline. Conversely, muscle atrophy reduces support for overlying tissues, allowing skin and fat to shift laterally. This is particularly noticeable in the lower face, where diminishing tone in the platysma and other supporting muscles contributes to a broader, less defined jaw contour. Neuromuscular adaptations further reduce muscle responsiveness, leading to progressive laxity and altered facial proportions.

Adipose Tissue Distribution

Fat distribution significantly affects facial width over time. Unlike the centralized fat deposits of youth, aging redistributes facial fat, increasing fullness in some areas while depleting others. This process is influenced by metabolism, hormones, and the structural integrity of fat compartments.

In younger individuals, facial fat is compartmentalized into distinct pads that provide lift and contour. With age, the ligaments holding these fat pads weaken, allowing fat to descend and shift outward. This lateral migration contributes to increased facial width, particularly in the lower face and jawline. Additionally, age-related changes in fat metabolism increase superficial fat accumulation in the buccal and submental regions, exaggerating the broadening effect.

Environmental And Lifestyle Influences

Beyond biological processes, environmental factors and lifestyle choices contribute to facial widening with age. Long-term exposure to stressors like sun damage, pollution, and diet accelerates structural changes in skin, muscles, and fat. Chronic sun exposure degrades collagen and elastin, leading to early skin laxity and altered fat distribution.

Smoking accelerates collagen breakdown and impairs circulation, reducing skin firmness and increasing sagging. Excessive alcohol intake can cause fluid retention and inflammation, leading to recurrent facial puffiness that may contribute to long-term structural changes. Diets high in processed foods and sugars promote chronic low-grade inflammation, affecting fat metabolism and skin integrity. Combined with genetic predisposition, these factors influence how significantly an individual’s face widens with age.