Traditionally, sagging skin on the face and other parts of the body was treated with surgical lifting procedures. During the last 2 decades, a wide range of non-invasive treatments such as ablative and non-ablative laser skin removal and radiofrequency (RF) have been introduced as alternative therapies to achieve different degrees and depths of tissue tightening through controlled heating of dermal tissues. Essentially, these treatments use infrared light or RF to cause controlled thermal injury up to 2 to 4 mm deep in the dermis. Volumetric tissue heating causes immediate collagen contraction and delayed neo-collagenogenesis over a period of 6 months, resulting in clinical skin tightening. Although traction has been demonstrated with these devices, there are several drawbacks, including inconsistent clinical results, the need for multiple treatments, and associated pain and expense. Recently, intensively focused ultrasound has been introduced into therapeutic equipment, providing depths of treatment much greater than the aforementioned technologies. In human cadaveric facial tissue, microthermal coagulation zones up to 7.8 mm deep with epidermal sparing have been reported. As such, thermal contraction of deeper dermal elements such as the superficial musculoaponeurotic system can lead to lifting and tightening of the skin.
The mechanisms of aging
Aging can be seen as an accumulation of changes in cells and tissues resulting from greater disruption of regulatory mechanisms, which leads to reduced resistance of the organism to stress and disease. The idea of greater disruption in aging is illustrated by the erosion of the orderly neuroendocrine feedback regulation of luteinizing hormone (LH), follicle-stimulating hormone (FSH), adrenocorticotropic hormone (ACTH), and growth hormone (GH) secretion. These changes manifest as menopause, andropause, adrenopause and somatopause. Skin aging is part of a slow decline in appearance and function that is largely attributed to the drastic decline in hormones in the body after adulthood. At the cellular level, several processes are involved in the physiology of aging and the development of some age-related diseases. The process of apoptosis means the process of non-traumatic and non-inflammatory cell death. Disorders of apoptosis are associated with an increased incidence of skin malignancies that are more common in the elderly, such as basal cell carcinoma, squamous cell carcinoma, and malignant melanoma. Cell senescence limits cell division in normal somatic cells and may play a central role in age-related diseases. Telomeres are considered a factor in cellular aging and may contribute to the genetic background of human aging and longevity. The limited proliferative potential of human cells is thought to be the result of telomere shortening that occurs during DNA synthesis at each cell division. Photoaging can accelerate telomere shortening and shift cells into senescence earlier. This could be the reason why different growth factors can affect the speed and quality of wound healing. Biochemical attacks also occur within aging cells, in part from the action of reactive oxygen species that are generated and not completely eliminated during the cell cycle. Aging-related changes also occur between and among cells through changes in the intercellular matrix, the exchange of trophic factors, the release of inflammatory cytokine mediators, and the degree of infiltration of other associated cell types. In addition, the amount and distribution of various growth factors can influence wound healing. Declining DNA repair combined with loss of melanin increases the risk of photo-carcinogenesis and may also lead to a decline in enzymatically active melanocytes (10-20% each decade) contributing to increased sensitivity to UV radiation. However, it is not known why free radical damage does not adversely affect all cells in the body (eg, gonadal germ cells).
Intrinsic Issues of aging

Smoking
It is commonly recognized that smoking greatly speeds up skin aging. Skin aging can even occur as a result of secondhand cigarette smoke exposure. Cigarette smoke contains nicotine, which is harmful to the skin’s microvasculature and slows down the healing process. By upregulating the expression of tropoelastin and metalloproteins, it also damages keratinocytes and fibroblasts. Furthermore, smoking decreases the production of procollagen while increasing the expression of tiny proteoglycans. Clinically, these consequences show up as wrinkled, pale skin. Direct toxic damage or oxidative stress can cause DNA abnormalities. Elastosis, telangiectasia, skin roughness, and premature wrinkles are all caused by nicotine-induced vascular constriction, and smoking has been directly linked to an increased risk of wrinkles. Research by Park et al. in 2018 showed that cigarette smoke not only increases oxidative stress but also triggers autophagy. Skin of smokers at 40 years old can resemble that of nonsmokers at 70 due to tobacco’s irreversible skin damage, though further harm can be prevented by quitting smoking. Wang et al. in 2018 found that applying tobacco extracts to skin and oral fibroblasts in vitro triggered senescence markers like premature cell cycle arrest, oxidative DNA damage, inflammatory cytokine and MMP secretion, and reduced expression of cell junction proteins like E-cadherin and Zonula occludens-1 (ZO-1).
Sleep
Lack of sleep doesn’t just affect how your face looks; it also impacts how socially engaged you are. With 50–70 million Americans experiencing sleep issues, it’s clear this is a widespread problem. Sleep plays a vital role in the body’s development and renewal processes. A 2015 study discovered that individuals who sleep well tend to have lower scores for intrinsic skin aging, as measured by SCINEXATM. On the flip side, inadequate sleep can result in more visible signs of skin aging such as wrinkles, uneven skin tone, and decreased skin elasticity. Additionally, slow recovery from skin damage can exacerbate these effects, potentially leading to reduced self-esteem regarding one’s appearance. When individuals don’t get sufficient sleep, they often exhibit physical manifestations such as downturned mouth corners, puffy eyes, under-eye dark circles, and drooping eyelids. Wrinkles, commonly associated with aging, can be influenced by sleeping positions or specific facial expressions. Sleep-related wrinkles are typically influenced by the pressure exerted on the face against a pillow, while expression wrinkles have diverse origins and appearances.
Harsh soaps
Aging often brings about dry skin, which can be exacerbated by hot showers and the use of alkaline bar soaps. Dryness, scaling, and roughness of the skin can also be caused by lipid solvents such as acetone, alcohols, and nonionic surfactants. The condition of the skin can be affected by various cleansing agents, even simple tap water. When the skin’s pH increases, it can disrupt the natural protective barrier called the “acid mantle,” disturb the balance of skin bacteria, and interfere with the functioning of proteins in the upper epidermis, which work best at an acidic pH. Additionally, a loss of skin fat can exacerbate dehydration, resulting in dry and flaky skin. To avoid skin damage, it’s advisable to use cleansers with a pH level of 5.5 or closer.
Menopause
Women’s skin ages faster when they have low estrogen levels. Because it helps with skin hydration, sebum production, improves stratum corneum barrier function, and raises collagen and elastin levels, estrogen is essential for maintaining the structural and functional integrity of the skin. Women’s skin often ages faster than expected after menopause, characterized by thinner skin, less collagen and elasticity, more wrinkles and dryness. Skin tissues that contain estrogen receptors, especially sebaceous glands and epidermal cells, are the main targets of this drop in estrogen levels. It is interesting to note that androgen hormone levels do not drop significantly at this time.
The hypoestrogenemic state of menopause affects the metabolism of dermal cells, which leads to a change in the content of collagen, a change in the concentration of glycoaminoglycans and a decrease in water content. Skin elasticity and strength decrease as a result of these changes, which are common indicators of skin aging. Collagen content can be determined by a number of techniques, such as direct skin biopsy, assessment of skin thickness, and analysis of collagen indicators in skin blisters. All of these techniques show a decline in collagen content during menopause. On the other hand, systemic or local administration of estrogen may counteract some of these effects. For example, topical estrogen has been shown to increase epidermal thickness and keratinocyte proliferation in just two weeks.
Skin thickness decreases by about 1.13% per year in estrogen-deficient women, but collagen content decreases by approximately 2% per year in postmenopausal women. For example, during the first five years after menopause, the amount of type I and III collagen in the skin can drop by as much as 30%. Age is not as closely related to this decline in skin thickness and collagen content as was the time of estrogen deficiency. The greatest loss was recorded in the first five years, after which the collagen content drops by 1%-2% per year.
Conclusion
Transangular intensity focused ultrasound can be used safely and effectively to improve the clinical appearance (texture and contour) of the upper arms, extensor knees, and medial thighs. Additional research is necessary to determine specific treatment parameters, as well as the need and timing of additional treatments to optimize clinical results on these and other body parts.
References:
- Alster, T.S., & Tanzi, E.L. (2005). Noninvasive lifting of arm, thigh, and knee skin with transcutaneous intense focused ultrasound. Dermatologic Surgery, 31(9), 1237-1239.
- Lee, S.Y., Park, K.H., Choi, J.W., & Kwon, K.R. (2007). Anti-wrinkle effect of a novel cosmetic containing retinol microspheres on Asian skin: a randomized, double-blind, controlled study. Journal of Cosmetic Dermatology, 6(3), 189-193.
- Weiss, R.A., McDaniel, D.H., Geronemus, R.G., & Weiss, M.A. (2005). Clinical trial of a novel non-thermal LED array for reversal of photoaging: clinical, histologic, and surface profilometric results. Lasers in Surgery and Medicine, 36(2), 85-91.
- Kim, Y.J., & Park, K.Y. (2018). Facial rejuvenation effects of low-level laser therapy (LLLT) with the 1444 nm neodymium: yttrium-aluminum-garnet (Nd:YAG) laser. Journal of Cosmetic and Laser Therapy, 20(7-8), 393-397.