The Physiology of Dermal Ageing

by L'AVES 29 October 2019

The skin serves as a protective barrier between the body’s internal organs and the environment. It is a complex organ composed of many cell types and structures. The main three layers of the skin are the epidermis, dermis and hypodermis (subcutaneous tissue). The subcutaneous tissue consists of adipose (fat) cells, which support the connective tissue framework.

 

As we get older, our skin starts to become drier, thinner and more fragile. It isn’t as smooth or tight as it used to be. It may bruise more easily and skin might become looser. You may get lines or wrinkles and parts of your skin may start to ‘droop’. You may even lose cartilage in parts of your face. Ageing skin is at risk of breakdown and ultimately failure. It has a thinner epidermis with flattened dermal ridges making it less resistant to shearing forces. The complex biochemistry of the dermis is altered with age and the delicate balance between those enzymes that control remodeling and repair of the dermis is also disrupted, contributing to the overall loss of connective tissue and atrophy of the skin.

Coupled with a reduced ability of the skin to regenerate and a less efficient protective immune functioning, it is not surprising that the skin of chronologically ageing individuals is at risk of breakdown and failure.

 

Changes in Connective Tissue

 

Approximately 20% of dermal thickness disappears as people become elderly. The connective tissue which gives our skin its strength and ‘bounce’ contains a number of components which you are sure to have heard of - collagen, elastin, and hyaluronic acid. These compounds are responsible for the connective tissue which keeps our skin looking youthful.

 

Collagen

 

The primary structural component of the dermis and the most abundant protein found in humans, collagen is responsible for conferring strength and support to human skin.

Over time, the structural proteins and main components of the skin deteriorate, resulting in the cutaneous signs of ageing. Type I collagen is the most abundant protein of the skin’s connective tissue. This tissue also contains other types of collagen (III, V, VII), elastin, proteoglycans, fibronectin and extracellular matrix proteins. Of the dry skin mass, 70% is comprised of collagen. The loss of collagen is considered the characteristic physiological finding in aged skin. In aged skin, collagen is characterized by thickened fibrils, organized in rope-like bundles that appear to be in disarray in comparison to the pattern observed in younger skin. In addition, lower levels of collagen are synthesized by aged fibroblasts. As we age, collagen production slows down and elastin has a bit less spring. Structural destruction and loss of dermal collagen fibre bundles lead to wrinkling and increased appearance of muscular attachments.

 

Elastin

 

Elastin is an essential part of various human tissues that depend on elasticity. These connective tissues include the skin, lung and arteries. Elastin provides these elastic tissues with the ability to stretch and recoil and plays a critical role in supporting and maintaining healthy cells.

 

The underlying age-related changes in elastin are not as well understood as the changes in collagen, but alterations in elastic fibers are so strongly associated with photo-aged skin that ‘elastosis’, an accumulation of formless elastin material, is considered characteristic of photo-aged skin. Decreases in skin elasticity and resiliency are observed in older skin. The connective tissue network gradually disappears with age. Consequently, skin elasticity is also gradually lost with age. The phenomenon of sagging skin often observed in the elderly may, in fact, be due in large part to this loss of elasticity.

 

Changes in Connective Tissue

 

Glycosaminoglycan’s (GAGs) - Hyaluronic Acid

GAGs, along with collagen and elastin, are among the primary constituents of the dermis and are responsible for conferring the outward appearance of the skin. These polysaccharide chains are also important molecules because they exhibit the capacity to bind water up to 1000 times their volume. There are numerous members in the GAG family, including hyaluronic acid, which is the one we will focus on in this section. These compounds render normal skin plump, soft and hydrated, and are believed to assist in maintaining proper salt and water balance.

 

Several studies suggest that GAGs, particularly hyaluronic acid, have been found to be reduced in amount in photo-aged skin. Some studies offer conflicting reports, however, suggesting no changes in the level of GAGs in aged skin. The fact that hyaluronic acid is synthesized in the epidermis as well as the dermis likely accounts for this discrepancy in findings. In skin that ages intrinsically, the total hyaluronic acid level in the dermis remains stable; however, epidermal hyaluronic acid diminishes almost completely.

 

Photo aged skin has been shown to be characterized by reduced levels of hyaluronic acid. Hyaluronic acid is found in young skin at the periphery of collagen and elastin fibers and where these types of fibres intersect. In aged skin, such connections with hyaluronic acid disappear. It is possible that the decreases in hyaluronic acid levels, which contribute to its disassociation with collagen and elastin as well as reduced water binding, may be involved in the changes noted in aged skin, including wrinkling.

 

Free Radicals

 

The ageing process, both intrinsic and extrinsic, is believed to be influenced by the formation of free radicals, also known as reactive oxygen species (ROS). But what is a free radical exactly?

We live in an oxygen-rich environment of about 21% O2. This allows most species on Earth to survive. However, this oxygen-rich environment also results in some negative outcomes, especially in terms of oxidation or the generation of free radicals. It is thought that free radical damage is involved in or responsible for a number of diseases and that it also plays a core role in the ageing process.

 

Oxidative Stress

 

Free radicals have somehow lost an electron. They can be formed during normal bodily functions such as when cells burn food for energy or even when the body is fighting off bacteria or viruses. Free radicals in general are not dangerous. But when our cells are exposed to pollution, radiation, cigarette smoke or certain chemicals, this process creates a larger quantity of free radicals in the body: a surplus of unbalanced cells looking to become balanced by scavenging for electrons. They will actually “steal” electrons from balanced cells and set off a chain reaction of damage. If there are no electrons available, or if free radical production is in excess, damage occurs and creates an environment of oxidative stress.

 

Substantial evidence exists to support that ageing is associated with, though more likely, the consequence of free radical damage by various reactive oxygen species (ROS). ROS include superoxide and hydroxyl radicals and other activated forms of oxygen such as hydrogen peroxide. During times of environmental stress, ROS levels can increase dramatically, causing significant damage to cell structures. This is known as oxidative stress.

The primary sites of production of ROS are the mitochondria in our cells. Ageing is associated with changes in the molecular structure of DNA, proteins, lipids, and prostaglandins – these are all markers of oxidative stress. The accumulation of these molecular changes, particularly in proteins, constitutes the basis of cell ageing. However, it is also recognized that ROS play a role in normal signaling processes and that their generation is essential to maintain our internal body’s environment.

 

Antioxidants and Free Radicals

 

Intrinsic vs. Extrinsic Ageing

The skin and hair are subject to both intrinsic or physiological ageing, and extrinsic or premature aging due to external factors. Intrinsic factors are related to individual genetic mechanisms which vary between individuals. Extrinsic factors that are well-established causes for skin ageing include ultraviolet radiation of the sun’s rays, cigarette smoking, poor diet (lacking in key ‘beauty nutrients’), alcohol consumption and lack of sleep.

Basically, it is the facets of the whole lifestyle that contribute significantly to prematurely aged skin.

 

When designing anti-ageing skincare, it is therefore important to thoroughly investigate the preventative side of anti-ageing as this will yield the best results for your products. In fact, research has shown that extrinsic ageing has the greatest influence over the individual ageing of our own skin. Some researchers think that as little as 3% of the skin-ageing processes are caused by genetic factors and that the rest is all lifestyle-based. This is exciting news for those of us in cosmetic formulation as it means we can potentially make a real difference.

 

It is now largely accepted that ageing is not ‘‘coded’’ into the genome although modifications of the coordination of gene functions are certainly involved. The hereditary genetic influences, which up to a few decades ago were thought to account for approximately 25% of the ageing process, are now considered to represent somewhere between 3 and 15%.

 

Degradation of Skin Cells

 

The most obvious sign of dermal ageing is the degradation of the tissue, i.e. the loss of skin-cells. This happens in 2 ways:

 

1. Cells simply stop multiplying because they reach the end of their telomere length. Telomeres are the ends of chromosomes (DNA strands) Think of telomeres as a bookend. They keep chromosomes protected and prevent them from fusing into rings or binding with other DNA. Telomeres play an important role in cell division. Each time a cell divides, the DNA unwraps and the information in the DNA is copied. The process does not copy all of the DNA information - the telomeres are not copied. When the cell is finished dividing, the DNA comes back together. The telomeres lose a little bit of length each time this happens. When a cell divides and copies DNA, the strands of DNA get snipped to enable the copying process. The places that are snipped are the telomeres. Since the telomeres do not contain any important information, more important parts of the DNA are protected.

 

The telomeres get shorter each time a cell divides, like a pencil eraser gets shorter each time it's used. When the telomere becomes too short, essential parts of the DNA can be damaged in the replication process.

Scientists have noticed that cells stop replicating when telomeres are too short. In humans, a cell replicates about 50 times before the telomeres become too short. While telomere shortening has been linked to the aging process, it is not yet known whether shorter telomeres are just a sign of ageing - like grey hair - or actually contribute to ageing.

 

2. Cells become senescent, they stop being able to reproduce themselves due to certain ‘genetic switches’ which allow the cell to exit from reproductive life.

 

Prevention is Key

Cosmetic chemists and dermatologists constantly warn us about the dangers of sun- exposure and instruct us to cover up. Depending on where you live in the world and the amount of UV exposure your skin receives, you should most certainly seek to avoid UV damage to your skin. Photo ageing is the number one cause of dermal ageing. We recommend three stages of prevention of excessive dermal ageing:

 

Primary prevention:

 

•  Avoid overexposure to the sun

 

Secondary prevention:

 

• Eat a healthy, balanced diet

• Avoid cigarette smoke

• Avoid environmental pollution

• Get enough sleep

• Get plenty of fresh air

• Don’t consume too much alcohol

 

Tertiary prevention:

 

• Dermo-cosmetic substances

• Anti-ageing cosmeceuticals

 

All 3 preventative strategies must be in place to be able to make a noticeable difference to the skin. There’s no point in quitting smoking while still eating junk food every day, or avoiding the sun while drinking too much alcohol every night.

 

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