Why does our skin form wrinkles as we age?
This post will outline the answer in a few steps:
- Under what conditions do materials form wrinkles, in general?
- How does the general theory of wrinkles apply to aging human skin?
- What underlying factors drive the physiological changes which result in wrinkles?
In the process, we’ll draw on sources from three different fields: mechanical engineering, animation, and physiology.
Why do Materials Wrinkle?
Imagine we have a material with two layers:
- A thin, stiff top layer
- A thick, elastic bottom layer
We squeeze this material from the sides, so the whole thing compresses.
The two layers want to do different things under compression:
- The thin top layer maintains its length but wants to minimize bending, so it wants to bow outward and form an arc
- The elastic bottom layer wants to minimize vertical displacement, so it wants to just compress horizontally without any vertical change at all.
Because the two layers are attached, these two objectives trade off, and the end result is waves - aka wrinkles. Longer waves allow the top layer to bend less, so a stiffer top layer yields longer waves. Shorter waves allow the bottom layer to expand/compress less vertically, so a stiffer bottom layer yields shorter waves. The “objectives” can be quantified via the energy associated with bending the top layer or displacing the bottom layer, leading to quantitative predictions of the wavelength - see this great review paper for the math.
Engineers do this with a thin metal coating on soft plastic. The two are bound together at high temperature, and then the whole system compresses as it cools. The end result is cool wrinkle patterns:
Other interesting applications include predicting mountain spacing (with crust and mantle as the two layers) and surface texture of dried fruit - see the review paper for more info and cool pictures.
The same thing happens in skin.
For our purposes, skin has three main layers:
- The epidermis is a thin, relatively stiff top layer
- The SENEB (subepidermal non-echogenic band, also sometimes called subepidermal low-echogenic band, SLEB) is a mysterious age-related layer, mostly absent in youth and growing with age, between the epidermis and dermis - more on this later
- The dermis is the thick base layer, containing all the support structure - blood vessels, connective tissue, etc
Both the SENEB and the dermis are relatively thick, elastic layers, while the epidermis is thin and stiff. So, based on the model from the previous section, we’d expect this system to form wrinkles.
But wait, if our skin has a thin stiff top layer and thick elastic bottom layer even in youth, then why do wrinkles only form when we get old?
Turns out, young people have wrinkles too. In youth, the wrinkles have short wavelength - we have lots of tiny wrinkles, so they’re not very visible. As we age, our wrinkle-wavelength grows, so we have fewer, larger wrinkles - which are more visible. The real question is not “why do wrinkles form as we age?” but rather “why does the wavelength of wrinkles grow as we age?”.
Based on the simple two-layer model, we’d expect that either the epidermis becomes more stiff with age, or the lower layers become less stiff.
This the right basic idea, but of course it’s a bit more complicated in practice. These guys use a three-layer model, cross-reference parameters from the literature with what actually reproduces realistic age-related wrinkling (specifically for SENEB modulus), and find realistic age-related wrinkles with these numbers:
(arrows indicate change from young to old). Other than the SENEB elastic modulus, all of these numbers are derived from empirically measured parameters - see the paper for details.
Age-Related Physiological Changes
We have two main questions left:
- Why do the dermis and epidermis stiffen with age?
- What exactly is the SENEB, and why does it grow with age?
I haven’t looked too much into stiffening of the dermis, but the obvious hypothesis is that it stiffens for the same reason lots of other tissues stiffen with age. At some point I’ll have a post on stiffening of the vasculature which will talk about that in more depth, but for now I’m going to punt.
The paper from the previous section notes that the epidermis stiffens mainly due to dehydration; rehydrating the epidermis reverses the stiffening (this is the basis of many cosmetics). A dehydrated epidermis makes sense, since both the SENEB and age-related problems in the vasculature will isolate the epidermis more from the bloodstream (although I haven’t seen direct experimental evidence of that causal link).
That leaves the mysterious SENEB. What is it, and why does it grow with age?
The name “subepidermal non-echogenic band” is a fancy way of saying that there’s a layer under the epidermis which is transparent to ultrasound imaging. That’s the main way the SENEB is detected: it shows up as a space between the epidermis and dermis on ultrasound images of the skin.
As far as I can tell, little is known about the SENEB. The main things we do know:
- SENEB grows with age; see numbers above
- SENEB is found in aged skin typically exposed to sunlight (“photoaged”, e.g. hands and face) but not in hidden skin (e.g. butt).
Most authors claim that the SENEB consists of elastin deposits. That matches what we know of solar elastosis, the build-up of elastin deposits in photoaged skin. But I haven’t seen anyone systemically line up the ultrasonic and histologic images and chemically analyze the SENEB layer to check that it really is made of elastin. (This may just be a case of different researchers with different tools using different names for things which are the same.)
Assuming that the SENEB does consist of accumulated elastin, why is elastin accumulating? Well, it turns out that elastin is never broken down in humans. It does not turn over. On the other hand, the skin presumably needs to produce new elastin sometimes to heal wounds. Indeed, many authors note that the skin’s response to UV exposure is basically a wound-healing response. Again, I haven’t seen really convincing data, but I haven’t dug too thoroughly. It’s certainly plausible that elastin is produced in response to UV as part of a wound-healing response, and then accumulates with age. That would explain why the SENEB grows in photoaged skin, but not in hidden skin.