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As we age, changes in our skin are inevitable. Fine lines, dryness, and sunspots are common signs we tend to expect. But for some, aging brings a lesser-known and more concerning skin condition: dermatoporosis.
Dermatoporosis is a chronic, progressive condition that results in extremely fragile and thinning skin. Often referred to as “chronic cutaneous insufficiency,” it primarily affects elderly individuals and is comparable to osteoporosis—but in the skin.
As we get older, our skin naturally becomes thinner and more fragile—but for some people, this goes a step further and becomes a condition known as dermatoporosis.
The term dermatoporosis was introduced by dermatologist Dr. Jean-Hilaire Saurat to describe a range of symptoms related to chronic skin fragility. In simple terms, it means the skin has lost its strength and resilience, making it more prone to bruising, tearing, and delayed healing. Over time, the skin’s natural protective barrier begins to break down, leaving it vulnerable to everyday wear and tear.
Dermatoporosis typically presents with the following symptoms:
Skin thinning – the skin appears almost translucent.
Easy bruising (purpura) – especially on the arms and hands.
Skin tears and lacerations – often from minimal trauma.
Pseudoscars (stellate scars) – small, white star-like scars that don’t fade.
Subcutaneous bleeding – visible pooling of blood under the skin.
There are two main types:
Primary dermatoporosis: This form is mostly caused by the natural aging process, often made worse by long-term sun exposure.
Secondary dermatoporosis: This occurs due to certain medications—most commonly corticosteroids (like steroid creams or tablets), which can thin the skin over time.
You might be surprised to learn that dermatoporosis is more common than many people think—especially in older adults. In fact:
A study of elderly patients in French hospitals found that around 32% of people aged 60 to 80 had signs of dermatoporosis.
In a Finnish study, researchers found that about 31% of patients over 60 had the condition, mostly affecting the arms.
Another large French study found the condition in nearly 38% of people over the age of 65—with women affected more often than men.
What’s also interesting is that dermatoporosis wasn’t just linked to age. Certain medications played a big role too. Strong topical steroid creams increased the risk more than fivefold, while oral steroids, blood thinners, and kidney problems were also associated with higher risk. Some patients with a skin condition called bullous pemphigoid had the highest rates of dermatoporosis—up to 64%.
Researchers have discovered that a key molecule called CD44—which sits on the surface of skin cells and binds to hyaluronic acid (HA)—plays a big role in keeping skin healthy. In mouse studies, when CD44 is reduced or blocked, the skin becomes noticeably thinner and weaker.
This finding helped lay the foundation for research into dermatoporosis.
Hyaluronic acid is a natural substance found in large amounts in the skin. It keeps the skin hydrated, plump, and elastic—basically everything we want healthy skin to be. But both CD44 and hyaluronic acid levels are found to be lower in people with dermatoporosis.
What’s more, exposure to UV rays—especially UVB and UVA from the sun—has been shown to reduce the production of both CD44 and hyaluronic acid in the skin. This helps explain why sun damage is such a major contributor to fragile, aging skin.
hyalurosome refers to a sort of “mini factory” on the surface of skin cells that helps produce hyaluronic acid (HA)—a key ingredient for keeping skin hydrated and firm. This little factory is made up of several important parts, including:
HA synthase 3 (HAS3) – the enzyme that makes hyaluronic acid
A special form of CD44 found in skin cells
The epidermal growth factor receptor (EGFR) – which helps with cell repair and renewal
All of these components work together to maintain strong, healthy skin. But in people with dermatoporosis, this hyalurosome setup doesn’t work as well. In fact, studies have shown that these key molecules are reduced in older or affected skin compared to younger, healthy skin.
Our skin is constantly renewing itself, and a big part of that process relies on special cells called stem cells. In healthy skin, there are two main groups of these important cells:
Lrig1+ stem cells – These are quiet, “resting” stem cells that serve as a backup reserve.
EGFR+/CD44v3+ stem cells – These are the active, hard-working cells that handle the daily task of renewing the skin.
In healthy skin, both groups work together to keep the surface fresh and functioning properly.
But in dermatoporotic skin, things change. Research has found that only the Lrig1+ stem cells remain active in the top layers of the skin, while the usual daily-renewing cells are missing. This means the skin has to rely solely on its backup system—kind of like running a marathon with only your second-string team.
In healthy skin, a protein called CD44 plays a key role in keeping things running smoothly. One of its jobs is to support a pathway called Wnt/β-catenin—which is like a communication system that tells skin cells when to grow and renew.
This pathway works closely with the hyalurosome, the tiny “skin-repair station” we mentioned earlier, and helps maintain the growth of the skin between hair follicles (known as the interfollicular epidermis). It’s especially active in a group of cells called the EGFR+/CD44v3+ cluster, which are responsible for daily skin renewal.
But in dermatoporotic skin, CD44 levels drop, and as a result, Wnt signalling slows down. Without this activity, the EGFR+/CD44v3+ cluster disappears—which means the skin loses one of its most important renewal systems.
This helps explain why dermatoporotic skin is thinner, slower to heal, and more fragile—it’s missing the very tools it needs to stay strong.
Calcium isn’t just important for bones—it also plays a key role in keeping your skin healthy. In the deeper layer of the skin (called the basal layer), there’s a special calcium channel known as Orai-1. This tiny protein helps bring calcium into skin cells and supports their growth and renewal, especially the cells called keratinocytes that make up most of our outer skin.
But in people with dermatoporosis, the amount of Orai-1 in the skin is reduced. That means the skin cells don’t get as much calcium as they need, which can slow down skin cell turnover and repair. This is one more reason why dermatoporotic skin becomes thinner, weaker, and more fragile over time.
Our skin cells go through a natural aging process, and one of the key signs that a cell has become senescent (meaning it’s old and no longer dividing) is the presence of a protein called p16 (short for p16^Ink4a^).
Scientists often use p16 as a marker for cellular aging, since it’s found in most aging or “retired” cells. In studies of dermatoporotic skin, researchers have found higher levels of p16-positive cells—especially in the top layer of the skin (the epidermis).
This means that the skin in dermatoporosis isn’t just fragile—it’s also made up of more aging cells that aren’t as active in repair and renewal, which helps explain the slower healing and thinning that comes with the condition.
Dermatoporosis isn’t just one condition—it progresses in stages, each with increasing severity. Understanding these stages can help with early detection and better management of the condition.
In the first stage, the skin starts to show signs of thinning (atrophy). You may notice:
Easy bruising (purpura)
Pseudo-scars – white, star-shaped marks that look like old scars but haven’t resulted from an actual injury
These are the earliest clues that the skin’s structure is becoming more fragile.
As the condition progresses, the skin becomes more delicate and prone to injury. In Stage II, skin lacerations less than 3 cm in size start to appear, often from minor bumps or friction that wouldn’t normally cause damage.
In Stage III, the tears become larger—more than 3 cm. These wounds can be painful and slow to heal, and they increase the risk of infection or complications, especially in older adults.
The most severe stage involves dissecting hematomas—large, deep bruises where blood collects under the skin and can spread between tissue layers. This stage is serious and usually requires medical attention to manage properly.
A topical formulation containing 5% ascorbic acid (vitamin C) has been shown to reduce the number of senile purpura (bruising) on the forearms of patients with scurvy—a condition also marked by skin fragility. In another case, an elderly patient with severe dermatoporosis saw significant improvement in blistering and spontaneous bruising after taking oral vitamin C supplements.
In addition to vitamin C, other soothing and barrier-repairing ingredients—like hyaluronic acid, retinoids, and niacinamide—may also be recommended by dermatologists to improve skin strength and hydration.
One effective approach is Platelet-Rich Plasma (PRP) therapy, which uses your body’s own growth factors to stimulate collagen production and improve skin strength. Another option are Collagen-stimulating injections that stimulates long-term collagen production, making the skin thicker, stronger, and more resilient.
Emerging treatments like growth factor serums and stem cell therapy are also being explored to boost natural repair processes and combat skin thinning at a deeper level.
CO₂ laser and microneedling are effective treatments for improving fragile, thinning skin caused by dermatoporosis.
CO₂ laser resurfaces the skin and boosts deep collagen production, helping to reduce atrophy, purpura, and improve firmness.
Microneedling uses tiny needles to stimulate natural healing and collagen, making it ideal for delicate skin with minimal downtime.
Dermatoporosis may be under-recognised, but it’s common—especially in older adults. If you or a loved one is experiencing frequent bruising, skin thinning, or slow-healing wounds, it’s important to seek help early.
With the right treatments, it’s possible to strengthen the skin, reduce symptoms, and improve quality of life.