First named in 2007 by Professor Jean Hilaire Saurat, a dermatologist, dermatoporosis is a skin disease related to skin aging. After a certain age, the skin becomes so fragile that it tears. What are the symptoms? What are the risk factors? Can this be avoided?
What is dermatoporosis?
As life expectancy increases, we are increasingly confronted with a new dimension of skin aging, which is no longer only cosmetic but also functional, as the skin loses its protective mechanical properties. We propose to summarize the different manifestations and effects of this chronic skin insufficiency/fragility syndrome under the generic term “dermatoporosis”. The molecular mechanisms surrounding the CD44 and hyaluronate expression seem to play an important role in the pathogenesis. Dermatologists should be aware of this emerging syndrome and act as main actors in its prevention and treatment. Randomized clinical trials should show which interventions are most likely to prevent and/or treat dermatoporosis.
Skin aging is one of the most visible signs in humans as they get older. It has received renewed interest as treatments have been identified that could prevent or mitigate it.
Read Also: HGH and Its Anti Aging Effects On The Skin
The concept of “failure” is well accepted for organs such as kidneys, liver, heart, and lungs. In the case of the skin, the chronic failure of its essential functions fits well with the concept of “failure” and therefore a new terminology is needed to describe this type of skin disease.
An acute, often fatal, skin failure is the sudden loss of its vital functions, such as in severe burns or toxic necrotic epidermolysis (Lyell syndrome). This is well described and nothing new.
What is new, however, is a chronic skin insufficiency syndrome associated with advanced age, a high cumulative dose of solar radiation and prolonged use of topical and/or systemic corticosteroids, which, with increased life expectancy, becomes an emerging clinical problem with significant morbidity, sometimes due to prolonged hospitalization. With increasing age, the progressive disappearance of hyaluronic acid, which stabilizes the intercellular structures and forms a viscoelastic network with collagen and elastin fibers, leads to a degeneration of the extracellular matrix, followed by the loss of the skin’s mechanical protective functions and great fragility.
The term “dermatoporosis” has recently been proposed in 2007 by Professor Jean Hilaire Saurat to cover all manifestations and effects of this chronic skin syndrome linked to the fragility of the skin that comes with aging.
Clinical manifestations of dermatoporosis
The clinical manifestations of dermatoporosis include morphological markers of fragility (skin atrophy, senile purpura, Stellate spontaneous pseudo scars) and the functional expression of skin fragility (skin tears, poor healing, subcutaneous bleeding). The first signs appear at the age of about 60 years, while the disease itself, with its associated complications, is observed between 70 and 90 years of age.
Skin atrophy is mainly observed in sun-exposed areas, especially on the back of the forearms and in pretibial areas. The skin is usually very thin, translucent, and wrinkled; dermal elastosis, senile purpura, and Stellate spontaneous pseudo scars are also observed.
The senile purpura is localized to the extremities and results from trauma associated with small hemorrhages in the dermis when there are no coagulation disorders. It affects about 10% of the population between 70 and 90 years of age, with women predominant, and is associated with pseudo scars in 90% of cases. These purple plaques then lead to brownish pigmented spots due to hemosiderin. Vitamin C deficiency can lead to bruising on the skin, which justifies a substitution treatment. Histologically, senile purpura is characterized by the red blood cells leaving the blood vessels.
Stellate spontaneous pseudo scars
These are called spontaneous skin injuries. They are observed in 20-40% of the population aged 70-90 years, with women being predominant. These lesions occur mainly on the backs of the hands and forearms and are accompanied by senile purpura in 30-50% of patients. There are currently three types of pseudo-scarring: linear, star-shaped, and irregular.
Deep dissecting hematoma
This serious complication represents a medical emergency and is the consequence of the mechanical fragility of the aged skin: the slightest shock can cause bleeding that can become lodged between the dermis and the subcutis or between the subcutis and the muscular fascia, and the dissection of these two levels deprives the affected areas of their vascularization and causes necrosis. The hematoma and necrotic tissue must be removed immediately to prevent further damage to the skin. Cutaneous dissection hematoma is most commonly found in the lower extremities of elderly patients (70 to 99 years of age) with dermatoporosis, with females being most predisposed (M/F ratio: 1/5) and in patients taking anticoagulants or corticosteroids. People with deep dissecting hematoma require long-term hospitalization.
Chronic post-traumatic injuries are a real problem in older people and the mechanisms of their slow and delayed recovery are not well understood. The reduced proliferative capacity of keratinocytes and fibroblasts and the production of metalloproteinases and various cytokines are clearly involved in this process.
Etiological classification of dermatoporosis
It is the most common form of dermatoporosis and is the result of chronological aging and chronic unprotected exposure to the sun. In analogy to osteoporosis, it is assumed that a genetic predisposition is often the origin of primary dermatoporosis, and the genes involved in the regulation of the components of the extracellular matrix are good candidates.
Secondary iatrogenic dermatoporosis
This form is due to long-term treatment with topical and/or systemic steroids known to modulate the expression of the genes for collagen I, III, IV and V, elastin, metalloproteinases 1, 2 and 3, tenascin and metalloproteinase inhibitors 1, 2 and 6. 5 There are no clinically significant differences between the two types of dermatoporosis, although ultrasound examinations may show thinner skin (0.5-0.7 mm) in secondary iatrogenic dermatoporosis. In addition, patients at risk for primary dermatoporosis develop secondary dermatoporosis earlier and more acutely under chronic corticosteroid treatment.
Different stages of dermatoporosis
Due to the prevalence of this disease in the elderly population, we believe it is important to distinguish between several stages of development, depending on the severity of the symptoms and their clinical impact. There are four stages:
Stage I: This stage is characterized by a severe thinning of the skin with senile purpura and Stellate spontaneous pseudo scars. The clinical assessment of the viscoelasticity of the skin is a good measurement parameter.
Stage II: In addition to the lesions observed in stage I, small localized lacerations are observed in the skin resulting from the separation between the dermis and epidermis.
Stage III: the skin cracks are more numerous and larger and can affect the entire surface of the extremities. There is clearly a delay in healing.
Stage IV: The progression of these lesions leads to the appearance of dissecting skin contusions, which constitute a medical emergency and require hospitalization.
Possible mechanisms of skin fragility in dermatoporosis
The mechanism of photoaging is well understood. As seen above, oxidative stress can be induced by ultraviolet light (UVA) and is involved in the aging process in general and in the skin in particular. Oxidative stress manifests itself through the production of reactive forms of oxygen and free radicals which cause, among other things, changes in nuclear and mitochondrial DNA and the activation of various matrix metalloproteinases with the associated biological consequences. For example, UV radiation activates growth factor receptors on the surface of keratinocytes, which leads to a signal that includes the activation of transcription factors of the AP-1 family in the cell nucleus, thereby disrupting collagen production by binding and sequestering factors that are required for the transcription of type I and type III Transforming growth factor-beta (TGF-beta). Hyaluronic acid and CD44-dependent signals are also suppressed by ultraviolet rays: in mice, UVA and UVB rays induce a strong decrease in hyaluronic acid and cutaneous CD44; this effect can be avoided by topical application of retinoids. In general, photo-induced changes in the extracellular matrix explain well the elastosis in the superficial dermis observed in people with sun damage.
Changes in the viscoelasticity of the skin
The extracellular matrix of the skin contains two main glycosaminoglycans, dermatan sulfate, which is closely linked to the collagen fibers, and hyaluronic acid, which occupies the space between the fibers. Collagen and elastin fibers are responsible for the elasticity of the skin, while hyaluronic acid determines its viscosity. The viscoelasticity of the skin, therefore, enables it to absorb the mechanical stresses to which it is exposed, disperse the absorbed energy, and return to its original structure. The changes in the extracellular matrix described above lead to fractures of the collagen fibers and to a reduction in hyaluronic acid, the main consequence of which is the progressive loss of this essential property of the skin, namely its viscoelasticity.
Defects in hyaluronic acid signaling/CD44
It has been observed that hyaluronic acid, the main component of the extracellular matrix, gradually decreases during the aging process. On the other hand, apart from its physical properties which are involved in the viscoelasticity of the skin, hyaluronic acid is a biologically active molecule that induces intracellular signals after binding to a membrane receptor called CD44. A study in mice has shown that the two main biological responses resulting from CD44 activation are the regulation of keratinocyte proliferation and the control of local hyaluronic acid homeostasis. Topical retinoids induce epidermal hyperplasia by activating the HB-EGF-dependent pathway. In mice, topical application of retinaldehyde increases the expression of CD44 and hyaluronic acid synthesizing enzymes (hyaluronic acid synthetases).
These studies indicate that the hyaluronic acid and CD44-dependent signaling pathway is affected in dermatoporosis and represents a good target for the development of new therapeutic strategies for this emerging syndrome.
Treatment of Dermatoporosis
Although a doctor could prescribe a prescription-strength retinoid or even HGH injections to help thicken and rejuvenate skin prevention remains the key to a good prognosis.
To prevent the skin condition from getting worse protection from the sun and moisturizing must become second nature to you. Do not expose yourself too much to the sun and protect yourself whenever you are exposed to it. It is recommended to use a high SPF sun protection with a protective spectrum that includes both UVA and UVB rays.
Good skin hydration is also indispensable for slowing down skin aging. For this, you could use hyaluronic acid-based creams, as hyaluronic acid production is significantly reduced in patients suffering from dermatoporosis. You may also consider using moisturizing oils that are rich in vitamin E such as Argan oil, Olive oil, and coconut oil. There are many companies offering decent moisturizing creams and oils such as Skinception, Eucerin, estheticshub, and much more. NB: Gilmore Health is not endorsing any products so do your due diligence!
For all skin types, especially those with dermatoporotic tendencies, it is advisable to opt for simple life changes from the age of forty by Limiting stress, promoting good sleep, reducing or even giving up smoking, finding natural alternatives to certain medicines (antidepressants, corticosteroids) and moisturizing your skin religiously.
Avoid prolonged exposure to the sun.
Eat foods rich in antioxidant that can help the body fight free radicals.
Compensate for the loss of hyaluronic acid: Cosmetic application of high-dose hyaluronic acid, supplemented by oral supplements, seems to be the only alternative to correct the decline in the body’s naturally produced hyaluronic acid and increase its internal production.