What are the origins of telangiectasia?

The mechanisms underpinning the dilation of vessels are poorly understood. However, several factors are suspected.

• Primitive anomaly of the facial vein circulation.

  Studies have reported that there appears to be a primary abnormality in the circulation of the facial vein in rosacea. Normally, the blood from the facial veins, which is cooler than the rest of the blood, flows downwards towards the jugular veins. When the temperature increases (physical activity or hyperthermia), the flow in the facial vein is reversed: the blood flows upwards through the angular vein, reducing the temperature of the arterial blood that reaches the brain, thus cooling it down.

  In the context of rosacea, there would be an inhibition of venous blood flow from the skin to the brain. This results in blood stagnation in the capillaries, leading to vessel dilation and inflammation. The area of rosacea being that of facial vein drainage, it can be thought that a venous abnormality could promote telangiectasias. However, the causes of its onset are still unclear.

• Exposure to UV rays.

  Rosacea predominantly affects individuals with fair skin and light eyes, who are more frequently subject to photoaging due to UV exposure. Biopsies of rosacea lesions typically reveal a solar elastosis, which is a deterioration of the elastic tissue in the dermis. UV radiation promotes photoaging by inducing matrix metalloproteinases (MMP), which degrade and suppress collagen production. It has been demonstrated that the impact of collagen degeneration mediated by MMP-1 on endothelial cells leads to the formation of vascular tubes. These vascular tubes resemble the lumen of telangiectasias. We therefore believe that UV exposure promotes the formation of telangiectasias.

• Repeated vasomotor flushes.

  Vasomotor flushes are reactions in response to physical exertion or strong emotions (anger, excitement) and can lead to skin reddening. During these situations, the autonomic nervous system responds by secreting adrenaline. The vessels dilate, warm blood rushes to the face and reddens the skin. It has been proven that repeated episodes of vasodilation associated with vasomotor flushes lead to a loss of vascular tone and a permanent dilation of the vessels. These dilated vessels can become permeable with a subsequent release of inflammatory mediators. This will then result in continuous skin inflammation and permanent telangiectasias.

• Sensory factors in vascular dysregulation.

  Various known triggers of rosacea (spicy food, alcohol, sudden temperature changes, UV radiation, physical exercise, stress) can potentially cause the appearance of telangiectasias. These factors would activate ion channels, such as TRPV1, involved in vasoregulation and pain perception (nociception). Once activated, these channels will upregulate substance P and CGRP, two vasodilators, and cause vasodilation, which in some cases can lead to telangiectasias.

• Pregnancy.

  Despite the limited number of studies on the subject, it is believed that rosacea telangiectasia during pregnancy is exacerbated. Indeed, during pregnancy, the production ofoestrogens increases. The oestrogens are known to be vasodilators. Therefore, being pregnant could potentially increase the occurrence of rosacea-related telangiectasia. It should be noted that these are only assumptions.

• Genetics.

  Finally, this condition could also be hereditarily transmitted. The presence of family history in individuals with rosacea has led researchers to hypothesise that unidentified genes are at the root of the disease, and concurrently, telangiectasias. It is also worth noting that individuals with light phototypes, as well as women, appear to be more susceptible to developing this skin disorder. However, further studies are necessary to confirm this hypothesis.