Chronic Rosacea

Disorders that cause redness or inflammation of facial skin are a subject the general public has little knowledge of and about which the medical community has a poor understanding. At least one person in every ten in the adult population has a significant problem with increased facial redness (flushing, blushing, or rosacea), making these conditions more common than diabetes or asthma.



Disorders of frequent flushing or blushing may appear to be trivial complaints to those who do not suffer from them, but can be major problems to those afflicted, affecting both their personal and professional lives. Similarly, persistent redness and inflammation of the face or nose (rosacea) is often dismissed as a minor problem and sufferers can become the subject for “humorous” remarks. The enlargement or distortion of the nose (rhinophyma) that sometimes is seen in patients with rosacea is commonly (and incorrectly) thought to result from alcohol abuse, enhancing the social stigmatization that these individuals endure.

The reality is that people who develop these conditions have physical problems that arise for reasons that are not of their own making and that are not related to dietary or alcohol indiscretion. They suffer not only the discomfort of their disorders (which can affect not only the skin but the eyes as well), but at times social stigmatization.



Although rosacea is more common than diabetes and clearly visible to all, it is largely unknown to misunderstood by the general public. Knowledge relating to the epidemiology, etiology, and pathogenesis of this facial disorder that affects adults in middle age is limited. There are effective treatments of most of the manifestations of rosacea, but the mechanism of many treatments (particularly antibiotics) is unclear. In spite of this for the majority of patients a careful approach by their clinician to the diagnosis, classification, and management of their disorder will yield good results.

The poor definition of rosacea was compounded by its assumed association with excessive consumption of alcohol. This deeply imbedded misconception in the minds of many members of the public has had the effect of stigmatizing patients with this disorder. The fact that the disorder is highly visible on the prominences of the face and difficult to mask cosmetically has made rosacea a skin condition that has a disproportionately large psychologic impact on sufferers.

To understand rosacea, a working knowledge of the structure and function of normal skin is necessary. This work will begin with a review of the structure and function of human skin with particular reference to the face as the basis for the discussion of the clinical features and postulated pathogenic mechanisms of the different subtypes of rosacea.

Flushing and blushing are reactive vascular changes in the face seen in normal individuals. These take place in response to various stimuli, especially heat, certain foods, alcohol or emotional swings. Frequent and prolonged flushing can be a manifestation of abnormal psychosocial sensitivity or systemic illness such as the carcinoid syndrome. Frequent flushing can also be the presenting complaint of some patients with rosacea or accompany the inflammatory skin changes. The various types of flushing, their causation, and mechanism of action are reviewed in the next section together with the available treatments for this troublesome condition.

The basis for clinical diagnosis of rosacea and its classification into subsets is described in the next section. This classification provides a common language and has helped to clarify the various components of this disorder. This helps
communication between researchers and physicians and ultimately will translate into better patient care.

There are four subtypes of rosacea :

  1. Erythematotelangiectatic rosacea (ETTR)
  2. Papulopustular rosacea (PPR) 
  3. Phymatous rosacea (PR)
  4. Ocular rosacea (OR)

 Each subtype is then graded according to disease severity. The grading system also assists clinicians in selecting therapy and in evaluating the patient’s response to therapy.

In the following sections we will review pathophysiology and a guide to the appropriate treatment.


What causes Chronic Rosacea?

The study into the pathophysiology of rosacea has long been hampered by the lack of specific diagnostic criteria. In addition, many studies fail to specify the breakdown of the various subtypes, which may potentially have varied pathogenic mechanisms. Nonetheless, several fundamental findings have recently been made, and our understanding of the pathophysiological factors underlying the development of rosacea will likely improve significantly in the near future. Numerous mechanisms have been proposed over the years, including vascular abnormalities, inflammation and dermal matrix degradation, climactic exposures, and various microbial and parasite organisms, and will now be examined at length.

1. Vascular abnormalities

Vascular abnormalities |Ungex

Since flushing is often exaggerated in rosacea patients, inherent vascular abnormalities have been proposed as a causative factor in the pathogenesis of this disorder (Wilkin 1994). In a small study, a normal physiological response to hyperthermia of shunting blood away from facial circulation in order to increase blood flow to the brain was absent in rosacea patients (Brinnel et al. 1989). Rosacea patients have also been shown to flush more easily in response to various thermal stimuli. In the case of oral exposure to heat, such as that seen with ingestion of hot liquids, a countercurrent heat exchange between the internal jugular vein and the common carotid artery may be produced, thus triggering an anterior hypothalamic thermoregulatory reflex, resulting in cutaneous vasodilation (Wilkin 1981).

Of note, a high expression of D2-40, a marker of lymphatic vessels, in the affected skin has been demonstrated in both early and long-standing disorder, suggesting lymphangiogenesis as an early pathological process in rosacea (Gomaa et al. 2007).


2. Inflammation and dermal matrix degradation

Abnormalities of dermal connective tissue as seen in rosacea patients may be caused by the preceding vascular derangements (Neumann & Frithz 1998). Thus, inherent or acquired vasculopathy and the increased expression of VEGF may lead to leaky blood vessels and dermal accumulation of cytokines and other inflammatory mediators with subsequent dermal matrix deterioration.

The newest findings involving the action of cathelicidin in the pathophysiology of rosacea gives further credence to the primary role of the immune system in rosacea (Yamasaki et al. 2007).


3. Climactic exposures

The notion that climactic exposures, most notably solar radiation, may lead to the development of rosacea has been advocated by many investigators (Wilkin 1994). This is supported by the observation that convex, sun-exposed surfaces are typically involved, sparing the sun-protected periorbital and submental areas. Prolonged ultraviolet (UV) radiation leads to the degradation of the elastic fiber network and collagen fibers in the dermis, resulting in the accumulation of solar elastotic material.

Additionally, despite a common misperception, rosacea patients do not show increased photosensitivity compared to the normal population. In fact, minimum erythema dose of either UV-A or UV-B radiation in rosacea patients is not decreased (Lee & Koo 2005). Thus, flares in response to sun exposure may actually be a reaction to heat rather than the light itself (Kligman 2006).


4. Demodex mites

Microscopic Demodex mites are a natural part of the human microbiome — the ecological community of microorganisms that live within and on the body. Two species of Demodex are found in humans. Demodex Folliculorum live in hair follicles, primarily on the face, as well as in the meibomian glands of the yyelids; Demodex Brevis live in the sebaceous glands of the skin.

While Demodex folliculorum are found on the skin of all humans, they frequently occur in greater numbers in those with rosacea. There has been much debate as to whether their increased numbers are a cause or result of rosacea. However, evidence appears to be mounting that an overabundance of Demodex may possibly trigger an immune response in people with rosacea, or that the inflammation may be caused by certain bacteria associated with the mites.

A severe infestation of Demodex mites, known as demodicosis, may mimic the symptoms of rosacea but fail to respond to traditional rosacea therapy.

Dr. Frank C. Powell, consulting dermatologist at Mater Misericordiae Hospital in Dublin, Ireland, noted that the mites are most plentiful in the same regions of the face that are most commonly affected by rosacea — the cheeks, nose, chin and forehead — and that large quantities of mites have been found in biopsies of rosacea papules and pustules.

According to research by Dr. Martin Schaller, assistant professor of dermatology at Ludwig-Maximilians University in Munich, Germany, a severe infestation of Demodex mites, known as demodicosis, may mimic the symptoms of rosacea but fail to respond to traditional rosacea therapy. Dr. Fabienne Forton, a dermatologist in private practice in Brussels, Belgium, suggested both an indirect and a direct role for the mites themselves in the development of the disorder. Skin infections and disruption of the skin barrier stimulate toll-like receptors to induce cathelicidin production, and the complaint of sensitive skin in rosacea patients often disappears when the number of mites is reduced to normal by treatment, she noted.


Nonetheless, several questions persist. First, a complete characterization of the additional proteases and protease inhibitors involved in the homeostasis of LL-37 is critical. Second, although the above findings represent a major breakthrough in the pathophysiology of rosacea, the initial insult or defect that eventuates in the overexpression of SCTE and cathelicidin LL-37 still needs to be identified. Finally, future research studies may attempt to develop specific mechanism-based treatments afforded by these new findings.



Appropriate Treatment

Both topical and oral therapeutic agents introduced in the previous chapter have been shown to be of significant value in the treatment of rosacea. Clinical improvement, however, is usually most apparent in the inflammatory lesions associated with the disease, including papules and pustules, whereas the effect of these agents on erythema and especially telangiectasias tends to be limited at best. On the other hand, lasers and similar devices can predictably attain considerable amelioration in these latter lesions, thereby significantly improving the quality of life in rosacea patients, especially those with the erythematotelangiectatic
subtype (Tan & Tope 2004).

Preoperative Care

Laser- and light-based treatment of rosacea is generally well-tolerated with relatively little preoperative preparation. Since makeup can both reflect and absorb various wavelengths of light, it is imperative that patients carefully remove all makeup and other facial products before the procedure. Most patients being treated for rosacea do not require topical anesthesia for pain control. As will be discussed below, epidermal cooling during the procedure helps to reduce patient discomfort. Additionally, topical anesthesia causes vasoconstriction, resulting in the loss of tissue chromophore. Nonetheless, a topical anesthetic cream, such as a mixture of topical 2.5% lidocaine and 2.5% prilocaine, or regional nerve blocks can be employed in exquisitely sensitive patients.

Finally, as mentioned above, melanin represents a competing chromophore when rosacea is being treated with lasers and light systems. This includes retinal melanin, thus obligating the practitioner to utilize wavelength-specific protective goggles both for the patient and the assisting staff.


Pulsed-dye Lasers

Pulsed dye laser (PDL) was the first laser to be designed in compliance with the theory of selective photothermolysis and was introduced in 1986. The original system emitted light with a wavelength of 577 nm, thus corresponding to one of the major oxyhemoglobin absorption peaks. Subsequently, the wavelength was increased to 585 nm and, later, to 595 nm in order to increase cutaneous penetration without a significant compromise to vascular selectivity. Both wavelengths are currently in use in the numerous systems available today. 

The duration of improvement in rosacea symptoms and signs following PDL treatments has not been adequately studied and appears to vary significantly. In one study, worsening of residual erythema was reported to occur anywhere between 6 months and 52 months following laser treatment, depending on the original number of treatment sessions (Tan et al. 2004). The longevity of improvement likely also depends on the frequency of post-treatment exposure to rosacea triggers.


Demodex Mites Treatment

As it was mentioned before, Demodex mites might play a role in causing chronic rosacea. Dealing with these tiny creature would help with treating rosacea.

Ungex Control shampoo was formulated for treatment of mild and severe stages of head demodicosis. Complex of natural oils, herbal extracts and minerals helps to boost the immune system of the skin. Stimulates metabolism of hair follicles and scalp infected with the skin parasites. The shampoo effectively reduces Demodex population.

This unique shampoo is exceptionally designed to help to eliminate Demodex mites from your hair and skin. It is formulated for dry skin and hair, this Shampoo gently cleanses away Demodex mites, alleviating skin inflammation issues, such as acne, rosacea, demodicosis, dandruff, hair loss, and itchiness.



The proof is in the results

Ungex has formulated a product which has helped thousands of people around the world deal with their acne, rosacea and seborrheic. When you work with us, we will ensure you receive the highest quality products and treatment plan to help permanently treat your acne.


Acne and Rosacea: Epidemiology, Diagnosis and Treatment by David J Goldberg

Rosacea Diagnosis and Management by Frank Powell

Causes of Rosacea: Demodex Mites & Microbes 


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Rosacea Treatment

What Are Demodex mites?

How to Kill Demodex Mites?

Can Demodex Mites Cause Seborrheic Dermatitis?