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I. Introduction

II. Normal Blood Vessels

1. Function of normal blood vessels
   
2. Structure of normal blood vessels
   

III. Rosacea Blood Vessels

1. Rosacea blood vessels undergo changes in function
2. Rosacea blood vessels undergo changes in structure

IV.  Summary of Functional and Structural Changes

V.  References

I.  Introduction

Rosacea is primarily a disorder of the facial blood vessels. Experts from across the world agree that vascular abnormalities are central to all stages and symptoms of rosacea:

• Dr. Ramelet states, "The skin alterations in all four stages of rosacea as well as histopathologic investigations demonstrate rosacea to be essentially a cutaneous vascular disorder." (1)
  
  
• In a recent medical review article, "Rosacea: Pathophysiology and Treatment", Dr. Wilkin stresses that rosacea is primarily a disorder of the facial blood vessels. (2)
  
  
• A study performed by Dr. Marks on dozens of facial biopsies indicates that all major rosacea symptoms such as facial erythema (redness), telangiectasia (broken blood vessels), and inflammatory papules are vascular in origin. (3)
  
  
• Dr. Wollina stresses, "The basic abnormality in rosacea seems to be microcirculatory..... It is primarily a vascular disorder." (4)
  
  
• Consistent with the above reports, numerous other medical researchers emphasize that blood vessel abnormalities are key to the development and progression of rosacea. (5-8)
  

Before discussing rosacea abnormalities, the reader must first understand the function and structure of normal blood vessels.

II.  Normal Blood Vessels

1.  Function of Normal Blood Vessels

The human facial skin is densely supplied by blood vessels of different shapes and sizes. In the facial skin, normal blood vessels serve several important functions:

•  
  • Blood vessels deliver oxygen and essential nutrients to the facial skin.
    
    
  • Blood vessels remove waste products that are generated from cells of the facial skin.
    
    
  • Blood vessels help to regulate internal body temperature. If internal body temperature gets too high it triggers an increase in blood flow through the facial blood vessels.  This releases large amounts of heat from the skin surface and helps decrease internal body temperature back down to normal levels.

2.  Structure of Normal Blood Vessels

In all simplicity, blood vessels are hollow tubes that serve as a highway system for the delivery of substances to and from certain areas of the body. The wall of an individual blood vessel is made up of several different physical layers, with each layer serving a specific purpose. The two most important layers of a vessel wall are the middle layer (comprised of vascular smooth muscle cells), and the inner layer (comprised of endothelial cells).

Vascular smooth muscle cells: This is the 'muscle' of the blood vessel. The main function of this muscular layer is to control blood flow:

Endothelial cells: Endothelial cells line the inside of the blood vessel wall. They are in direct contact with the flowing blood. These cells are important regulators of blood vessel diameter.   Endothelial cells normally release potent dilator substances which diffuse to nearby smooth muscle cells and cause the muscular layer to relax. This results in blood vessel dilation and increased skin blood flow.

III.  Rosacea Blood Vessels

1.  Rosacea Blood Vessels Undergo Changes in Function

Rosacea blood vessels often experience changes in function. These blood vessels become hyper-responsive to internal and external stimuli. Three different functional changes may take place: (1) Rosacea blood vessels may dilate to a substance that normal blood vessels do not respond to at all, (2) Rosacea blood vessels may open up more widely than normal blood vessels, and (3) Rosacea blood vessels may stay open for abnormally long periods of time. In many rosacea sufferers, all three of these changes take place. This hyper-responsiveness lays the foundation for rosacea, resulting in increased blood flow through the facial skin. (9 - 12)

2.  Rosacea Blood Vessels Undergo Changes in Structure

Clinical studies on rosacea sufferers demonstrate that in addition to the above listed functional changes, rosacea blood vessels may undergo extensive structural changes. Experts stress that these changes are ultimately responsible for the progression of all rosacea symptoms. (7, 13)  Structural changes may include:

•  
  • Permanent dilation of blood vessels (telangiectasia): Clinical studies on rosacea sufferers demonstrate that a significant portion of facial blood vessels are 'broken'; these vessels are permanently fixed in a dilated state. (13-18)
    
    
  • Damage to vascular smooth muscle: In rosacea subjects, the muscular layer of facial blood vessels is often found to be damaged and abnormally thin. (3, 14, 18-20)
    
    
  • Damage to endothelial cells: In rosacea sufferers, the inner layer of the blood vessel wall is often found to be severely damaged and dysfunctional. (18, 21)
    
    
  • Growth of new vessels: In addition to the above structural changes, experts have found that abnormal growth of new blood vessels may occur in rosacea sufferers. (2, 18, 22) This is called angiogenesis (an-gee-O-gen-esis).
    
    
  • Orientation of blood vessels closer to the surface of facial skin: Medical reports on rosacea sufferers indicate that blood vessels may become oriented so that they are closer to the surface of the facial skin. (23, 24)
    
    
  • Fusion of blood vessels: In rosacea subjects, abnormal fusion of damaged blood vessels may also occur. (18)

IV.   Summary of Functional and Structural Changes

As the reader now knows, rosacea is primarily a facial vascular disorder in which the affected blood vessels are functionally and structurally abnormal. In rosacea, the functional changes usually occur first. Over time, this functional hyper-responsiveness may then lead to blood vessel damage and subsequent structural changes. This results in more blood flow through the facial skin -- causing more inflammation and damage -- making the condition worse. This is why rosacea is a chronic and progressive disease; each vascular change feeds the underlying fire.

V. References

1. Ramelet, A.A. Rosacea: a reaction pattern associated with ocular lesions and migraine? Arch Dermatol 130: 1448, 1994.
   
   
2. Wilkin, J.K. Rosacea. Pathophysiology and treatment. Arch Dermatol 130: 359-362, 1994.
   
   
3. Marks, R. Histogenesis of the inflammatory component of rosacea. Proc R Soc Med 66: 742-745, 1973.
   
   
4. Wollina, U. The response of erythematous rosacea to ondansetron. Br J Dermatol 140: 561-562, 1999.
   
   
5. Borrie, P. "The state of the blood vessels of the face in rosacea - II". Br J Dermatol 67: 73-75, 1955.
   
   
6. Brinnel, H., J. Friedel, M. Caputa, M. Cabanac, and E. Grosshans. Rosacea: disturbed defense against brain overheating. Arch Dermatol Res 281: 66-72, 1989.
   
   
7. National Rosacea Society. "Rosacea Review". Spring. 1999. Drake,L.
   
   
8. Marks, R. and J.N. Harcourt-Webster. Histopathology of rosacea. Arch Dermatol 100: 683-691, 1969.
   
   
9. Lowe, N.J., K.L. Behr, R. Fitzpatrick, M. Goldman, and J. Ruiz-Esparza. Flash lamp pumped dye laser for rosacea-associated telangiectasia and erythema. J Dermatol Surg Oncol 17: 522-525, 1991.
   
   
10. Wiemer, D.R. Rhinophyma. Clin Plast Surg 14: 357-365, 1987.
    
    
11. Elliott, R.A.J., L.E. Ruf, and J.G. Hoehn. Rhinophyma and its treatment. Clin Plast Surg 7: 277-288, 1980.
    
    
12. Thiboutot, D.M., P.C. Donshik, D.M. Hoss, and W.H. Ehlers. Acne Rosacea: Inflammatory and papulo-squamous disorders of the skin and eye. Am Fam Physician 50: 1691-1692, 1994.
    
    
13. Balch, P. and J. Balch. "Rosacea". In: Prescription for nutritional healing, 1999, p. 462-464.
    
    
14. Wollina, U. Rhinophyma--unusual expression of simple-type keratins and S100A in sebocytes and abundance of VIP receptor-positive dermal cells. Histol Histopathol 11: 111-115, 1996.
    
    
15. Applebaum, J. and J.S. Nelson. "Telangiectasia and miscellaneous vascular lesions". In: Lasers in Plastic Surgery and Dermatology, edited by B.M. Achauer, Vander KamV.M., and M.W. Berns. New York: Thieme Medical Publishers, 1992, p. 70-91.
    
    
16. Motley, R.J., S. Barton, and R. Marks. "The significance of telangiectasia in rosacea". In: Proceedings of an International Symposium, Cardiff, edited by R. Marks and G. Plewig. Cardiff: Martin Dunitz Ltd, 1988, p. 339-344.
    
    
17. Gratton, D. The many faces of rosacea. J Cutan Med Surg 2 Suppl 4: S4-S4, 1998.
    
    
18. Neumann, E. and A. Frithz. Capillaropathy and capillaroneogenesis in the pathogenesis of rosacea. Int J Dermatol 37: 263-266, 1998.
    
    
19. Sobye, P. "Aetiology and pathogenesis of rosacea". Acta Derm Venereol 30: 137-157, 1950.
    
    
20. Delektorsky, V.V., L.S. Ananieva, A.M. Vavilov, and B. Ryzhkova. "Nekotorye osobennostti ultrastruktury kapillyarnogo rusla sosochkovogo sloya dermy u bolnykh eritematoznoy stadley rozatsea.". Vestn Dermatol Venereol 5: 8, 1978.
    
    
21. Nunzi, E., A. Rebora, F. Hamerlinck, and R.H. Cormane. Immunopathological studies on rosacea. Br J Dermatol 103: 543-551, 1980.
    
    
22. Pierard, G.E., C. Pierard-Franchimont, and C.M. Lapiere. Proliferation and hyperplasia of vascular endothelium in human skin. Am J Dermatopathol 7: 477-488, 1985
    .
    
23. Wilkin, J.K. "The red face: Flushing disorders". Clin Dermatol 11: 211-223, 1993.
    
    
24. National Rosacea Society. "Rosacea Review". Summer. 1998. Drake,L.

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