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Educational information

I Overview

 

 

This overview is intended to provide the reader with a basic understanding of the importance of normal human skin function, the processes of normal skin at the cellular level, and the contributing factors to and effects of aging on normal skin.

 

When we think of aging skin, whether a result of natural aging, photodamage, or the environment, we think of wrinkles, creases, sleep lines, large pores, rhytides, sagging skin, folds, uneven skin tone and texture, dryness, and hyper and hypopigmented areas. These unwelcome changes are a result of changes in the normal functioning of the skin. In order to initiate improvement and maintain healthy skin, the normal functions of the skin must be reestablished.

 

Normal skin function is a result of the cellular components of the skin working as they were intended. As a prelude to understanding the mechanisms of action for the Dermesse skin care system, a brief explanation of normal cellular functioning follows.

 

 

 

Anatomy of the Skin


Skin is a waterproof, flexible, but tough protective covering for your body.  It is the body's largest organ, covering the entire outside of the body. It functions as a protective shield keeping out water, insects, heat and cold, sunlight, dirt, and gases. It also keeps in body fluids such as water and blood, hormones, minerals, vitamins, and heat.

Additionally, the skin plays an important role in protecting the body from microorganisms. The skin accomplishes this is several ways; Through the continual shedding of the upper layer of the skin (desquamation), through the existing normal flora of the skin, and through the excretion of sebum and sweat which contain fatty acids and lactic acid respectively all of which assist in protecting against unwanted microbes.

Over different parts of the body, the thickness and color of the skin and the number of sweat glands, sebaceous glands, hair follicles, and nerves vary. The top of the head has many hair follicles; the soles of the feet have none. The soles and the palms have much thicker epidermis and keratin layers. The fingertips and toes contain many nerves and are extremely sensitive to touch.

The skin tends to change throughout a person's lifetime. A baby's skin has a much thicker fat layer (subcutaneous) and a much thinner layer of protective keratin. As people age, they lose much of the underlying fat, the dermis and epidermis become thinner, the elastic fibers in the dermis become fragmented, and the skin becomes more wrinkled. The flow of blood in the skin also decreases with age; so damaged skin heals more slowly in older people. Older skin also makes less protective oil, so the skin dries out more easily.

 

 

The skin is composed of three layers, the epidermis, the dermis, and the subcutaneous layer. Each layer performs specific tasks.

 

 

Cross-Section of Human Skin:

 

             
 
   
  
  
  
  
  
  
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EPIDERMIS

 

 

Epidermis

(protection

   layer)

The epidermis is the thin translucent outer layer of the skin. The   epidermis itself has several layers determined by the cellular content:

      
  • Stratum Corneum
           This is the uppermost layer and contains continually shedding, dead, flattened, non-nucleated, and non dividing corneocytes, which are transformed keratinocytes. The keratin present in this layer is a protein formed from the remains of the dead keratinocytes and protects the skin from harmful substances.
  •   
  • Keratinocytes       
           This layer contains living keratinocytes (squamous cells), which help provide the skin with what it needs to protect the rest of the body. Keratinocytes make the transformation from being living cells to the dead cornified cells of the stratum corneum.
  •   
  • Basal Layer
           The basal layer is the inner layer of the epidermis, containing basal cells. Basal cells continually divide, forming new keratinocytes and replacing the old ones that are shed from the skin's surface. The cycle from cell division of a keratinocyte to exfoliation takes approximately 40 days or roughly 6 weeks. The body is willing to expend the energy necessary to accomplish this process due to the importance of healthy skin as a protector.
      
  • The lowest level of the epidermis contains melanocytes, which are cells that produce melanin, the dark colored pigment of skin.  The function of melanin is to provide pigmentation and is the first physiochemical defense against the damaging ultraviolet rays of the sun. Melanocytes produce pigment granules, called melanosomes, which are picked up by keratinocytes. One melanocyte provides pigmentation to approximately 36 keratinocytes.


 

DERMIS

 

Dermis

(structural

   layer)

The dermis is the middle layer of the skin and is responsible for water binding, wound repair, and diffusion regulation involving hormones, salts, and other metabolic   substances. It contains pain and touch receptors, whose tentacles reach up to the skin surface, and many of the functional glands of the skin: sweat glands, sebaceous glands (which   produce the oil sebum to help moisturize the skin), and hair follicles. Also within the dermis lie blood vessels that provide nutrition to the skin and   nerves that branch throughout the layers of the skin.

Important components of the dermis and their function include:

      
  • Proteins       

The dermis is held together by a fibrous insoluable protein called collagen which is the most abundant protein in the body. Elastin is a        protein substance that forms the principal constituent of yellow elastic tissue and gives the skin it’s resiliency and feel. Glycosaminoglycans (GAGs) produce a highly hydrated, gel-like matrix that helps to maintain water balance, and act as a support system for the components of the dermis. Hyaluronic acid andchondroitin sulfate (found in cartilage and bone) are glycosaminoglycans.

  • Fibroblasts:    Fibroblasts are responsible for producing collagen, elastin, and   glycosaminoglycans.
  • Blood Supply:    A blood   supply is necessary to transport nutrients to the normally functioning   skin and to remove waste products generated through cellular metabolism. An adequate blood supply must be   present.  The blood   vessels present are the arterioles which bring oxygenated blood from the   heart and lungs; veinules which return oxygen-depleted blood back to the   heart and lungs; and capillarieswhich are the primary   sites for exchange of oxygen and nutrients.
     
     

 

 

SUBCUTANEOUS FAT

Subcutaneous

       Fat

(cushioning

     layer)

The subcutaneous fat layer is the deepest layer of skin and   insulates the body from heat and cold and serves as an energy storage system. It consists of a network of   collagen and fat cells and it helps conserve the body's heat while protecting other organs from injury by acting as a "shock absorber."

 

·          Adipose Cells

     This layer consists of cells containing fatty deposits, called Adipose cells.

 

      
  • Subcutaneous Fat

   The subcutaneous fat lies on the muscles and bones, to which the whole skin structure is attached by connective tissues. The attachment is quite loose, so the   skin can move fairly freely.

 

  The subcutaneous fat is organized into fat lobules, which are separated by collagen fibers. When these lobules become grossly distended and engorged with too much fat the areas of attachment become more obvious and the skin cannot move as easily and gives rise to cellulite. These characteristic cellulite  patterns tend to develop from the teens onwards.

 

      
  • Other

   Blood vessels and nerves are present in   the dermis and it may also house the hair follicles when they are in the growing phase.


 
 

                 
   

 

   
   

 

   
   

 

   

 

 

 

               FDA INFORMATION ON COSMECEUTICAL CLASSIFICATION

                         COSMECEUTICAL

While the Food, Drug, and Cosmetic Act does not recognize the term "cosmeceutical," the cosmetic industry uses this word to refer to cosmetic products that have medicinal or drug-like benefits.

The Food, Drug, and Cosmetic Act defines drugs as those products that cure, treat, mitigate or prevent disease or that affect the structure or function of the human body. While drugs are subject to a review and approval process by FDA, cosmetics are not approved by FDA prior to sale. If a product has drug properties, it must be approved as a drug.

 

Dermesse system approach

 

The signs of aging are a result of cellular damage and a reduction in normal cellular activity resulting from sun damage and environmental factors, commonly termed extrinsic ageing, or the natural aging process which is largely determined by genetics, referred to as intrinsic ageing.12,14,15,16 In order to combat the signs of aging, an effective skin care program must produce results at the cellular level. The DermesseÔ products do just that.

 

The importance of correcting skin damage at the cellular level is evident. For the serious patient, cover-up cosmetics or quick cure products are not appropriate and do not offer long-term results.

 

The Dermesse products have been formulated specifically for this program to enhance the effects of the prescription ingredients, hydroquinone and tretinoin, and to return skin functioning to its normal 6 week cycle.

 

Prescription strength 4% hydroquinone is included in the DermesseÔ product line and the prescription strength tretinoin is available through the pharmacist with a physician’s prescription.

 

The inclusion of hydroquinone and tretinoin in the program provide significant benefits to the patient as documented in numerous investigative and clinical publications.

 

  • Safety and efficacy in the treatment of fine facial wrinkles, mottled hyperpigmentation, and skin roughness.1,2,4

 

  • Significantly reduces fine wrinkling, mottled hyperpigmentation, roughness, and laxity.2

 

  • Long lasting results and sustained clinical improvement with the use of tretinoin for up to 4 years.3

 

  • Restoration of collagen and increase in collagen formation.5,8,10,13      

 

  • Produces histological changes such as epidermal thickening, granular layer thickness, and stratum corneum compaction.2,4,6,11

 

  • Improvement in coarse wrinkling, sallowness, and looseness with perceptible improvement. 7

 

  • Increased blood flow and angiogenesis.9          

 

  • Deposition of glycosaminoglycans and lightening of actinic lentigines. 10

 

  • Hydroquinone 17,18 is a known skin lightening agent that acts at the cellular level by inhibiting melanin production by melanocytes.

 

REFERENCES: Available upon request

1. Nyirady J, Bergfeld W, Ellis C, Levine N, Savin R, Shavin J, Voorhees JJ, Weiss J, Grossman R. Tretinoin cream 0.02% for the treatment of photodamaged facial skin: a review of 2 double-blind clinical studies. Cutis. 2001 Aug;68(2):135-42.
2. Weinstein GD, Nigra TP, Pochi PE, Savin RC, Allan A, Benik K, Jeffes E, Lufrano L, Thorne EG.
Topical tretinoin for treatment of photodamaged skin. A multicenter study. Arch Dermatol. 1991 May;127(5):659-65.
3. Bhawan J, Olsen E, Lufrano L, Thorne EG, Schwab B, Gilchrest BA. Histologic evaluation of the long term effects of tretinoin on photodamaged skin. J Dermatol Sci. 1996 Mar: 11(3):177-82.                                                                                                 4. Olsen EA, Katz HI, Levine N, Shupack J, Billys MM, Prawer S, Gold J, Stiller M, Lufrano L, Thorne EG. Tretinoin emollient cream: a new therapy for photodamaged skin. J Am Acad Dermatol. 1992 Feb;26(2 Pt 1):215-24.
5. Griffiths CE, Russman AN, Majmudar G, Singer RS, Hamilton TA, Voorhees JJ.
Restoration of collagen formation in photodamaged human skin by tretinoin (retinoic acid). N Engl J Med. 1993 Aug 19;329(8):530-5.
                                                                                               6. Gilchrest BA. Treatment of photodamage   with topical tretinoin: an overview. J Am Acad Dermatol.1997 Mar;36(3 Pt 2):S27-36.            7. Leyden JJ, Grove GL, Grove MJ, Thorne EG, Lufrano L. Treatment of photodamaged facial skin with topical tretinoin. J Am Acad Dermatol. 1989 Sep;21(3 Pt   2):638-44.                                                                                                                                                   8. Bhawan J. Short- and long-term histologic effects of topical tretinoin on photodamaged skin. Int J Dermatol. 1998 Apr;37(4):286-92.       9. Kligman AM, Grove GL, Hirose R, Leyden JJ. Topical tretinoin for photoaged skin. J Am Acad Dermatol. 1986 Oct;15 (4 Pt 2): 836-59.     10. Griffiths CE, Voorhees JJ. Topical retinoic acid for photoaging: clinical response and underlying mechanisms. Skin Pharmacol. 1993;6 Suppl 1:70-7.                                                                                                                                                                                11. Lever L, Kumar P, Marks R. Topical retinoic acid for treatment of solar damage. Br J Dermatol. 1990 Jan;122(1):91-8.                         12. Jenkins G. Molecular mechanisms of skin ageing. Mech Ageing Dev. 2002 Apr;123(7):801-10.                                                          13. Griffiths CE. The role of retinoids in the prevention and repair of aged and photoaged skin. Clin Exp Dermatol. 2001 Oct;26(7):613-8.
14. Wlaschek M, Tantcheva-Poor I, Naderi L, Ma W, Schneider LA, Razi-Wolf Z, Schuller J, Scharffetter-Kochanek K.
Solar UV irradiation and dermal photoaging. J Photochem Photobiol B. 2001 Oct;63(1-3):41-51.
15. Scharffetter-Kochanek K, Brenneisen P, Wenk J, Herrmann G, Ma W, Kuhr L, Meewes C, Wlaschek M.
Photoaging of the skin from phenotype to mechanisms. Exp Gerontol. 2000 May;35(3):307-16.                                                                                                  16. Contet-Audonneau JL, Jeanmaire C, Pauly G. A histological study of human wrinkle structures: comparison between sun-exposed areas of the face, with or without wrinkles, and sun-protected areas. Br J Dermatol. 1999 Jun;140(6):1038-47.
17. Denton, C., A.B. Lerner and T.B. Fitzpatrick, Inhibition of Melanin Formation by Chemical Agents, Journal of Investigative Dermatology, :119-135, 1952.
18. Jimbow, K., H. Obata, M. Pathak and T.B. Fitzpatrick, Mechanism of Depigmentation by Hydroquinone, Journal of Investigative Dermatology, 62:436-449, 1974.

 

Note: Several references and sources of information on tretinoin have been presented in this section. It is recommended that any additional information on tretinoin be researched by the individual accounts.

 

 

 

 THE DERMESSE REGIMEN APPROACH (weeks 1 - 18)

 

 SKIN REPAIR PHASES

This prescription strength skin care program produces results at the cellular level. You will experience different reactions and results as you progress through the three phases of 6 weeks per phase. The total rejuvenation process will take 18 weeks. Real results take time and this program.

 

Mild Regimen: The Mild Regimen provides a slow and comfortable approach to skin health. The reaction is minimized resulting in reduced skin stimulation. The treatment program requires a longer time frame due to the gentle approach of the regimen. This regimen is effective for patients with thin or sensitive skin since it will allow the patient to build tolerance to the program and thereby eventually progress to a more intense regimen for added improvement.

Benefits of the Mild Regimen  

  • Provides skin hydration
  • Smoothes rough areas
  • Slight improvement in skin tone and color
  • Minimal effect on sun damaged areas
  • Minimizes clogged and enlarged pores
  • Allows patient to build tolerance
  • Effective in controlling acne breakouts

 

Standard Regimen: The Standard Regimen is an effective yet patient tolerant program that is ideal for treating patients with minimal to moderate skin damage. Emphasis is on helping to eliminate fine lines and wrinkles, correcting skin color imperfections, and slowly building tolerance in the skin.

Benefits of the Standard Regimen

  • Reduce pore size            
  • Create smooth skin      
  • Provide adequate hydration
  • Improve skin tone and color
  • Improve skin texture
  • Repair minor sun damage

 

Aggressive Regimen: The Aggressive Regimen provides maximum correction for patients with significant pigmentation problems and skin damage. Positive results are    evident in patients with dark pigmentation spots, deep sun damaged skin, or patients exhibiting other unsightly aesthetic skin irregularities associated with aging.

Benefits of the Aggressive Regimen

  • Improves areas of deep skin damage
  • Improves skin texture            
  • Reduces large pores
  • Improves areas of pigmentation
  • Creates an even skin tone
  • Improves areas of scarring

Regimen requires the shortest length of time for improvement

 

Maintenance Regimen: The Maintenance Regimen is to be implemented after completion of one of the treatment regimens. It is designed to allow the patient to maintain the improvements and benefits that they achieved during the treatment period.

 

Cleanser, Toner, Sun Protection daily.

Hydroquinone products and Exfoliator— twice/week.

 

 

TIPS

EXFOLIATOR can be used less often if redness is too intense.

Use tretinoin and BALANCER every other night for the first week of treatment.

SKIN LIGHTENER is used at night for spot treatment.  

 

 

 

SKIN REPAIR PHASES (18 weeks)

 

This prescription strength skin care program produces results at the cellular level. You will experience different reactions and results as you progress through the three phases of 6 weeks per phase. The total rejuvenation process will take 18 weeks. Real results take time and this program will produce results if you stay with the program.

 

1)   Weeks 1 - 6 Action:

The top layer of the skin exfoliates and new skin cells begin developing in the dermal layer. Melanin production by melanocytes is reduced.

Reaction:

  • Flaking and light peeling, sensitive feeling
  • Possible redness and a dry feeling
  • Some fading of discolored areas, fading of freckles
  • Wrinkles and lines may appear more prominent

NOTE: some acne patients experience a worsening of their breakouts. This is temporary.

 

2)   Weeks 7 – 12 Action:

The new skin cells are migrating to the surface and new collagen and elastin is being produced. Melanin production continues to be inhibited.

Reaction:

  • Improvement in wrinkles is noticeable
  • Pore size is reduced creating smoother looking skin
  • Lightening of the skin continues
  • Redness and dry feeling subside

 

3)   Weeks 13 – 18   Action:

All cellular stimulation is functioning correctly. New skin cells are on a regular 6 week cycle, melanin production is controlled, and elastin and collagen deposition is optimized.

Reaction:

  • Even skin tone and smoothness
  • Skin is self hydrating
  • Redness is gone
  • Improvements in elasticity evident, wrinkle reduction

 

 

 

 
 Fitzpatrick Skin Type Classification

 

Skin Type
 
 

I         Always burns, never tans. Extremely fair skin, blonde or red haired,

          freckled complexion, blue or green eyes. Example: Irish or Scottish.

II        Always burns, tans minimally. Fair skinned, sandy to brown hair, blue, green, or brown eyes.   Caucasian.

III       Sometimes burns, tans gradually. Average skin, brown hair and brown eyes.

IV       Burns minimally, always tans. Olive skin, brown or black hair, dark brown or black eyes. Caucasian, 

          Mediterranean type.

V        Rarely burns, tans well. Dark brown skin, black hair, black eyes. Middle Eastern, Hispanic, some African.

VI       Never burns, deeply pigmented. Black skin, black hair, black eyes. African.



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