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PILOSEBACEOUS FOLLICLE DISFUNCTION

ACNE. =. PILOSEBACEOUS FOLLICLE DISFUNCTION. PATHOGENESIS. FUNCTIONAL DISFUNCTIONS OF THE SEBACEOUS GLANDS. MULTIFACTORIAL ETHIOLOGY. HYPERSEBORRHEA. FOLICULAR HYPERKERATOSIS. SAPROFITE MICROFLORA PROLIFERATION. FREE RADICALS AND FATTY ACIDS PRODUCTION. INFLUENCING. SKIN & MUCOSES.

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PILOSEBACEOUS FOLLICLE DISFUNCTION

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  1. ACNE = PILOSEBACEOUS FOLLICLE DISFUNCTION

  2. PATHOGENESIS FUNCTIONAL DISFUNCTIONS OF THE SEBACEOUS GLANDS

  3. MULTIFACTORIAL ETHIOLOGY HYPERSEBORRHEA FOLICULAR HYPERKERATOSIS SAPROFITE MICROFLORA PROLIFERATION FREE RADICALS AND FATTY ACIDS PRODUCTION

  4. INFLUENCING SKIN & MUCOSES INTERNAL ORGANS MIND THERE IS ALSO A PSYCHOLOGICAL ASPECT

  5. VICIOUS CIRCLE

  6. Ingestion of big amount high glycemic index food Decreases endogen retinoics efectivity on inhibition of follicle cells proliferation. + insuline Follicle hyperkeratinization + sebum Increases cell mitosis in all tissues Aviable Androgens + of androgens synthesis in gonades Precursors synthesis in the liver INFLUENCE OF THE OCCIDENTAL DIET ON ACNE APPEARANCE

  7. 4 CAUSES INCREASE OF THE CUTANEOUS SEBUM SECRETION ABNORMAL KERATINISATION OF THE HAIR FOLLICLE WALLS BACTERIAL INFECTIONS INFLAMMATION ANSWERS

  8. SKIN STRUCTURE

  9. HAIR FOLLICLE STRUCTURE Hair Skin surface sebum follicle Sebaceous gland

  10. HYPERSEBORRHEA PUBERAL HORMONAL FLUCTUATIONS INCREASE OF THE ANDROGENIC SECRETION DILATED PORES OILY SKIN / PROACNEIC SKIN

  11. ABNORMAL KERATINISATION HIGHER LEVELS OF ANDROGENS CORNEOCYTES MATURING PROCESS ALTERED DETATCHMENT OF CORNEOCYTES IN GROUPS HYPERSEBORRHOEA + CRNCT. = PORES OBSTRUCTED

  12. BACTERIAL INFECTIONS MICRO-AIR ATMOSPHERE INSIDE THE SEBACEOUS GLANDS SAPROFITE BACTERIAS MICRO FLORA DEVELOPMENT LIPIDS HYDROLISIS BY BACTERIAL ENZYMES (LIPASES) FATTY ACIDS RELEASE IRRITATION / PROINFLAM.

  13. INFLAMMATION ANSWERS TISSULAR CHEMIOTACTIC FACTORS + LEUCOCYTES MIGRATION TO THE ALTERED SEBACEOUS GLAND PUS & FREE RADICALS FORMATION MORE IMPORTANT INFLAMED LESIONS

  14. Puberal increase of testosterone & dihydrotest. secretion Sebaceous gland hyperactivity Increase of sebum production Cell turn over increase Increase of P.A. bct Comedones production Abnormal keratinization Release of P.A. cell mb fragments Chymiotaxis Intense inflammation

  15. SEBUM ACCUMMULATION UNDER KERATINIC CAP DUCTAL HYPERCORNIFICATION COMEDONES EARLY INITIAL LESION OF THE PROACNEIC SKIN + NON- INFLAMED LESION OF ACNE OPEN COMEDONE = BLACK HEAD CLOSED COMEDONE = WHITE HEAD

  16. Closed comedone Open comedone Infected comedone Inflammed comedone

  17. COMEDONE ALTERATION OF THE KERATINIZATION PROCESS QUANTITY & QUALITY CHANGES OF THE KERATIN INCREASING OF THE DUCTAL EPITELIUM TURN-OVER PRODUCTION OF A KERATIN CAP BLOCKAGE OF THE SEBUM PRODUCED

  18. FOLLICULAR HYPERKERATOSIS Follicle duct full of keratin, sebum and bacterial micro-flora Keratinic epitelium that follows the upper epidermis Same type of ripening that epidermis Keratinization = cornification Quality & quantity alteration of the Keratinization Detachment of the corneocytes by an accumulative form

  19. ABNORMAL KERATINIZATION

  20. BACTERIAL MICRO-FLORA CHANGE Micro air atmosphere of the sebaceous glands Saprophyte micro-flora proliferation Propionilbacterium Acnes and other micro-organisms Increase of some bacterial enzymes production (lipases & proteases) Hydrolysis of the lipids by bacterial lipases fatty acids (F.A) F.A. with irritative and pro-inflammatory characteristics BCT INFECTIONS

  21. CORNEOCYTES ACCUMMULATION + HYPERSEBORRHOEA COMEDONE CLOSED OPENED

  22. INFLAMMATORY ANSWERS PUS INFLAMMATION FOLLICLE WALLS BREACKAGE FREE RADICALS BCTR PUS SURROUN- DING TISSUES IN- FLAMMATION +++ CELLULAR DETRITUS

  23. CLINICAL MANIFESTATIONS OPENED NON INFLAMMATORY COMEDONES CLOSED PAPULES PUSTULES PILOSEBAC. UNIT CLOSED COMEDONE OPEN COMEDONE INFLAMMATORY NODES CISTES SCARS PÁPULE PUSTULE CISTES

  24. ETHIOLOGY ( influencing factors ) HORMONES: puberty, menstrual cycles, hormonal fluctuations STRESS: hormonal repercussion, (suprarenal, hipotal./ hipofis.) DEAD CELLS ACCUMMULATION INSIDE THE GLANDS PORES BACTERIAL COLONISATION AND ALLERGIC ANSWERS STEROIDS DRUGS CLORATED COMPONENTS EXPOSITION ( cloroacne)

  25. Frequent septic manipulation Lesions get a severe stage Post acne scars

  26. ANTIACNE TREATMENT Active ingredients group of chemical & natural nature The target of the ingredients are the 4 causes of acne Synergic & polyvalent answers, combining ingredients Non medical or cosmetic treatment is giving an immediate result Minor forms (comedones) have good results with an adequate cosmetic tr. Severe inflammatory forms may require medical treatment Cosmetic treatments are a good complement for the medical ones Sudden changes of the products can create irritative answers

  27. ANTIACNE TREATMENT (Actions) SEBUM REGULATOR EXFOLIATOR KERATOLITIC PORES DESCA- LORER SAPROFITE MICRO- FLORA INHIBITOR DESPIGMENTATOR PURIFIER & IMPURITIES REMOVER MOISTURIZERER

  28. PRODUCT DESCRIPTION

  29. APPLICATION PROTOCOL 1 REMOVE SEBUM EXCESS WITH DEGREASING SOLUTION APPLY MASK DURING 3 TO 6 HOURS 2 3 REMOVE MASK WITH SPONGES AND WATER 4 APPLY MAINTENANCE CREAM MORNING AND NIGHT 5 CLEANSE THE SKIN WITH FACIAL GEL CLEANSER DAILY 6 DAILY APPLY ROLL-ON OCCASIONAL TRTMNT SEVERAL TIMES COMBINATION WITH SALYCILIC-PEEL 10% UNDER PROFS. CRITERIA COMBINATION WITH BLUE LIGHT PHOTOTHERAPIE OF PHOTOGEN S.

  30. Thank you for your attention

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