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Ageing and Geriatric dermatoses
- 1. Ageing and Geriatric dermatoses Dr Manasa S J
- 2. Overview ▪ Introduction ▪ Ageing- Intrinsic, Extrinsic ▪ Histopathology of ageing ▪ Special conditions ▪ Physiological skin changes in old age ▪ Dermatoses in old age ▪ Treatment
- 3. Introduction
- 4. Introduction ▪ Geriatric population- > 65 years ▪ In India, 72 million- 2001 179 million- 2031 ! ▪ Needs emphasis
- 5. Ageing An inevitable, continuous and gradual process..
- 6. Ageing ▪ Ageing is inevitable in every organ system ▪ The implications of skin ageing are broad ▪ Genetic program(Intrinsic) and damage by UVR, alcohol, smoking, poor nutrition(Extrinsic)
- 7. Mechanism ▪ Cellular senescence- Telomere shortening ▪ Alteration in cell differentiation- Increased MMPs - Reduced collagen production - Reduced expression of elastin gene and synthesis ▪ Oxidative damage ▪ Role if DNA- Premature aging synd.
- 8. Chronological ageing Repeated cell divisions Progressive telomere loss Critical telomere shortening p53 activation Cell arrest Senescence
- 9. UV rays ▪ Mutations in key regulatory genes(thymidine dimers, oxidation of guanine bases) ▪ Regulates activity of MMPs and MMP inhibitors ▪ Telomere shortening, activation of p53
- 10. Oxidative damage ▪ Normal metabolic processes ▪ UV rays ▪ Stress ▪ Smoking MMPs
- 11. ROS Activates receptors of epidermal growth factor, IL-1, TNF-α Nuclear transcription complex Activator protein 1 Blocks TGF α and TGF β Inhibits transcription and synthesis of collagen MMPs Degradation of collagen and elastin Cysteine rich growth regulatory factor (CYR61) Reduces type I procollagen synthesis, TGF-β receptor level, and induces AP-1 , MMP-1
- 12. ▪ Massive accumulation of ‘elastotic’ material in upper and mid dermis ▪ Degradation and dysregulation of elastin and fibrillin production ▪ Incomplete, accumulates in dermis, reduces structural integrity of skin, inhibits new collagen synthesis ▪ Increased elastase levels-neutrophils attracted by inflammatory mediators ▪ Thus, excessive unbalanced synthesis of elastic fiber components that undergo partial degradation results in formation of amorphous elastotic material
- 13. Intrinsic ageing ▪ Chronological ageing/natural ageing ▪ Genetically programmed- limited num of cell divisions (Replicative senescence) ▪ Observed best on upper inner aspects of arms and buttocks (Photoprotected) ▪ Dryness, homogenous colour, atrophy and fine wrinkling
- 14. Extrinsic ageing ▪ Photoageing ▪ Damaging effects of ultraviolet radiation ▪ Face, upper chest (decollete), extensor forearms, dorsal hands and neck ▪ Rough texture, dryness, dyspigmentation, fine and coarse wrinkles and telangiectases
- 15. Extrinsic ageing variants ▪ Atrophic- fine facial wrinkles, atrophy, telangiectases and/or erythema, focal depigmentation and hyperpigmentation (lentigines and/or patchy hyperpigmentation) ▪ Proliferative exhaustion (Fitzpatrick skin type I–II) ▪ Predisposition to pre‐cancerous and cancerous skin lesions
- 16. Extrinsic ageing variants ▪ Hypertrophic- homogenous colour, coarse wrinkling ▪ Protective hyperplasia (Fitzpatrick skin type III– IV) ▪ Less tendency to development of skin cancers
- 17. Similarities and differences between the variants ▪ Same degree of collagen damage ▪ Hypertrophic photoageing- more elastotic damage - occur in younger subjects
- 20. Extrinsic ageing in skin of color ▪ More inherent protection due to increased melanin in darker skin types ▪ Pigmentation irregularities >> wrinkling ▪ Wrinkles not readily apparent until after the age of 50 yrs and to a much lesser extent compared with fairer skin
- 21. Tobacco and extrinsic ageing ▪ Deleterious effects on elastic fibres ▪ Increase in area of elastic fibres due to elastic fibre degradation ▪ Reduces new collagen synthesis; induces matrix metalloproteinase
- 22. Histology
- 27. Histologic Changes in Ageing Skin ▪ Thinning of epidermis, dermis and decreased number of fibroblasts ▪ Decreased melanocytes,langerhans cells ▪ Reduction and disintegration of collagen and elastic fibers ▪ Reduction of cutaneous microvasculature, size and vessel density ▪ Decreased skin appendages, including sebaceous, sweat, and apocrine glands ▪ Reduced number of nerve endings ▪ Decreased volume of subcutaneous fat
- 28. Comparative histology Intrinsic/Chronological ▪ Thinned out epidermis, lower proliferative rate, modest cellular irregularity, reduplication of lamina densa ▪ Reduced collagen and elastin ▪ Absent Grenz zone ▪ Normal microvasculature ▪ No inflammation Extrinsic/Photoageing ▪ Epidermis thickened initially, higher proliferative rate, marked cellular irregularity & reduplication of lamina densa ▪ Reduced collagen and increased elastin in matrix ▪ Grenz zone seen ▪ Abnormal accumulation of BM like material ▪ Inflammation marked
- 32. Skin ageing of neck ▪ Assumes several different phenotypes depending on anatomical location ▪ Poikiloderma of Civatte- extrinsic photoageing of lateral neck ; reticulated erythema and dyspigmentation of lateral aspect of neck ▪ Coarse wrinkling, a bronzed or sallow coloration, and minimal telangiectases – hypertrophic variant of photoageing
- 33. Dermatoporosis ▪ Chronic cutaneous insufficiency/ fragility syndrome ▪ Advanced age, sun exposure, steroid use ▪ Integrity of skin is severely compromised Stage 1 Pronounced skin thinning, purpura and stellate pseudoscars Stage 2 Limited lacerations + Stage1 Stage 3 Numerous and extensive lacerations and delay in wound healing Stage 4 Dissecting haematomas
- 35. Favre Racouchot syndrome ▪ Nodular elastoidosis with cysts and comedones ▪ Multiple comedones, follicular cysts, furrows, and yellowish nodules ▪ MC- periorbital region
- 36. Syndromes of premature ageing
- 38. Physiological changes ▪ Thinning of epidermis ▪ Reduced adhesion of corneocytes(Dryness) ▪ Reduced aquaporin gene expression(Hydration) ▪ Reduced melanocytes and Langerhans cell(Malignancy and infection) ▪ Flattening of rete ridges(Blisters & delayed healing) ▪ Reduced synthesis of Vit D(Osteomalacia/porosis)
- 39. Physiological changes ▪ Reduced collagen and elastin(Wrinkles, tensile strength) ▪ Solid hyaluronic acid(Hydration) ▪ Fibroblast changes(Wound healing) ▪ Reduced support to microvasculature(Purpura) ▪ Decreasing Pacinian corpuscle(Touch) ▪ Reduced sebaceous, eccrine, apocrine secretion ▪ Reduced SC fat(Sensitivity to cold) ▪ Altered B & T cell functions(Infections)
- 40. Geriatric dermatoses ▪ Physical factors Pressure sores (decubitus ulcers) Xerosis Pruritus Asteatotic dermatitis ▪ Infections Bacterial- Impetigo/folliculitis, Cellulitis Viral- Herpes zoster, Molluscum contagiosum Fungal- Onychomycosis,Tinea pedis, Tinea cruris, Intertrigo Infestations- Pediculosis, Scabies
- 41. ▪ Eczematous reactions-Nummular eczema, Seborrheic dermatitis, Contact dermatitis ▪ Photodermatoses-Solar elastosis,Nodular elastoidosis,Cutis rhomboidalis nuchae,Poikilodermic changes ▪ Neoplastic changes ▪ Benign-Seborrheic keratosis, Skin tags, Cherry angiomas, Leukoplakia,Keratoacanthoma, Actinic keratosis ▪ Malignant-Actinic cheilitis,BCC,SCC,Malignant melanoma ▪ Immunological-Bullous pemphigoid ▪ Psychodermatoses-LSC, Prurigo ,Neurotic excoriations, Delusion of parasitosis, Dermatitis artefacta ▪ Vascular compromise-Chronic venous insufficiency ▪ Cutaneous drug reactions ▪ Nutritional changes
- 46. Pruritus of senescence ▪ 50% of people beyond 60 yrs ▪ MC- Xerosis ▪ Pruritus of multiple aetiologies- Scabies, underlying illness, depression ▪ Slow reduction of sebum production, failure of skin to retain waterdryness and fine crackingitching ▪ Dystrophic changes in afferent nerve terminals ▪ Water‐induced itching- variant of senescent pruritus;
- 47. Treatment ▪ No clear guidelines ▪ Specific treatment for individual diseases
- 48. Chronic pruritus
- 50. THANK YOU
- 51. Questions 1. A man is as old as his skin- Discuss (Sep 2005, LE) 2. Discuss advantages and disadvantages off antiageing treatment (Oct 2008, LE) 3.Facial rejuvenation DNB 4. Antiageing Questions
Editor's Notes
- Ageing is inevitable in every organ system, yet no organ conveys to the outside world an aged appearance as does the skin. The implications of skin ageing are broad and include not only cosmetic concerns of appearance but also medical issues and social concerns
- UV radiation activates growth factor receptors on the surface of fibroblasts and keratinocytes, resulting in signal transduction through a protein kinase cascade and subsequent activation of AP-1 in the nucleus. This then stimulates MMP production in both the dermis and epidermis and leads to the degradation of collagen and elastic fibres. More specifically, it is proposed that UV activation of membrane receptors stimulates MAP kinase signal transduction pathways, via stimulation of GTP-binding proteins including ras, rac and cdc42. In support of this, activation of the three MAP kinases, ERK, jnk and p38 within 1 h of acute UV radiation has been demonstrated (Fisher et al., 1998). This activation is then succeeded by increased expression of the transcription factors c-jun and c-fos that, together with other protein factors form the transcription factor complex AP-1 (Karin and Hunter, 1995). Elevated levels of AP-1 are then responsible for inducing expression of key members of the MMP family responsible for the degradation of dermal matrix.
- Mitochondrial Damage. Mitochondria are cellular organelles that produce energy (adenosine triphosphate) by consuming oxygen. Although equipped with antioxidant defense systems, continuous generation of ROS damages mitochondrial DNA (mtDNA). To date, machinery to remove bulky DNA lesions has not been identified in mitochondria, although they display capacity for base excision repair relevant to repair of oxidative damage. Still, mtDNA mutation frequency is approximately 50-fold higher than that of nuclear DNA, and photodamaged skin has higher mtDNA mutation frequency than sun-protected skin, displaying large DNA deletions135–138 and resulting in decreased mitochondrial function, leading to further accumulation of ROS and compromising the cell’s ability to generate energy. Also, a correlation was noted between decreased mitochondrial function and increased MMP-1 levels without concomitant increase of MMP-1-specific TIMP,136 exacerbating collagen degradation135– 138 and aggravating skin photoaging. Protein Oxidation. Proteins are affected by oxidative damage, and photodamaged skin shows accumulation of oxidized, damaged proteins in the upper portions of the dermis. In vitro studies suggest that UVA is a major contributor and the accumulation of such proteins further inhibits proteasomal function and the ability of the cell to successfully degrade additional damaged proteins Basement membrane damage. In sunexposed skin, the basement membrane becomes thicker and multilayered in part as a result of damage through MMP activation, affecting molecular transfer between the epidermis and the dermis and compromising epidermal health ROS induces the transcription of tropoelastin, a component of the mature elastic fibers. Fibulins 2 and 5 and fibrillin-1, components of the microfibrillar fraction of the dermal elastic fiber are also increased in the elastotic material.
- All mammaliann cells are genetically programmed to undergo a limited number of cell divisions. There is an irreversible arrest of this division known as replicative senescence
- HGPS, Bloom Synd, Wiedemann– Rautenstrauch syndrome