The Ageing Skin

The human skin, identified as being the largest organ by both weight and

magnitude, is made up of multiple conjoined strata’s and is accountable for

numerous fundamental processes such as percutaneous water loss,

temperature conservation and immune protection. Intriguingly, the skin is also the

initial projection of the physiological signs of ageing, a process described as a

succession of complex biological developments that have the potential to

damagingly affect the skins external presentation, as well as its functional and

mechanical practices. Considering this, researchers declare that modern society’s

necessity of beauty to be a youthful façade, expounds the great efforts

being undertaken to guarantee the preservation of a youthful appearance. This

information reiterates the significance of understanding the mechanisms that underly

the ageing skin as it will ensure the suitable and safe use of interventions and

modalities.


Intrinsic and extrinsic ageing


It is critical to consider the two individual developments of skin ageing, intrinsic

ageing and extrinsic ageing.


Intrinsic ageing: Also termed chronological ageing or physiological aging, is a series

of biochemical molecular amendments instrumental of one’s genetic predisposition.

It is hypothesised these alterations are consequential of the shortening of telomeres,

the diminishment of antioxidant enzyme activity and lessened elastin gene

expression.


Extrinsic ageing: Also recognised as photoaging. Extrinsic ageing has the ability to imbricate intrinsic ageing. Extrinsic ageing is marked as a biochemical means that is

successive of external factors such as mechanical, lifestyle and environmental bearings, for instance; accumulated exposure to ultraviolet radiation (UVR), pollution

or cigarette smoking.

It is important to remark, divergent to most bodily organs, the ageing skin is

subject to both intrinsic and extrinsic ageing advances.






Alterations of the ageing epidermis


The epidermis, whilst also yielding cutaneous hydration, is liable for the body’s

defence against environmental and external insults and as the skin moves through

the ageing processes, this strata undergoes various modifications:


  • Amplified skin vulnerability, fragility and transparency: It is proposed this is credited to the 6.4 per cent per decade decline in epidermal thickness resultant of amplified apoptosis toward the granular layer, cytological atypia and increased keratinisation.

  • Pigmentation, guttate amelanosis and solar lentigo lesions: Research has testified this is due to the 20 per cent per decade diminution in the number of effective melanocytes within the basal layer in aggregation with a significant growth in the size of melanocytes.

  • Xerosis, dermatitis, eczema and associated pruritus: This is attributed to trans epidermal water loss (TEWL) inclusive of the insufficient morphological and functional qualities of sebaceous gland cells. Post preliminary hypertrophy the size of the sebaceous gland cells regress and consequently their secretory output perishes, eventually succeeding a reduction in sebum formation and surface lipid levels.

  • Decreased desquamation and altered immune function, skin infection, pathological disease and delayed wound healing: This is said to be consequential of the striking attenuation in Langerhans cells and the decrease in mitotic cell activity and re-epithelisation.


Alterations of the ageing dermis


The dermis offers a sturdy, flexible and supportive layer to the epidermis and

remarkably displays the most extreme and dramatic reformations instrumental of

skin ageing:


  • Reduced skin strength and resilience and a thin, lax and wrinkly skin surface: This is hypothesised to be consequential of dense bundles of fragmented, disorganised and insoluble collagen and elastin conformations. Studies profess this is indebted to downgraded collagen synthesis and degradation due to weakened fibroblast activity, in addition with the upregulation of collagen degradation enzymes, such as matrix metalloproteinases (MMP) via the assembly of reactive oxygen species (ROS).

  • Skin pallor and sallowness: This is affirmed to be successive of lessened vascularity resultant of a loss of vertical capillary loops.

  • Telangiectasia: This is avowed to be momentous of the thinning of dilated vessel walls.


The Dermal Clinician and treatment and management options of the

ageing cutaneous


Skin protection: UVR protection through routine and consistent use of protective

sunscreens in aggregation with reduced exposure to UVR is proposed to be vital

in protecting the cutaneous from gross variations that are linked with cumulative

sun exposure.


Skin care: Throughout cutaneous maturation the skin’s protective barrier can

become compromised, though daily administration of a gentle skincare regimen

can restore, repair and maintain the integrity of the barrier.

Topical antioxidants can potentially assist in lessening UV-induced oxygen

free radicals and skin impairment accompanied with UVR. Such antioxidants

include, L-ascorbic acid, ferulic acid, alpha lipoic acid and coenzyme Q10.


Alpha hydroxy acids (AHA) such as ascorbic acid, glycolic acid, lactic acid,

citric acid and malic acid can recover the skins elasticity and overall exterior

through encouraging epidermal thickness, mounting collagen production,

cultivating perfusion of the dermis and increasing moisture retainment in the

epidermis.


Topical tretinoin can intensify epidermal thickness, diminish keratinocyte

atypia, modify distribution melanin granule dispersal and increase collage and

fibroblast activity in the dermis.


Chemical peeling solutions: It is hypothesised chemical peels have the potential

to expose a smoother skin surface through the craft of an orderly wound to

stimulate regeneration.


Dermabrasion and microdermabrasion: This involves the stimulation and

production of new collagen through the replacement of abraded skin post

treatment.


Non-ablative therapies: This encompasses initiation of a thermal injury to the

papillary and upper reticular dermis to promote a wound healing response and

encourage fibroblast activation, regeneration of subsurface collagen and

neocollagenesis.


To summarise, skin ageing is a complicated progression and it is crucial to not

only postulate a vaster understanding of the underlying physiological and biological

developments correlated with cutaneous ageing, but to also ruminate the

psychological considerations for ageing patients in order to accelerate the undertaking of holistic treatment and management approaches to ensure healthy ageing skin.




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