The role of Dermal Clinician’s in the management and treatment of scarring associated with Acne.



Acne scarring is the most common ramification of Acne Vulgaris and research declares 95 per-cent of acne sufferers will extant with various degrees of consequent acne scarring. Acne scarring emanates from the damage caused to the skin during the healing of active acne lesions and has the ability to induce overwhelming psychological, psychosocial and physical distress due to its bodily disfigurement. Successful treatment and management of acne scarring remains a challenge, however research advises early intervention is vital due to the correlation between the severity of acne scars and the duration between initial development of acne lesions and the commencement of acne treatment.


The pathogenesis of acne scarring


The subsequent scarring ensuing the inflammation accompanying Acne Vulgaris progresses from an exchange of numerous mechanisms, such as inflammation, granulation tissue formation and matrix remodelling. The formation of Acne scars transpires when an inflammatory lesion associated with Acne Vulgaris erupts into the sebaceous follicle and principates a perifollicular abscess. Typically, the inflammatory reaction is compressed, and the abscess is repaired with no supplement scarring, however, if encapsulation is defective, multichannel fistulous tracts will advance, and scar formation will befall. The type of scar that is formed is governed by the extent, the depth and the hosts response to the inflammation. It is also noteworthy to consider that some patients are more susceptible to the development of acne scarring as they encompass an altered inflammatory cell profile and consequently encounter an extended inflammatory response at the follicle culminating in collagen disruption and destruction.


Classification of acne scarring

Acne scars are established based on their tissue response to inflammation. Mostly, there are two categories of acne scars, those which are resultant from amplified tissue formation and those which are produced by deficient tissue formation. Hypertrophic and keloidal scars are associated with excessive collagen deposition and decreased collagenase activity. Specific to hypertrophic scars, they exhibit erythematous, raised, firm lesions in conjunction with thick hyalinised collagen bundles within the original site of injury. By comparison keloidal scars depict as red or purple papules and nodules with dense collections of hyalinised acellular collagen in whorls that proliferate outside of the original wound margin and often grow without retreat. Both hypertrophic and keloidal scars commonly display on the back, shoulders, trunk and jawline. In contrast, atrophic scars are more collective and are affiliated with the destruction of collagen and elastin due to inflammation in the deep dermis. Atrophic scars commonly appear on the face and primarily present as erythematous lesions that become hypopigmented as time advances. Atrophic scars are further divided into three sub-groups contingent on the depth, shape and degree of collagen lost.

  • Ice-pick scarring (less than 2mm): Narrow, deep and sharply demarcated “V” shaped epithelial tracts that extend vertically into the deep dermis or subcutaneous layer. Credits to 60-70 per-cent of Acne scars.

  • Rolling scarring (4-5mm): Undulating “M” shaped tracts resultant from dermal tethering of the dermis to the subcutis. Attributes to 15-20% of Acne scarring.

  • Boxcar scarring (1.5-4mm): Oval or round, shallow or deep, sharply demarcated “U” shaped epithelial tracts that extend into the dermis, however they do not taper at the base. Responsible for 20-30 per-cent of Acne scars.

It is crucial to establish the type of scarring present in order to generate and tailor a befitting treatment plan for patients. Whilst other deviating descriptors have formerly been used to classify Acne scars, they are subjective and therefore research advocates that Clinicians comply with the sanctioned nomenclature to ensure unity of terminology and allow for treatment contrasts across a variation of studies.


Interprofessional Practice and how Dermal Clinicians can aid in the management and treatment of acne scarring


The treatment of Acne scarring exposes as a challenge for both Clinician and patient, despite there being an abundance of treatment and management selections available there is no guaranteed uniform modality to completely and dependably remove scars, thus, research instructs when treating Acne scars the goal should be to give the skin a more acceptable physical appearance. Considering this, as Dermal Clinicians, when treating post-acne scarring patients it is imperative to educate and impart realistic expectations whilst also residing within our scope of practice.


The ways in which Dermal Clinicians can work interprofessionally to aid in the treatment and management of acne scars are outlined below:

  • Ablative lasers

The epithelium, papillary dermis and reticular dermis are removed to stimulate re-epithelialisation, extracellular collagen synthesis and remodelling

  • Non-ablative lasers

Using thermal production, the skin is resurfaced to promote collagen remodelling in the dermis

  • Fractional resurfacing

Microscopic thermal wounds are created to induce dermal remodelling and re-epithelialisation

  • Chemical peels

A controlled wound healing process is engendered which results in the elimination of dead cells to prompt re-epithelialisation and increase collagen and elastin production

  • Skin Needling

Microchannels in the dermis are formed to initiate and increase collagen and elastin production

  • Dermabraison

The epidermis and part of the dermis is removed via either a rotating motorised hand piece with a wire brush or a diamond tipped handpiece to promote re-epithelialisation and re-pigmentation

  • Radio-frequency (RF)

A skin injury is created to encourage a wound healing response in order to inspire the remodelling of dermal collagen

  • Subcision

Fibrotic adhesions are loosened in order to form a gap for future collagen deposition in successive wound healing

  • Isotretinoin

Prevents post-acne scar formation

  • Topical retinoids

Motivates collagen formation, elastin fibres and dermal collagen synthesis

  • Soft Tissue Augmentation

Soft tissue volume is replaced, and collagen production is encouraged

  • Punch Excision

Scar tissue is excised via a punch biopsy to promote a controlled wound healing process

  • Radiotherapy

Prevents recurrence of post-acne scar formation by decreasing fibroblast activity and encouraging cellular apoptosis


Considering the above information, it is essential to remark that research recommends in order to maximise patient clinical outcomes that Dermal Clinicians execute a combination of these therapies whilst working interprofessionally alongside other medical specialists in the treatment of post-acne scarring.



References

Pandey, A., Swain, J.P., & Minj, A. (2015). Assessment of Microneedling Therapy in the Management of Atrophic Facial Acne Scars. Journal of Evidence Based Medicine and Healthcare, (57), 8911. https://doi-org.wallaby.vu.edu.au:4433/10.18410/jebmh/2015/1256

Basta-Juzbašić, A. (2010). Current therapeutic approach to acne scars. Acta Dermatovenerologica Croatica: ADC, 18(3), 171–175. Retrieved from https://search-ebscohost-com.wallaby.vu.edu.au:4433/login.aspx?direct=true&db=mnh&AN=20887698&site=eds-live

Cohen, B. E., Brauer, J. A., & Geronemus, R. G. (2016). Acne scarring: A review of available therapeutic lasers. Lasers in Surgery & Medicine, 48(2), 95–115. https://doi-org.wallaby.vu.edu.au:4433/10.1002/lsm.22410

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