Retacnyl Mechanism of Action

Pharmacology: Pharmacodynamics: Tretinoin applied to the skin is responsible for a variety of effects on cellular systems. It stimulates mitosis and the renewal of epidermal cells, inhibits the formation of keratin, promotes repair of conjunctive tissue and can avert and even achieve regression of cutaneous tumours induced by various carcinogenic agents. These properties form the basis for the use of tretinoin in dermatology in the treatment of cutaneous disorders such as acne, psoriasis, ichthyosis and actinic keratosis.
In acne, tretinoin acts on one of the essential aetiological factors which is the keratinisation of the lower part of the pilosebaceous follicle. The keratinised cells adhere strongly to each other, obstructing the pilosebaceous orifice which dilates, forming the microcomedone. The sebaceous gland, plugged by the effect of sebum production, becomes encysted, forming a microcyst or closed comedone. This closed comedone may evolve into an open comedo or blackhead. The microcysts are the site of a microbial pullulation of Staphylococcus albus and Propionibacterium acnes.
These organisms liberate lipases which prematurely transform triglycerides into free fatty acids which emerge in the dermis through the follicle wall, giving rise to an inflammatory reaction with a degree of suppuration, corresponding to the formation of papules and pustules. In the course of this suppurative phase, deep cystic nodules can be formed. Their evolution is prolonged, interspersed with inflammatory phenomena. The activity of tretinoin is based on a mechanism of action which has an application at every state in the pathogenesis of acne.
Tretinoin opposes and averts the formation of those elements which cause acne: by stimulation of the follicular epithelium, the increased proliferation of non-coherent keratinised cells is intensified. These unattached corneal cells are evacuated together with sebum towards the surface of the skin. The corneal plug cannot evolve and the formation of new elements is thus forestalled.
Tretinoin provokes the expulsion of retentive elements (open comedones, microcysts). Beyond the superficial desquamation of the epidermis, tretinoin exerts a deep action at the level of the follicular epithelium: it stimulates the proliferation of free corneal cells which, in association with the reduction in coherence of the corneal plug, lead to the expulsion of microcysts or of the comedone.
Tretinoin accelerates the evolution of inflammatory elements (papules, pustules). Applied at the onset of the inflammatory phase, tretinoin increases the permeability of the follicular wall to irritants responsible for inflammatory phenomena (fragments of keratin, free fatty acids) and equally accelerates the evolution of papules and pustules and their elimination. It thus prevents the transformation of these lesions into cystics nodules.
Pharmacokinetics: Absorption of tretinoin through intact human skin is low and it is not known whether it is absorbed from denuded skin, wounds, or mucous membranes. Tretinoin is rapidly absorbed but equally rapidly eliminated by metabolism and excretion. Cutaneously a small percentage passes the stratum corneum, in the order of 0.6% to 6% of the applied dose.