Facial Aesthetic Medicines

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madman

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The realm of aesthetic medicine is broad, and there are now countless medications and topical agents used in the practice of aesthetic medicine. This chapter examines the most commonly used injectable and topical medications for aesthetic medicine.




BOTULINUM TOXINS

Since the 1990s botulinum toxins have been used in aesthetic medicine. Botulinum toxin is a neurotoxin produced by the bacteria Clostridium botulinum. Originally used for the medical purpose of treating blepharospasm, botulinum toxins are now approved by Food and Drug Administration (FDA) for a wide range of indications. The first use in aesthetic medicine was noted when treatment of blepharospasm resulted in the additional benefit of reducing crow’s feet lines produced by constriction of the vertical portion (lateral aspect) of the orbicularis oculi muscle. Interestingly, botulinum toxins were not approved to treat crow’s feet lines until 2013. In its first use as aesthetic medicine, botulinus toxins were used to treat vertical glabellar lines and horizontal forehead rhytids.

Mimetic lines are produced by the contraction of facial muscles. Mimetic lines are commonly seen in the forehead, glabella, and lateral orbicularis (crow’s feet areas) but can also be identified in other facial subunits such as the lower face and midface (Fig. 1).
Mimetic lines are amenable to treatment with botulinum toxins because the mechanism of action of botulinum toxins is to paralyze or weaken muscles by inhibiting the release of acetylcholine from the neuromuscular junction (Fig. 2).

The botulinum toxin polypeptide chain has a heavy (H) chain and a light (L) chain linked by a disulfide bond. Intramuscular injection of botulinum toxins acts at the neuromuscular junction to cause muscle paralysis by inhibiting the release of acetylcholine from presynaptic motor neurons. The heavy (H) chain of the toxin is an irreversible binder to high-affinity receptors at the presynaptic surface of cholinergic neurons. The toxin-receptor complex is endocytosed into the cell, and the disulfide bond between the 2 chains is cleaved. The toxin is then released into the cytoplasm. The light (L) chain interacts with different proteins (SNAP 25, vesicle-associated membrane protein, and syntaxin) in the nerve terminals and prevents the fusion of acetylcholine vesicles with the cell membrane.1,2 The peak of the effect occurs approximately 7 days after injection. Doses of all commercially available botulinum toxins are expressed in terms of units of biological activity. One unit of botulinum toxin corresponds to the calculated median intraperitoneal lethal dose (LD50) in female Swiss-Webster mice.1 The affected nerve terminals do not degenerate, but the blockage of neurotransmitter release is irreversible. The function is recovered by the sprouting of nerve terminals and the formation of new synaptic contacts; this usually takes approximately 3 months.





Commercially Available Types of Neurotoxins for Aesthetic Use
There are now on the market several brands of neurotoxins using different formulations of botulinum toxin. Several are FDA approved for nonaesthetic uses (eg, Myobloc), whereas others (Botox, Dysport, Xeomin, Jeuveau) are FDA approved for use to treat mimetic rhytids.

-Botox (onabotulinum A)
-Dysport (abobotulinum A)
-Jeuveau (prabotulinum toxin A)
-Xeomin (incobotulinum toxin A)



*Current Practical Use of Neurotoxins

*Contraindications to Neurotoxin Use for Aesthetic Purposes

*Adverse Effect of Neurotoxin Treatment


HYALURONIC ACID FILLERS

-Technique for Injection
-Contraindications
-Adverse Reactions and Complications



NONHYALURONIC ACID FILLERS
-Calcium Hydroxylapatite—Radiesse
-Poly-L-Lactic-Acid Filler—Sculptra
-Polymethylmethacrylate Fillers—Bellafill, ArteFill



CHEMICAL PEELS
-Superficial Peeling Agents
-Medium Depth Agents
-Deep Peel Agents



TOPICAL AESTHETIC MEDICATIONS
-Tretinoin
-Hydroquinone
-Growth Factors
-Vitamin C
 
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madman

Super Moderator
Fig. 1. Facial musculature for neurotoxin injection sites.
Screenshot (10631).png
 

madman

Super Moderator
Fig. 2. Mechanism of action of botulinum toxin. (From Rowland LP. Stroke, spasticity, and botulinum toxin. N Engl J Med. 2002 Aug 8;347(6):382-3. DOI: 10.1056/NEJMp020071; with permission.)
Screenshot (10632).png
 

madman

Super Moderator
Fig. 3. Complications of neurotoxins. (A) Eyelid ptosis. Treat with 0.5% apraclonidine drops, 1 to 2 drops tid. (B) Brow ptosis. Add 1 to 3 units of neurotoxin above the superiorly placed lateral brow to decrease the activity of the vertical fibers of the orbicularis oculi, which depresses the lateral brow.
Screenshot (10633).png
 

madman

Super Moderator
Fig. 4. (A) Typical packaging for hyaluronic acid fillers. Note syringe and Luer-lock needles included. (B) Microcannulas for injection of dermal fillers.
Screenshot (10634).png
 

madman

Super Moderator
KEY POINTS

*Botulinum toxin functions by paralyzing or weakening muscles of facial expression and thereby diminishing the appearance of mimetic lines

*Hyaluronic acid fillers have a wide variety of clinical applications in facial aesthetic medicine, and variation in filler density determines indication for location and depth of injection

*Chemical peels predictably rejuvenate the face and vary in depth of penetration from superficial to deep; chemoexfoliation coagulates proteins in the skin and induces regeneration of collagen and keratinocytes


*Topical aesthetic medicines are gaining popularity for the treatment of acne, photodamage, fine rhytids, and dyschromia

*Patients with significant horizontal forehead rhytids often have a standing static elevation of the brow by activation of the frontalis— be judicious with neurotoxin injection to avoid brow ptosis

*Inadequate weakening of the lateral frontalis can result in lateral brow “peaking” and can be corrected with a small amount of neurotoxin in the lateral frontalis

*The depth of penetration of a chemical peel depends on the mechanism of chemoexfoliation

*Nonself-neutralizing peels such as GA will continue to keratocoagulate for the duration of their contact with the skin and can reach deeper layers by prolonged skin contact

*Self-neutralizing chemical peels, such as salicylic acid, reach an endpoint after which they no longer penetrate the dermis

*Patients should wait for 6 to 12 months after stopping isotretinoin (Accutane) before undergoing surgical or nonsurgical cosmetic procedures such as laser resurfacing or chemical peels
 
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