Botox is a brand name of OnabotulinumtoxinA, which is perhaps most famous for its cosmetic uses. The most popular use of Botox is the treatment of glabellar frown lines, crow’s feet, and other facial wrinkles or creases. However, it was actually first used in the 1980s by ophthalmologists (eye doctors) to treat eye conditions such as blepharospasm (uncontrollable blinking) and strabismus (crossed eyes). Since then, it has also been used to treat other medical conditions such as achalasia (spasm of the lower esophageal sphincter), hyperhidrosis (excessive sweating), and chronic migraines or headaches, etc.
Botox or OnabotulinumtoxinA is also known as botolinum toxin type A. Botulinum toxin is a neurotoxin that is produced by Clostridium botulinum, which is a spore-producing anaerobic bacterium. The toxin has seven serotypes: type A, type B, type C, type D, type E, type F, and type G. Each of these types has specific molecular properties or characteristics. However, excessive levels of any of these can be potentially life threatening.
How is Botox or OnabotulinumtoxinA (botulinum toxin type A) used in the treatment of wrinkles and facial creases?
Botulinum toxin primarily blocks cell communication by preventing the release of neurotransmitters, which results in a temporary paralysis of the local muscles. This, in turn, causes the smoothening of the skin and reduction in wrinkles, particularly crow’s feet, frown lines and lines on the forehead. This paralysis can last up to several months before follow up treatment is needed. The general safety and easy tolerability of the procedure has made this a popular option for cosmetic purposes.
What is the mechanism of action of botulinum toxin? (What happens in the cells when botolinum toxin is injected in the body?)
Botulinum toxin contains a heavy polypeptide chain and a light polypeptide chain. The heavy polypeptide chain is an important component of the toxin because it targets and binds with the axon terminals of the neurons (nerve cells) at or near the site of injection. One region of the heavy polypeptide chain binds to the surface of the target nerve cell(s), while another region of the heavy chain transports the light polypeptide chain across the membrane of the nerve cell(s). After its attachment to the axon terminals and cell absorption of the light polypeptide chain via endocytosis, the toxin (through its light polypeptide chain) exerts zinc-dependent protease activity on the SNARE complex (protein components essential to exocytosis).
Specifically, botulinum toxin type A degrades the SNAP-25 protein, which is essential for vesicle fusion and release of acetylcholine (an essential chemical for communication between cells) from the axon endings. The proteolysis of the SNARE proteins prevents neurosecretory vesicles from binding with the synapse plasma membrane, and thus, neurotransmitter release is inhibited.
After all this activity in the cells, the end result is a paralyzed muscle (or muscles). The lack of movement of these muscles help reduce the appearance of wrinkles on the area where Botox was injected.
What are the risks or adverse effects of Botox?
Some adverse effects that have been noted with the use of botulinum toxin include local pain, hematoma formation, and ptosis (drooping) of the eyelid, etc.