Botox: Identity, Uses, and Results
Actual name: Botulinum Toxin Type-A
In the Biomedical Research: An International Journal of Medical Sciences, Jiang et al. (2017) emphasized that Botulinum Toxin Type-A, Botox for commercial purposes, has been commonly used to treat many cases of muscle tension disease for more than 50 years. The reason that this well-known toxin has been affective in treatment is that it paralyzes the cholinergic nerve. The cholinergic nerves include all thepreganglionic sympathetic and preganglionic parasympathetic nerves: the postganglionic parasympathetic nerves, thesomatic motor nerves to skeletal muscles, and some nerves to sweat glands and to certain blood vessels” (Mosby’s Medical Dictionary, 2009).”
Simply put, Botox’s main purpose is to block physiological function, causing muscle paralysis. It is not meant for healing, rejuvenation, correction, or prevention; in pain-related cases, it relieves pain symptoms by causing nerve dysfunction only.
Jiang et al. (2017) explained that Botulinum Toxin causes paralysis especially at the muscle-nerve joints, resulting in complete muscle relaxation. Though Botox is “one of the most toxic substances in the world,” its safety has been illustrated in numerous scholarly studies as long as repeated injections do not occur within 3 months. Also, repeated injections after the first 3-month period have never been understood, and there is no substantial research that can show the impacts of this toxin and/or repeated injections in humans after a specific period of time (Jiang, et al., 2017, p. 490).
According to United Health Care Drug Policy, Jiang et al. (2017), Gracies et al. (2015), Intiso et al. (2014), Nalysnyk et al. (2013), Dutra et al. (2017), Mancini, Sandrini, Moglia, Nappi, & Pacchetti (2005), and many other credible, scholarly sources, the studies that have targeted the use of Botulinum Toxin Type-A in humans have, so far, reported results of small randomized exploratory studies. The results of the majority of studies were based on very small samples.
The FDA does not approve of the cosmetic use of Botox. For non-cosmetic use, the Botulinum Toxin Type-A “is FDA approved for the prophylaxis of headaches in adult patients with chronic migraine (≥15 days per month with headache lasting 4 hours a day or longer). Safety and effectiveness of Botox have not been established for the prophylaxis of episodic migraine (14 headache days or fewer per month). Treatment with Botox is not intended to substitute for usual standard of care rehabilitation regimens” (UnitedHealthcare Commercial Drug Policy, 2017). Though the United Healthcare Drug Policy specifically noted that all credible studies on Botox have used very small samples, it reported the toxin’s effectiveness in very specific pain-related conditions listed and explained here.
Overall, the successful and safe results of the use of Botulinum Toxin Type-A have only been reported in pain-related conditions that required immediate paralysis of the nerves.
BOTOX CAUSES BONE LOSS
Dutra et al. (2016) from the Department of Orthodontics, University of Connecticut Health Center, the Department of Oral and Maxillofacial Diagnostic Sciences, University of Connecticut Health Center, and the Department of Oral and Maxillofacial Radiology, University of Connecticut Health Center reported substantial results after completing a study on a sample of mice.
*Disclaimer: Please note that Greg Martin Skin is strictly against any form of animal testing and remains a cruelty-free company. The scholarly studies published on this page are strictly for research purposes.
Dutra et al. (2016) explained that the objective of their study was “to evaluate the cellular and matrix effects of Botulinum Toxin Type-A (Botox) on mandibular condylar cartilage (MCC) and subchondral bone,” which has never been done before (Dutra, et al., 2016, p. 2).
“Botox (0.3 unit) was injected into the right masseter of 5-week-old transgenic mice (Col10a1-RFPcherry) at day 1. Left side masseter was used as intra-animal control. The following bone labels were intraperitoneally injected: calcein at day 7, alizarin red at day 14 and calcein at day 21. In addition, EdU was injected 48 and 24 hours before sacrifice. Mice were sacrificed 30 days after Botox injection. Experimental and control side mandibles were dissected and examined by x-ray imaging and micro-CT. Subsequently, MCC along with the subchondral bone was sectioned and stained with tartrate resistant acid phosphatase (TRAP), EdU, TUNEL, alkaline phosphatase, toluidine blue and safranin O. In addition, we performed immunohistochemistry for pSMAD and VEGF” (Dutra et al., 2016, p. 2).
- “Botox injection leads to decrease in tissue density and bone volume. There was a significant decrease in bone volume in the Botox injected side in comparison to control, as revealed by a 21.44% decrease in BFV (p < 0.05, Fig 1C ), as well as a 17.4% decrease in Trab. Thickness (p < 0.05), Fig 1D ) and an 18.37% increase in Trab. Spacing (p < 0.05, Fig 1E ). Furthermore, we observed a significant decrease in tissue density (4.10% decrease, p < 0.05, Fig 1F ) at the injected side after unilateral Botox injection (Dutra et al., 2016, pp. 4-5).”
- Botox injection leads to decrease in condylar width (Dutra et al., 2016, p. 6).
- Botox leads to decrease in bone turnover (Dutra et al., 2016, p. 6).
- Botox injection leads to decrease in chondrocyte proliferation anddifferentiation and increases cell apoptosis (Dutra et al., 2016, p. 6).
- Botox leads to decrease in proteoglycan secretion (Dutra et al., 2016, p. 6).
- Botox injection leads to decreased expression of pSMAD1/5/8 and VEGF (Dutra et al., 2016, p. 7).
Discussion of Results
Even though “Botox is being used as a cosmetic procedure to reduce the thickness and tonicity of themassetermuscle and create a slimmer oval shape face,” it could “potentially unload the mandible and cause anatomical changes as well as osteopenia of the mandibular ramus, alveolar bone and subchondral bone” (Dutra et al., 2016, p. 2).
Muscular loading plays an essential role in maintaining bone volume and density. It has been shown that reducing the volume of thigh and calfmuscles by Botox injections cause reduced bone volume and mineral content in the limbs. Rafferty et al. (2012) studied the short-termand long-terms effects of a single Botox injection into themasseter of rabbits and found decreased bone volume of the subchondral bone at the injected side, 4 and 12 weeks after injection, suggesting that the bone loss caused by masseter paralysis persists with time. Tsai et al. (2010) tested the effects of injecting the temporalismuscle in addition to masseter with Botox, and observed reduced bonemineral density not only in themandible, but also in the skull of rats. A pilot clinical investigation evaluated cone-beamcomputed tomography of condyles of women presenting oral-facial pain who were treated with Botox injections into the masticatorymuscles or not. All women who received Botox injections presented with decreased subchondral bone density in comparison to women who were not exposed to Botox (Dutra et al., 2016, pp. 10-11).
The above studies were all consistent with the results found by Dutra et al. (2016) “on reduced bone volume and quality in the subchondral bone of the Botox injected side condyle” (Dutra et al., 2016, p. 11).
For regularly updated scholarly articles on Botulinum Toxin Type-A (Botox), the latest technological advancements used in cellular healing, restoration, and rejuvenation, and ingredients used in skincare lines, please explore the Greg Martin Skin LATEST RESEARCH page.