Since ancient times, the symbolic and aesthetic significance of breasts as a feature of the female body has long been recognized by the world. From Dong Yining’s “Qinyuanchun – Beauty’s Breasts” (沁园春-美人乳) to Yu Dafu’s “Lost Sheep” (迷羊), “A kind of soft and smooth breast that is the same as touching a wheat flour doughnut. To Yu Dafu’s “Lost Sheep”, “a soft and smooth, with the same touch on the wheat flour dough like touch, and in my whole body through a current”. All of them show that a pair of full, round, firm, symmetrical and healthy breasts is the common pursuit of human beings. Since the birth of gel prosthesis in the 1960s, breast augmentation has been used clinically for decades all over the world. Qualified implant materials have been proven to be harmless to human body through a lot of researches and experiments, and have been approved by FDA in the United States. However, there are still problems to be solved in its clinical application. Peritoneal contracture is a common and serious complication after breast augmentation surgery, which is caused by the dysfunction of inflammatory cells, fibroblasts and extracellular matrix in the body during the process of isolation of the implant material with tight collagen. 92% of the peritoneal contracture occurs within 1 year after the surgery, and the reason for its occurrence is still not very clear. Based on the existing research data, it can be inferred that its possible etiology are: 1, bacterial infection; 2, the surface of the prosthesis; 3, the choice of incision site; 4, the level of prosthesis placement; 5, foreign body causing aseptic inflammation (prosthesis oozing, talcum powder, iodine povidone) and so on. Among them, glossy prosthesis material, axillary incision access and postmammary placement level are considered to be risk factors for periosteal contracture. In addition, there are studies that support the role of chronic inflammation of tissues under bacterial or aseptic conditions in the formation of contracture of the envelope. Current non-surgical treatments for pericardial contracture include: 1. Leukotriene inhibitors: such as zalustat, have been shown to prevent and reduce established pericardial contracture; however, the risk of serious complications from leukotriene inhibitors, such as liver failure, far outweighs the benefits of treating pericardial contracture. 2, glucocorticoid drugs: local anti-inflammatory effect can reduce the incidence of contracture, but there are delayed wound healing, prosthesis placement hernia, and tissue thinning and other steroid-related complications, so it can not be widely used. 3, other drugs: small-scale studies found that (such as mitomycin C, pirfenidone and some smooth muscle function regulators, etc.) for pericardial contracture has a certain therapeutic effect, but due to the small sample size of the study and the successive emergence of adverse reactions, it is difficult to be used as a routine clinical drug therapy. 4.Physical therapy: such as massage, extracorporeal ultrasound, pulsed electromagnetic field therapy, etc. only has a certain therapeutic effect on pericardial contracture. At present, there is no method that can predict, prevent and treat contracture. This means that if symptoms of contracture such as breast distortion, hardening or even breast pain occur after surgery, there is a risk of reoperation. Surgically Removed Implant Covered by Contractured Peritoneum And in recent years, with the further understanding of Botulinum Toxin A (BoNT-A) and the mechanism of the occurrence of contracture of the peritoneum, doctors and scientists believe that Botulinum Toxin A, which we usually use to slim down the face and calves, can be used as a new peritoneal contracture treatment method. This is because they found a special kind of fibroblasts with contractile function properties within the contracted periosteal tissue. (It is also often found in granulation tissue to promote wound contraction and disappears when the wound grows back, but it is abnormally persistent and functional in hyperplastic scars and keloids.) The presence of this specialized cell can lead to an overreaction of the body to risk factors, promoting fibroblast proliferation and deposition of ECM components of the extracellular matrix, which can lead to overgrowth of the encapsulated tissue. This cell proliferation and ECM remodeling can, on the one hand, lead to the activation of intertissue transforming growth factor β1 (TGF-β1), which further phosphorylates Smad2/3, thereby regulating the expression of the corresponding genes and inducing the transformation of fibroblasts into myofibroblasts. On the other hand, it can cause enhanced extracellular stress, which activates multiple intracellular signaling systems through cytoskeletal protein transduction, further amplifying the fibrotic cascade response. These myofibroblasts transformed from intrinsic fibroblasts and circulating migrating bone marrow-derived fibroblasts will further lead to pericyte contracture. Fibroblasts are transformed into myofibroblasts by activated TGFβ1 So what role can Botulinum Toxin A play in the prevention and treatment of periosteal contracture? Studies have shown that BoNT-A can reduce the thickness of the peritoneum by: 1. regulating the cell cycle of fibroblasts and down-regulating fibroblast proliferation, as well as regulating the activity of matrix metalloproteinase MMP, which promotes the breakdown of collagen type 1 and type 3. The dotted line shows the thickness of the peritoneal tissue, you can see that with the increase in the dosage of botulinum toxin A, the thickness of the peritoneum has a significant reduction 2, effectively reduce the inter-tissue TGF β1, reduce smad2 phosphorylation, thus reducing the conversion of intrinsic fibroblasts into myofibroblasts, reducing the peritoneal contracture. It can be seen that after the application of botulinum toxin A, there is a significant reduction in the level of intertissue TGFβ1. 3, by pre-reducing the pectoralis major muscle force, can effectively prevent the occurrence of periosteal contracture, which may be related to the reduction of extracellular stress.