China
Africa
Explore chapters and articles related to this topic
Injectable Poly-L-Lactic Acid for the Arms
Published in Neil S. Sadick, Illustrated Manual of Injectable Fillers, 2020
Daniel Dal’Asta Coimbra, Betina Stefanello
The biological mechanism generating the desired augmenting effect is most likely mediated by macrophages and foreign body giant cells that recognize PLLA as a foreign body. They recruit and stimulate fibroblasts via transforming growth factor beta to proliferate and differentiate into myofibroblasts. (Myo)fibroblasts encapsulate PLLA particles with collagen type III and deposit fibrotic collagen type I in the capsule periphery. Hence PLLA is degraded in human tissue at a much slower pace than previously assumed by several authors, and the use of PLLA for augmentation should be given further consideration (5).
Animal Models for Studying Soft Tissue Biocompatibility of Biomaterials
Published in Yuehuei H. An, Richard J. Friedman, Animal Models in Orthopaedic Research, 2020
At approximately the third day, formation of collagen fibres by the fibroblasts becomes histologically visible.22 In addition, a network of capillaries is formed to provide oxygen to support the fibroblast synthesis of collagen. In front of the newly formed collagen matrix, the macrophages still continue to phagocytize the dead material hereby creating an environment for other fibroblasts to settle. This process continues until the wound is completely closed. The tissue formed is called granulation tissue. Already at the sixth day of wound healing, maturation of the collagen fibres starts. By means of collagen synthesis and lysis, remodelling of the collagen network occurs. Meanwhile, myofibroblasts are responsible for wound contraction, hereby reducing the wound surface. Finally, the number of cells will decrease, leaving scar tissue behind. The functional characteristics of this newly formed tissue are less effective compared to the original tissue, The wound strength will never reach its original value and scar tissue is nonelastic.22-24
Actions of Dopamine on the Skin and the Skeleton
Published in Nira Ben-Jonathan, Dopamine, 2020
Wound contraction and remodeling: myofibroblasts decrease the size of the wound by gripping the wound edges and contracting, acting like smooth muscle cells. Collagen is then realigned along tension lines, and cells that are no longer needed are removed by apoptosis. Freshly healed epidermis and dermis are formed by the appropriate cells.
Hyalocytes in proliferative vitreo-retinal diseases
Published in Expert Review of Ophthalmology, 2022
Charlotte H. Jones, Wei Gui, Ricarda G. Schumann, Stefaniya K. Boneva, Clemens A. K. Lange, Koen A. van Overdam, Toco Y. P. Chui, Richard B. Rosen, Michael Engelbert, J. Sebag
Myofibroblasts are the contractile components of fibrocellular membranes. Their contractile properties and their ability to produce newly formed collagen have been demonstrated in numerous studies of the diabetic vitreo-retinal interface [68,87]. In particular, ultrastructural analyses of the co-localization α-SMA filaments and collagen type I and III proved the presence of hyalocytes in fibrocellular membranes of diabetic eyes [84]. Hyalocytes and myofibroblasts are usually embedded in thick layers of native vitreous collagen. In addition, newly-formed collagen and fibrous long-spacing collagen were seen in diabetic retinopathy representing a remodeling process of vitreous cortex collagen [79,84,88]. Pathologic changes at the vitreo-macular interface were present in all eyes irrespective of the presence of tractional fibrocellular membranes.
The effect of platelet-rich fibrin on wound healing following strabismus surgery
Published in Cutaneous and Ocular Toxicology, 2022
Betul Tugcu, Havvanur Bayraktar, Cansu Ekinci, Zafer Kucukodaci, Mustafa Tunali, Fadime Nuhoglu
The wound contraction is important in wound healing because it results in the closure of the wound23. Myofibroblasts are playing a major role in wound contraction and remodelling of the granulation tissue24. For this reason, fibroblast-to-myofibroblast differentiation represents a key event during the remodelling phase of wound healing. PRF consists of TGF-β, which is causing migration of fibroblast and differentiation to myofibroblast during wound healing. Myofibroblasts exhibit contractile properties, due to the expression of α-SMA in microfilament bundles. In the present study, more intense staining for α-SMA was detected in the PRF group compared to the control group and this is also consistent with the hypothesis that PRF facilitates wound healing as a biocatalyst in literature16. Besides, this difference in α-SMA related to myofibroblast activity might be an important feature in wound remodelling for the preference to use PRF. Therefore, further studies are warranted to confirm these preliminary findings.
PDGF as an Important Initiator for Neurite Outgrowth Associated with Fibrovascular Membranes in Proliferative Diabetic Retinopathy
Published in Current Eye Research, 2022
Evy Lefevere, Inge Van Hove, Jurgen Sergeys, David H. W. Steel, Reinier Schlingemann, Lieve Moons, Ingeborg Klaassen
Besides vascular pathogenesis, neuroglial cell migration/proliferation and fibrosis at the vitreoretinal interface are linked to proliferative DR (PDR). Importantly, fibrovascular membrane (FVM) formation is a serious sight-threatening complication of PDR as it may result in tractional retinal detachment.6 Extensive neurite sprouting occurs during the formation of fibrovascular membranes (FVMs) and may originate from any type of neuron including photoreceptors, bipolar, amacrine and ganglion cells, as well as from retinal glial cells.7–9 The role of these neurites in FVM formation is unknown, but it has been speculated that vascular growth is stimulated by neurotrophic factors derived from neurons and Müller cells and that the neurite outgrowths may also serve as a scaffold for the newly formed vessels.7,8,10 During progression of the disease, in which myofibroblasts play a central role in a wound-healing-like response, fibrosis leads to FVM formation. In addition, Müller glial–mesenchymal transition has been postulated as an alternative fibrinogenic mechanism associated with membrane formation in PDR.11 More precise knowledge of the molecular mechanisms underlying FVM development and progression may enable novel pharmacological interventions to be identified.