scholarly journals CALCIFICATION OF ARTERIES IN PATIENTS WITH ATHEROSCLEROSIS: CAUSES AND MECHANISMS OF DEVELOPMENT

2021 ◽  
pp. 17-35
Author(s):  
V. К. Кazymyrko ◽  
Т. S. Silantieva ◽  
L. N. Іvanitska ◽  
А. G. Dubkova ◽  
V. V. Кutovyi
Keyword(s):  
Stem Cells ◽  
Connective Tissue ◽  
Arterial Wall ◽  
Soft Tissues ◽  
Extracellular Fluid ◽  
Cartilage Tissue ◽  
Arterial Calcification ◽  
Elastic Fibers ◽  
Mineral Phase ◽  
Tissue Calcification

The paper shows analogies between the mechanisms of calcification of arteries, various tissues and bone mineralization. In calcification the same mechanisms are involved, as at ossification of an organic matrix of a bone, including participation of stem cells. In the arteries and capillaries of various organs found polypotent precursors – mesenchymal stem cells, presumably responsible for the pathological mineralization of the arterial wall. Circulating in the blood and present in the intima of the human atheromatous aorta colony-forming stem cells of the stromal line of differentiation. Adventitia cells or pericytes are considered as a pluripotent mesenchymal reserve for replenishment of some cellular forms of connective tissue. Bone marrow stem cells of the stromal line of differentiation with the presence of pluripotent stromal cells in the blood and granulomas (plaques) and their transformation into bone tissue cells are involved in atherogenesis. Smooth muscle cells (SMCs) and myofibroblasts of the arterial wall adventitia have an osteoblast-like phenotype. Collagen and elastic fibers are involved in the calcification of blood vessels and soft tissues. Calcification of granulomas (plaques) accompanies their inflammatory morphogenesis, accompanied by the development of scar tissue. It often accompanies and completes the inflammation in them. This process is observed with the gradual replacement of the parenchyma of some organs with connective tissue. The mineral phase in bones and soft tissues, represented by calcium (Ca) and phosphate (P), contacts with nucleators - specific areas of collagen fibers. Non-collagen proteins are also involved in arterial calcification. With the progression of atherosclerosis and calcification of granulomas/plaques by cells present in the arterial wall, osteonectin is expressed. Osteopontin content is associated with Ca deposits in them; in particular, it correlates with the Ca level in the coronary arteries. In the processes of ossification and calcification, phosphatases play a certain role. In areas of calcification of granulomas/plaques, osteoprotegerin is found, which inhibits the activity of alkaline phosphatase in the aorta and prevents calcification of the media. Arterial wall calcification and inflammation are inhibited by fetuin-A and matrix γ-carboxyglutaric protein (MGP). The rate of bone formation and tissue calcification depends on the concentration of Ca and P in plasma and extracellular fluid. With their high concentration in the extracellular fluid, the mineral phase appears where it normally does not exist. Lipids are among the initiators of granuloma / plaque calcification in the arteries. The role of inflammation and necrosis in the calcification of the arteries is confirmed by experiments on animals with repeated intravenous injections of adrenaline, which causes focal necrosis of the middle membrane, which then undergoes calcification. In arterial walls, heart muscle, bone and cartilage tissue, osteonectin, osteocalcin, osteopontin, bone sialoprotein are often formed. In general, the mechanisms of arterial and soft tissue calcification are poorly understood. There are no effective remedies for calcification.

scholarly journals Spontaneous perforation of the stomach and duodenum in children with Ehlers‑Danlos syndrome

2021 ◽  
Vol 1 (1) ◽  
pp. 176-182
Author(s):  
M. A. Amanova ◽  
A. N. Smirnov ◽  
V. V. Kholostova ◽  
A. G. Mannanov ◽  
S. A. Voina ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Collagen Synthesis ◽  
Soft Tissues ◽  
Clinical Manifestations ◽  
Elastic Fibers ◽  
Ehlers Danlos Syndrome ◽  
Vascular Type ◽  
The Individual ◽  
Rupture Of The Spleen ◽  
Danlos Syndrome

Ehlers-Danlos syndrome is based on hereditary systemic dysfunction of the connective tissue caused by impaired collagen synthesis. Depending on the individual mutation, the clinical manifestations of the syndrome can range from mild to life-threatening. The result of a violation of collagen synthesis is the proliferation of elastic fibers, loss of compactness and disorientation of collagen fibers, fragility of the vessel wall and expansion of their lumen. And, given that connective tissue fibers are present in almost every organ, the manifestations of Ehlers-Danlos syndrome are polymorphic and generalized, which often complicates the verification of this disease. The most clinically important is the Ehlers-Danlos Syndrome IV (vascular) type, which occurs as a result of mutations in the COL3A1 and COL1A1 genes and manifests itself in a tendency to spontaneous rupture of large arteries and hollow organs (intestinal perforation, strokes, rupture of the spleen, etc.), poor wound healing, fragility soft tissues, impaired hemostasis. The article describes our own experience of treating 4 patients with spontaneous ruptures of internal organs, including those of a recurrent nature.

scholarly journals Articular cartilage tissue engineering with stem cells implanted onto nanoscaffolds and platelet-rich plasma

2017 ◽  
Vol 3 (3) ◽  
pp. 322
Author(s):  
Hadeer A. Abbassy ◽  
Laila M. Montaser ◽  
Sherin M. Fawzy
Keyword(s):  
Tissue Engineering ◽  
Stem Cells ◽  
Articular Cartilage ◽  
Soft Tissues ◽  
Platelet Rich Plasma ◽  
Cartilage Tissue Engineering ◽  
Cartilage Regeneration ◽  
Cartilage Tissue ◽  
Cartilage Defects ◽  
Great Promise

<p class="abstract">Musculoskeletal medicine targets both cartilage regeneration and healing of soft tissues. Articular cartilage repair and regeneration is primarily considered to be due to its poor regenerative properties. Cartilage defects due to joint injury, aging, or osteoarthritis have low self-repair ability thus they are most often irreversible as well as being a major cause of joint pain and chronic disability. Unfortunately, current methods do not seamlessly restore hyaline cartilage and may lead to the formation of fibro- or continue hypertrophic cartilage. Deficiency of efficient modalities of therapy has invited research to combine stem cells, scaffold materials and environmental factors through tissue engineering. Articular cartilage tissue engineering aims to repair, regenerate, and hence improve the function of injured or diseased cartilage. This holds great potential and has evoked intense interest in improving cartilage therapy. Platelet-rich plasma (PRP) and/or stem cells may be influential for tissue repair as well as cartilage regenerative processes.  A great promise to advance current cartilage therapies toward achieving a consistently successful modality has been held for addressing cartilage afflictions. The use of stem cells, novel biologically inspired scaffolds and, emerging nanotechnology may be the best way to reach this objective via tissue engineering. A current and emergent approach in the field of cartilage tissue engineering is explained in this review for specific application. In the future, the development of new strategies using stem cells seeded in scaffolds and the culture medium supplemented with growth factors could improve the quality of the newly formed cartilage<span lang="EN-IN">.</span></p>

scholarly journals The Efficacy of Polycaprolactone Threads in Zygomatic and Mandibular Lifting: Consecutive Study from a Single Practitioner’s Experience

2017 ◽  
Vol 2 (1) ◽  
Keyword(s):  
Connective Tissue ◽  
Soft Tissues ◽  
Neck Region ◽  
Lower Eyelid ◽  
Ageing Process ◽  
Elastic Fibers ◽  
Muscular Tissue ◽  
Facial Skin ◽  
Eyelid Skin ◽  
The Face

The ageing process brings with it characteristic changes to the dermal facial skin scaffolding, and it’s fat component. Connective tissue of the skin begins to wear thin, and elastic fibers undergo a collapse, causing noticeable weakening in prominent facial regions such as the cheeks, eyebrows, mandibular area and neck [1]. It is the dermatocalasis of facial and neck soft tissues, including the Superficial Muscular Aponeurotic System (SMAS), and the muscular tissue, that is culpable for the distinctive signs of ageing of the face [2]. Of all the facial ageing signs, emphasis can be placed on; The profile of the mandibular margin (which lacks previous clarity) resulting in the down-ageing of the jaw line, The presence of horizontal wrinkles on the forehead at which vertical ones add on to at the glabellar area, A downward sliding of the zygomatic malar region (middle face) being observed, The appearance of the lachrymal furrow and deepening of the naso-buccal and mandibularbucco areas, The production of adipose bubbles resulting in the eyelid skin becoming saggy and protruding in correlation to the lower eyelid and Plasmatic parcel and cutaneous flabbiness disappearing from around the neck region [3].

Novel Biologic Therapy for Untreated Diseases of Vascular Calcification

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2326-2326 ◽  
Author(s):  
Demetrios T. Braddock ◽  
Dillon Kavanagh ◽  
Xiaofeng Li
Keyword(s):  
Connective Tissue ◽  
Vascular Calcification ◽  
Knockout Mice ◽  
Elastic Fiber ◽  
Extracellular Atp ◽  
The Body ◽  
Medial Wall ◽  
Arterial Calcification ◽  
Yale University ◽  
Tissue Calcification

Abstract Diseases of medial wall vascular and connective tissue calcification associated with low plasma pyrophosphate (PPi) range from orphan diseases such as Pseudoxanthoma Elasticum (PXE) and Generalized Calcification of Infancy (GACI) to ubiquitous diseases of medial wall vascular calcification affecting every aging adult such as hardening of the arteries associated with aging. Although recognized as a potent mineralization inhibitor for over a generation, PPi has never been established as a causative agent in the broad class of connective tissue diseases and effective therapeutics capable of treating the calcifications driving the morbidity and mortality of these conditions is lacking. We have recently demonstrated that elevation of plasma PPi using a novel biologic containing the pyrophosphate generating enzyme ENPP1 is curative in rodent models of the rare orphan disease GACI - a severe lethal neonatal disease of arterial calcification. Here, we demonstrate the efficacy of this approach in a more common disorder of vascular and connective tissue calcification and low plasma PPi called PXE. PXE is a monogenic, hereditable connective tissue disease characterized by aberrant mineralization of the skin, eye, and vasculature. PXE is associated with loss of function mutations in the ABCC6 gene - a multi-pass ATP dependent membrane transport protein. Two opposing theories regarding the genetic etiology of PXE are held - a metabolic hypothesis postulating that ABCC6 mutations deprive the body of a global mineralization inhibitor, and a cellular hypothesis postulating that ABCC6 mutations compromise a stem cell progenitor locally present within specific tissues. Both etiologies are proposed to account for the regional mineral and elastic fiber alterations present in the disease. Although the substrate of ABCC6 is unknown, patients with PXE (and ABCC6 knockout mice) have plasma [PPi] at about 20-30% of unaffected (or wild-type) individuals. Furthermore, transfections of ABCC6 into HEK cells increase extracellular [ATP] in vitro. ATP is metabolized into PPi by the extracellular enzyme ENPP1, and the combined findings support the notion that ABCC6 mutations decrease extracellular [ATP] thereby limiting ENPP1 production of PPi by limiting the enzymatic substrate of the enzyme. Here, we demonstrate that subcutaneous administration of ENPP1-Fc, a fusion protein containing the enzyme ENPP1, normalizes serum PPi concentrations in ABCC6 knockout mice. Furthermore, we show that normalization of serum PPi by this means potently inhibits the regional connective tissue calcifications present in ABCC6 knockout mice. Our findings provide in vivo experimental evidence for the metabolic basis of PXE. Furthermore, because ENPP1 is downstream of ABCC6, the efficacy of ENPP1-Fc is surprising and indicates that reduced extracellular [ATP] may not be the etiology for the decreased plasma PPi concentrations reported in PXE patients as previously proposed. Finally, the efficacy of ENPP1-Fc on the connective tissue calcifications in PXE suggests that elevation of plasma PPi by this means may be efficacious in spectrum of severe and poorly treated connective tissue calcification disorders associated with low plasma PPi. Disclosures Braddock: Yale University: Patents & Royalties: Yale University owns a patent on the technology, in which Demetrios Braddock is listed as an inventor.

scholarly journals The Symmetric 3D Organization of Connective Tissue around Implant Abutment: A Key-Issue to Prevent Bone Resorption

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1126
Author(s):  
Giovanna Iezzi ◽  
Francesca Di Lillo ◽  
Michele Furlani ◽  
Marco Degidi ◽  
Adriano Piattelli ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Connective Tissue ◽  
Inflammatory Cell ◽  
Soft Tissues ◽  
Three Dimensional ◽  
Collagen Fibers ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Oral Epithelium ◽  
Implant Abutment

Symmetric and well-organized connective tissues around the longitudinal implant axis were hypothesized to decrease early bone resorption by reducing inflammatory cell infiltration. Previous studies that referred to the connective tissue around implant and abutments were based on two-dimensional investigations; however, only advanced three-dimensional characterizations could evidence the organization of connective tissue microarchitecture in the attempt of finding new strategies to reduce inflammatory cell infiltration. We retrieved three implants with a cone morse implant–abutment connection from patients; they were investigated by high-resolution X-ray phase-contrast microtomography, cross-linking the obtained information with histologic results. We observed transverse and longitudinal orientated collagen bundles intertwining with each other. In the longitudinal planes, it was observed that the closer the fiber bundles were to the implant, the more symmetric and regular their course was. The transverse bundles of collagen fibers were observed as semicircular, intersecting in the lamina propria of the mucosa and ending in the oral epithelium. No collagen fibers were found radial to the implant surface. This intertwining three-dimensional pattern seems to favor the stabilization of the soft tissues around the implants, preventing inflammatory cell apical migration and, consequently, preventing bone resorption and implant failure. This fact, according to the authors’ best knowledge, has never been reported in the literature and might be due to the physical forces acting on fibroblasts and on the collagen produced by the fibroblasts themselves, in areas close to the implant and to the symmetric geometry of the implant itself.

Effects of in vitro low oxygen tension preconditioning of buccal fat pad stem cells on in Vivo articular cartilage tissue repair

Life Sciences ◽  
2021 ◽  
pp. 119728
Author(s):  
Fatemeh Dehghani Nazhvani ◽  
Leila Mohammadi Amirabad ◽  
Arezo Azari ◽  
Hamid Namazi ◽  
Simzar Hosseinzadeh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Articular Cartilage ◽  
Tissue Repair ◽  
Cartilage Tissue ◽  
Low Oxygen ◽  
Fat Pad ◽  
Buccal Fat Pad ◽  
Low Oxygen Tension

scholarly journals Cell Source-Dependent In Vitro Chondrogenic Differentiation Potential of Mesenchymal Stem Cell Established from Bone Marrow and Synovial Fluid of Camelus dromedarius

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1918
Author(s):  
Young-Bum Son ◽  
Yeon Ik Jeong ◽  
Yeon Woo Jeong ◽  
Mohammad Shamim Hossein ◽  
Per Olof Olsson ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Synovial Fluid ◽  
Cartilage Regeneration ◽  
Cartilage Tissue ◽  
Chondrocyte Differentiation ◽  
Differentiation Potential ◽  
Proliferation Capacity

Mesenchymal stem cells (MSCs) are promising multipotent cells with applications for cartilage tissue regeneration in stem cell-based therapies. In cartilage regeneration, both bone marrow (BM-MSCs) and synovial fluid (SF-MSCs) are valuable sources. However, the cellular characteristics and chondrocyte differentiation potential were not reported in either of the camel stem cells. The in vitro chondrocyte differentiation competence of MSCs, from (BM and SF) sources of the same Camelus dromedaries (camel) donor, was determined. Both MSCs were evaluated on pluripotent markers and proliferation capacity. After passage three, both MSCs showed fibroblast-like morphology. The proliferation capacity was significantly increased in SF-MSCs compared to BM-MSCs. Furthermore, SF-MSCs showed an enhanced expression of transcription factors than BM-MSCs. SF-MSCs exhibited lower differentiation potential toward adipocytes than BM-MSCs. However, the osteoblast differentiation potential was similar in MSCs from both sources. Chondrogenic pellets obtained from SF-MSCs revealed higher levels of chondrocyte-specific markers than those from BM-MSCs. Additionally, glycosaminoglycan (GAG) content was elevated in SF-MSCs related to BM-MSCs. This is, to our knowledge, the first study to establish BM-MSCs and SF-MSCs from the same donor and to demonstrate in vitro differentiation potential into chondrocytes in camels.

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