elastin and Rupture

The study aimed to investigate the polymorphism of fibrillin-2 (FBN2) and elastin genes in patients with Achilles tendon rupture and to compare the results with a control group of participants who did not experience such an injury.. In this prospective study, 106 consecutive patients in whom traumatic Achilles tendon rupture was diagnosed and treated were included. The control group consisted of randomly selected 92 athletes (10 women and 82 men) 85 of whom had practiced sports in the past, aged 40-76 years, who during their sports career did not experience Achilles tendon ruptures. Material for genetic tests was obtained by the swab from the oral cavity epithelium of all the study population.. 102 (96%) of patients with traumatic Achilles tendon ruptures were people with polymorphism B or heterozygotes for the elastin gene. 97 (92%) of patients with traumatic Achilles tendon ruptures were people with polymorphism B and heterozygotes for the FBN2 gene. Patients with homozygote A of the elastin gene and homozygote A of the FBN2 gene demonstrated a considerably lower incidence rate of sport-related Achilles tendon rupture. The type of sport that led to the Achilles tendon rupture and the amount of experience practicing it, as well as BMI and drug usage, did not contribute to a higher rate of incidence of any additional musculoskeletal problems or a longer time to return to their pre-injury sports activity. Polymorphisms of the fibrillin 2 (P=.0001) and elastin (P=.0009) genes impact the occurrence of traumatic injury to the Achilles tendon. However, it does not affect the length of full recovery time (P =.2251).. Minimally invasive and, above all, safe collection of genetic material from the epithelium of the oral cavity in order to assess the polymorphic state of the FBN and elastin genes may allow the identification of a group of players at risk of Achilles tendon rupture resulting in long-term injury, which will significantly affect their sports career in the future.. Level II, Prognostic Study.

Topics: Achilles Tendon; Elastin; Female; Fibrillin-2; Humans; Male; Polymorphism, Genetic; Prospective Studies; Rupture; Tendon Injuries

Elastic fibers containing elastin play an important role in tendon functionality, but the knowledge on presence and function of elastin during tendon healing is limited. The aim of this study was to investigate elastin content and distribution in intact and healing Achilles tendons and to understand how elastin influence the viscoelastic properties of tendons. The right Achilles tendon was completely transected in 81 Sprague-Dawley rats. Elastin content was quantified in intact and healing tendons (7, 14, and 28 days post-surgery) and elastin distribution was visualized by immunohistochemistry at 14 days post-surgery. Degradation of elastin by elastase incubation was used to study the role of elastin on viscoelastic properties. Mechanical testing was either performed as a cyclic test (20× 10 N) or as a creep test. We found significantly higher levels of elastin in healing tendons at all time-points compared to intact tendons (4% in healing tendons 28 days post-surgery vs 2% in intact tendons). The elastin was more widely distributed throughout the extracellular matrix in the healing tendons in contrast to the intact tendon where the distribution was not so pronounced. Elastase incubation reduced the elastin levels by approximately 30% and led to a 40%-50% reduction in creep. This reduction was seen in both intact and healing tendons. Our results show that healing tendons contain more elastin and is more compliable than intact tendons. The role of elastin in tendon healing and tissue compliance indicates a protective role of elastic fibers to prevent re-injuries during early tendon healing. PLAIN LANGUAGE SUMMARY: Tendons transfer high loads from muscles to bones during locomotion. They are primarily made by the protein collagen, a protein that provide strength to the tissues. Besides collagen, tendons also contain other building blocks such as, for example, elastic fibers. Elastic fibers contain elastin and elastin is important for the extensibility of the tendon. When a tendon is injured and ruptured the tissue heals through scar formation. This scar tissue is different from a normal intact tendon and it is important to understand how the tendons heal. Little is known about the presence and function of elastin during healing of tendon injuries. We have shown, in animal experiments, that healing tendons have higher amounts of elastin compared to intact tendons. The elastin is also spread throughout the tissue. When we reduced the levels of this protein, w

Topics: Achilles Tendon; Animals; Biomechanical Phenomena; Elastin; Female; Rats; Rats, Sprague-Dawley; Rupture; Tendon Injuries; Wound Healing

The proteins ELN and FBN2 are important in extracellular matrix function. The ELN rs2071307 and FBN2 rs331079 gene variants have been associated with soft tissue pathologies. We aimed to determine whether these variants were predisposing factors for both Achilles tendinopathy (AT) and anterior cruciate ligament (ACL) ruptures. For the AT study, 135 cases (TEN group) and 239 asymptomatic controls were recruited. For the ACL rupture study our cohort consisted of 141 cases (ACL group) and 219 controls. Samples were genotyped for both the ELN rs2071307 and FBN2 rs331079 variants using TaqMan assays. Analysis of variance and chi-squared tests were used to determine whether either variant was associated with AT or ACL rupture with significance set at p<0.05. The GG genotype of the FBN2 variant was significantly over-represented within the TEN group (p=0.035; OR=1.83; 95% CI 1.04-3.25) compared to the CON group. We also found that the frequency of the G allele was significantly different between the TEN (p=0.017; OR=1.90; 95% CI 1.11-3.27) and ACL groups (p=0.047; OR=1.76; 95% CI 1.00-3.10) compared to controls. The ELN rs207137 variant was not associated with either AT or ACL rupture. In conclusion, DNA sequence variation within the FBN2 gene is associated with both AT and ACL rupture.

Topics: Achilles Tendon; Adult; Anterior Cruciate Ligament Injuries; Case-Control Studies; Elastin; Female; Fibrillin-2; Fibrillins; Genotype; Humans; Male; Microfilament Proteins; Middle Aged; Risk Factors; Rupture

Plaque with dense inflammatory cells, including macrophages, thin fibrous cap and superficial necrotic/lipid core is thought to be prone-to-rupture. We report a time-resolved laser-induced fluorescence spectroscopy (TR-LIFS) technique for detection of such markers of plaque vulnerability in human plaques.. The autofluorescence of carotid plaques (65 endarterectomy patients) induced by a pulsed laser (337 nm, 0.7 ns) was measured from 831 distinct areas. The emission was resolved spectrally (360-550 nm range) and temporally (0.3 ns resolution) using a prototype fiber-optic TR-LIFS apparatus. Lesions were evaluated microscopically and quantified as to the % of different components (fibrous cap, necrotic core, inflammatory cells, foam cells, mature and degraded collagen, elastic fibers, calcification, and smooth muscle cell of the vessel wall).. We determined that the spectral intensities and time-dependent parameters at discrete emission wavelengths (1) allow for discrimination (sensitivity >81%, specificity >94%) of various compositional and pathological features associated with plaque vulnerability including infiltration of macrophages into intima and necrotic/lipid core under a thin fibrous cap, and (2) show a linear correlation with plaque biochemical content: elastin (P<0.008), collagen (P<0.02), inflammatory cells (P<0.003), necrosis (P<0.004).. Our results demonstrate the feasibility of TR-LIFS as a method for the identification of markers of plaque vulnerability. Current findings enable future development of TR-LIFS-based clinical devices for rapid investigation of atherosclerotic plaques and detection of those at high-risk.

Topics: Calcinosis; Carotid Artery Diseases; Carotid Artery, Common; Collagen; Elastin; Endarterectomy, Carotid; Feasibility Studies; Fiber Optic Technology; Fibrosis; Foam Cells; Humans; Lasers; Lipids; Necrosis; Predictive Value of Tests; Reproducibility of Results; Rupture; Sensitivity and Specificity; Spectrometry, Fluorescence; Time Factors

Rupture of the chordae tendineae cordis (CTC) is a well-known cause of mitral regurgitation. Despite its importance, the mechanisms by which the CTC is protected and the cause of its rupture remain unknown. CTC is an avascular tissue. We investigated the molecular mechanisms underlying the avascularity of CTC and the correlation between avascularity and CTC rupture.. We found that tenomodulin, which is a recently isolated antiangiogenic factor, was expressed abundantly in the elastin-rich subendothelial outer layer of normal rodent, porcine, canine, and human CTC. Conditioned medium from cultured CTC interstitial cells strongly inhibited tube formation and mobilization of endothelial cells; these effects were partially inhibited by small-interfering RNA against tenomodulin. The immunohistochemical analysis was performed on 12 normal and 16 ruptured CTC obtained from the autopsy or surgical specimen. Interestingly, tenomodulin was locally absent in the ruptured areas of CTC, where abnormal vessel formation, strong expression of vascular endothelial growth factor-A and matrix metalloproteinases, and infiltration of inflammatory cells were observed, but not in the normal or nonruptured area. In anesthetized open-chest dogs, the tenomodulin layer of tricuspid CTC was surgically filed, and immunohistological analysis was performed after several months. This intervention gradually caused angiogenesis and expression of vascular endothelial growth factor-A and matrix metalloproteinases in the core collagen layer in a time-dependent manner.. These findings provide evidence that tenomodulin is expressed universally in normal CTC in a concentric pattern and that local absence of tenomodulin, angiogenesis, and matrix metalloproteinase activation are associated with CTC rupture.

Topics: Aged; Aged, 80 and over; Animals; Cells, Cultured; Chordae Tendineae; Dogs; Elastin; Endothelium, Vascular; Enzyme Activation; Female; Heart Valve Diseases; Humans; Male; Matrix Metalloproteinases; Membrane Proteins; Mice; Mice, Inbred ICR; Middle Aged; Neovascularization, Pathologic; Rabbits; Rupture; Swine

Extracellular matrix (ECM) molecules such as elastin and collagen provide mechanical support to the vessel wall and are essential for vascular function. Evidence that genetic factors influence aortic ECM composition and organization was concluded from our previous studies showing that the inbred Brown Norway (BN) rat differs significantly from the outbred Long-Evans (LE) and the inbred LOU rat with respect to both thoracic aortic elastin content and internal elastic lamina (IEL) rupture in the abdominal aorta and iliac arteries. Here, we measured aortic elastin and collagen contents as well as factors that may modulate these parameters [insulin growth factor (IGF)-I, transforming growth factor (TGF)-beta(1), and matrix metalloproteinase (MMP)-2] in seven inbred rat strains, including BN and LOU. We also investigated whether IEL ruptures occur in strains other than BN. We showed that LOU, LE, BN, and Fischer 344 (F344) rats were significantly different for aortic elastin content and elastin-to-collagen ratio, whereas LE, Lewis, WAG, and Wistar-Furth (WF) were similar for these parameters. BN and F344 had the lowest values. BN was the only strain to present numerous IEL ruptures, whereas F344, LE, and WF presented a few and the other strains presented none. In addition, IGF-I and TGF-beta(1) levels in the plasma and aorta differed significantly between strains, suggesting genetic control of their production. Because inbred rat strains provide interesting models for quantitative trait locus analysis, our results concerning elastin, collagen, IEL ruptures, and cytokines may provide a basis for the search for candidate genes involved in the control of these phenotypes.

Topics: Animals; Aorta, Abdominal; Aorta, Thoracic; Blood Pressure; Collagen; Elasticity; Elastin; Heart Rate; Iliac Artery; Insulin-Like Growth Factor I; Male; Matrix Metalloproteinase 2; Organ Size; Phenotype; Rats; Rats, Inbred BN; Rats, Inbred F344; Rats, Inbred Lew; Rats, Inbred WF; Rats, Long-Evans; Rupture; Species Specificity; Transforming Growth Factor beta; Transforming Growth Factor beta1

The theory that "viable" valve grafts have superior durability because the donor cell population of the leaflets survives implantation and functions normally, thus maintaining leaflet integrity, is still not definitively proven. The postulate has been investigated for grafts produced and used at Green Lane Hospital by examining a series of 155 removed at reoperation following up to 21.3 years of implantation.. Leaflet cellularity at explantation was assessed histologically. An additional 55 cases were also assessed by tissue culture. Cell origin for six positive cultures was determined by comparison of DNA of the culture with that of the recipient's blood cells.. Grafts known to be nonviable at implantation lacked leaflet fibroblasts but sometimes showed ongrowth of fibrous tissue derived from the recipient's aorta. Grafts potentially viable at implantation showed three main patterns of fibroblastic growth: (1) relatively sparse, scattered cells; (2) focal hyperplastic growth with intervening acellular tissue that was prone to rupture; and (3) widely disseminated, vigorous growth causing abnormal thickening. The first pattern was associated with recipient cells, and both the second and third patterns were associated with nonrecipient cells.. Donor cells surviving implantation do not maintain a normal leaflet architecture and may lead to failure by producing loss of leaflet flexibility.

Topics: Anti-Bacterial Agents; Aortic Valve; Cell Division; Cell Lineage; Cell Survival; Collagen; Cryopreservation; Culture Techniques; DNA; Drug Therapy, Combination; Elastin; Fibroblasts; Follow-Up Studies; Graft Survival; Humans; Hyperplasia; Middle Aged; Pliability; Proteoglycans; Reoperation; Rupture; Sterilization; Tissue Survival; Transplantation Chimera; Transplantation, Homologous

A light and electron microscopy investigation was performed on a Leeds-Keio ligament removed because of rupture 18 months after implantation to repair an anterior cruciate ligament. The investigation showed fibrous connective tissue on the plane of the main stress force. There was elastin and adequate vascularization interspersed with Type I collagen fibrils in the area most distant from the ligament. The tissue near the Dacron fibers was highly cellular with a matrix of infrequent, thin collagen fibrils and abundant fine granular material. The growth of the host tissue occurred in and around a Leeds-Keio ligament in response to tensile stresses.

Topics: Adult; Anterior Cruciate Ligament; Collagen; Connective Tissue; Elastin; Extracellular Matrix; Female; Humans; Polyethylene Terephthalates; Prostheses and Implants; Prosthesis Failure; Running; Rupture

The tunica media and intima of descending thoracic aortas from commercially killed pigs showed variations in mechanical properties along their length in a region extending from just in front of the first intercostal artery to the sixth intercostal artery. Along this region circumferential toughness, measured as work of fracture from a tear test, increased, longitudinal and circumferential ultimate tensile strength increased and longitudinal and circumferential stress-strain gradients of excised strips increased further away from the heart. These increasing mechanical properties are positively correlated with an increase in collagen mass fraction and an increase of radius/thickness ratio away from the heart over this region.

Topics: Animals; Aorta, Thoracic; Collagen; Elastin; In Vitro Techniques; Rupture; Stress, Mechanical; Swine; Tensile Strength

Topics: Animals; Aorta; Aorta, Abdominal; Aorta, Thoracic; Biomechanical Phenomena; Collagen; Dogs; Elastin; Rupture; Stress, Mechanical

Topics: Aneurysm; Animals; Aorta, Thoracic; Arteries; Arteriosclerosis; Cardiovascular Diseases; Collagen; Copper; Deficiency Diseases; Elastin; Pedigree; Rupture; Swine; Vascular Diseases