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Biomedical subjects

E Livne

Publications and source records attributed to E Livne.

63 records · Page 4Linked to original sources
PubMed1983

Changes in the structure and chemical composition of the mandibular condylar cartilage of the neonatal mouse.

The cartilage of the mandibular condyle of growing mice was used to monitor changes in the content of protein, DNA, hydroxyproline, hydroxylysine, uronic acid, calcium and phosphate. Protein and DNA increased in a stepwise fashion with one spurt seen during the first 2 weeks of post-natal life a second immediately after weaning. Hydroxyproline increased during the entire growth period, i.e. until the 8th post-natal week. Hydroxylysine increased only until week 4. The content of the uronic acid fluctuated and showed highs and lows throughout the growth period. Both calcium and phosphate increased in an almost parallel fashion from birth until the stage of tissue maturation. Morphological studies indicated that the hyaline type of cartilage in the newborn is gradually replaced by a fibrous tissue, which reveals a markedly different structure and composition.

Animals↗
PubMed1983

Glucocorticoid hormone adversely affects the growth and differentiation of cartilage cells in neonatal mice.

Condylar cartilage of neonatal mice served as an experimental model to study the late in vivo effects of a single dose of a fluorinated synthetic analogue of cortisol on cartilage cell growth and development. Forty-eight hours after the administration of triamcinolone hexacetonide, the proliferative rate of chondroprogenitor cells decreased significantly. However, by the 6th day a marked recovery took place when the total number of 3H-thymidine labelled cells increased by 52.9%, and by 13 days hormone-treated condyles revealed an increase of 93.1% in the total number of labelled cells. At the same time, the magnitude of the chondroprogenitor zone increased by 194.4% and it was found to contain a large population of fibroblast-like cells. The latter were found to synthesize type I collagen and fibronectin, lacked any specific organization and occupied larger portions of the condylar head. Twenty days following the administration of the hormone the newly-formed mass of fibroblast-like cells penetrated the underlying cartilage, split it and formed a direct communication with the marrow cavity. Ultrastructural examination further substantiated the fibroblastic nature of the newly-formed cell population. Hence, it seems very possible that if a corticosteroid hormone is administered to newborn animals it possesses the capacity to affect the normal differentiative pathway of pre-chondroblasts and shift their developmental pathway toward the fibroblastic cell line.

Animals↗
PubMed1979

Skeletal changes in the condylar cartilage of the neonate mouse mandible.

Histological and histochemical qualitative and quantitative determinations are provided concerning the skeletal changes taking place in the growth center of the mandibular condyle in the neonatal ICR mouse. This study followed the changes in both the major matrical components (collagen, acidic glycosaminoglycans and glycolipids) as well as in the various cartilage cells throughout the maturational period of the neonatal condyle. It was found that the transformation of neonatal condylar cartilage to its mature form involved a significant decrease in its acid glycosaminoglycan content concomitant with a rapid increase in its collagen content. In addition, significant quantitative changes were found within the zone of hypertrophic chondrocytes. The period of highest growth activity along the mandibular posterior vertical dimension (ramus) was between birth and weanling 3rd postnatal week). At this time interval, the adaptive abilities of the growing condyle appeared maximal. A high degree of correlation was noted between the overall reduction in the height of the condylar cartilage and that of its hypertrophic zone. Further, the increase in the ramal height was highly correlated with the structural changes characteristic of the neonatal condyle.

Age Factors↗
PubMed1979

Age-related degenerative changes in the mouse mandibular joint.

The mandibular joints of ageing male ICR mice were studied by light and electron microscopy. A high incidence of degenerative joint disease was found relatively early in adult life, osteoarthrosis being evident by the seventh month. Initially the pathological changes were those of chondromalacia confined to isolated foci on the articular surface of the condylar cartilage. Later, characteristic signs of osteoarthrosis were noted, namely fibrillation, fibrous ankylosis, lipping and subchondral osteosclerosis. Ultrastructural examination indicated a marked heterogeneity in the articular lesions. Deep fissures and extensive cracks spread to the underlying matrix, and these were associated with severe alterations in its macromolecular structure. It is proposed that ageing chondrocytes produce a matrix which is increasingly incapable of withstanding normal mechanical forces, and this leads to the morphological changes recognized first as chondromalacia and then as osteoarthrosis.

Aging↗
PubMed1976

Retardation of bone growth in triamcinolone-treated mice.

Immature mice were treated for up to 8 weeks with daily doses of triamcinolone diacetate. The epiphyseal cartilage plate and its surrounding bone from the humeral head were studied histologically at regular intervals. Concomitantly, roentgenographic measurements were performed on the humeri in toto. By the tenth injection significant morphological changes were noted in the cartilaginous plate, followed by complete cessation of bone growth. Severe triglyceride accumulation appeared in the experimental livers and humeral bone marrow. Osteoporosis also occurred and became severe from the fifth week of triamcinolone administration. Possible explanations for the above findings are discussed.

Animals↗
PubMedDate not supplied

Metalloproteinases (MMPs -2, -3) are involved in TGF-beta and IGF-1-induced bone defect healing in 20-month-old female rats.

Matrix metalloproteinases are important in the physiological and pathological degradation of extracellular matrix including that of bone and cartilage. The process of bone defect healing is associated with formation of cartilage callus and cancelous bone. With maturation and aging, the response of skeletal tissues to injury is limited. The ability of growth factors to enhance bone defect healing in aged rats was studied. Partial bone defects were induced in femurs of aged rats. A single dose of IGF-1, TGF-beta+IGF-1 or saline was inserted in the defect and bones were examined after 2 and 4 weeks. Morphology revealed that after 2 weeks of treatment with TGF-beta the defects were filled with mesenchyme-like tissue and delicate bone trabeculae. Positive staining for metalloproteinase-2 (MMP-2) was shown at the sites of new bone formation. In defects treated with IGF-1 or TGF-beta+IGF-1 nodules of cartilage and fine bone trabeculae along with positive staining for both MMP-2 and MMP-3 were demonstrated in the healing defects. After 4 weeks radiology revealed mineralization in defects treated with TGF-beta and less pronounced mineralization after treatment with IGF-1, or with TGF-beta+IGF-1, whereas only partial healing of the defects was observed in control specimens. MMP-2 and MMP-3 were detected at sites of new bone formation after treatment with TGF-beta, IGF-1, and TGF-beta+IGF-1. It is concluded that TGF-beta and IGF-1 induced bone defect healing in aged rats. TGF-beta induced bone formation while IGF-1 induced cartilage and than bone formation via endochondral ossification. The localization of MMP-2 and MMP-3 in the healing defects reflected the synthesis of bone or cartilage matrices in the defect, reflecting the involvement of MMPs in the process of bone formation and endochondral ossification. The ability to induce bone defect healing in aging is of great clinical importance and understanding the involvement of MMPs in this process can contribute to future treatment with growth factors to enhance bone defect healing in 20-month-old female rats.

Journal Article↗
PubMedDate not supplied

Characterization of alkaline and acid phosphatases from skeletal muscles of young and old rats.

Alkaline phosphatase (ALP) and acid phosphatase (ACP) specific activities were measured in gastrocnemius muscles of female Wistar rats ranging in age from 2 to 30 months. ALP activity reached a peak at 12 months, with a subsequent slow decline with age. ACP activity increased sharply up to 12 months of age, followed by a slower elevation up to the age of 30 months. Using histochemical staining techniques and electron microscopy, the presence of ALP was demonstrated in the sarcolemma of gastrocnemius muscles, as well as in some capillaries around muscle fibers. ALP and ACP were isolated further from muscles of young (12 months) and old (30 months) animals by applying ion-exchange chromatography and separation on a Sephadex G-200 column. The purity of ALP was shown on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). From a calibrated Sephadex G-200 column and SDS-PAGE, the molecular mass of ALP was determined as 116 kilodaltons (kDa), a dimer of two 56-kDa monomers. The ACP major peak of the Sephadex G-200 column revealed a molecular mass of 40 kDa. No differences in molecular mass or in amino acid analysis were detected between ALP(s) from young and old animals, indicating that most probably the decline of activity with age is due to some post-translational events, as has been shown in the past for many other enzymes and proteins.

Journal Article↗
PubMedDate not supplied

Differential response of articular cartilage from young growing and mature old mice to IL-1 and TGF-beta.

Osteoarthritic lesions are observed in temporomandibular joint cartilage of ICR mice aged 7 months and older, accompanied by reduced proliferation and matrix synthesis. Transforming growth factor-beta (TGF-beta), is a multifactorial growth factor affecting matrix synthesis and cell proliferation in bone and cartilage, whereas interleukin-1 (IL-1) is involved in cartilage degradation. In order to establish the repair capacity of cartilage in aging, the response of cartilage from young and old animals to TGF-beta and IL-1 was studied. Mandibular condyles from young (1-month-old) and old (18-month-old) mice were cultured for up to 72 h in medium supplemented with TGF-beta1 or IL-1alpha. TGF-beta increased protein (+9.26%) and DNA (+36.0%) contents in young animals and DNA content (+19.49%) in old animals. Incorporations of [(3)H]thymidine and [(35)S]sulfate were enhanced in young (+254% and +116%, respectively) and in old (+22.6% and +6.88%, respectively) and animals and activity of alkaline phosphatase was induced in old animals. Treatment with IL-1 resulted in reduced DNA content in young (-35.76%) and old (-33.33%) animals, but acid phosphatase activity was induced in old animals. It is concluded that TGF-beta can induce anabolic activity even in cartilage from old animals indicating repair response in articular cartilage in aging.

Journal Article↗