Assessing the safety of an epiphyseal plate biopsy in a translational lamb model

Author(s):  
Richard T. Epperson ◽  
Dustin L. Williams ◽  
Brady Rogers ◽  
John Maxwell ◽  
Peter Stevens
Keyword(s):  
1972 ◽  
Vol 69 (4) ◽  
pp. 659-688 ◽  
Author(s):  
V. Stanescu ◽  
R. Stanescu ◽  
J. A. Szirmai

ABSTRACT Microchemical determinations of glycosaminoglycans and collagen were preformed in isolated histological zones from sections of tibial epiphyseal plate biopsies obtained from children with growth disorders (pituitary dwarfism, congenital myxoedema, Turner's syndrome, Noonan's syndrome, mucopolysaccharidosis type VI, vitamin D resistant rickets and achondroplasia). Alternate sections were used for histochemical localization of glycosaminoglycans and proteins. The values were compared with those found in comparable zones of the growth plate from normal children of the same age. The chondroitin sulphate concentration (% of defatted dry wt.) in the normal epiphyseal plate increased from the resting zone towards the proliferating/hypertrophic zone; collagen exhibited a reverse trend. In some of the pathological biopsies the concentration of chondroitin sulphate was slightly decreased whereas that of collagen was slightly increased. A marked increase in the collagen concentration was found in achondroplasia. The solubility profiles of the cetylpyridinium complexes of the chondroitin sulphate fraction showed three main peaks with slight but characteristic differences in the various zones of the normal cartilage plate. Significant shifts in the proportion of these peaks were observed in several pathological biopsies, indicating possible deviations from the normal molecular characteristics of the chondroitin sulphate. Analysis of the main chondroitin sulphate fraction, obtained from pooled samples of normal tibial growth plate after fractionation on the macroscale, indicated that all three peaks contained both chondroitin-4 sulphate and chondroitin-6 sulphate and that they probably differed in their molecular weight.


1983 ◽  
Vol 11 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Peter C. Amadio ◽  
Michael G. Ehrlich ◽  
Henry J. Mankin

2008 ◽  
Vol 17 (1) ◽  
pp. 76-83
Author(s):  
Thomas G. Bowman ◽  
Riann Palmieri-Smith

Objective:To present the case of an 18-year-old collegiate decathlete with a Salter-Harris type I epiphyseal plate fracture of the proximal humerus.Background:A collegiate decathlete was playing flag football and fell on an outstretched arm. He was taken to the emergency room and diagnosed with a type I epiphyseal plate fracture.Differential Diagnosis:AC sprain, dislocation or subluxation, rotator cuff tear, labral tear.Treatment:Active and passive range of motion exercises were completed after two days of immobilization. He then started strengthening exercises and returned to competitive activity in 10 weeks.Uniqueness:Proximal humeral epiphyseal plate fractures are uncommon injuries, especially in athletes over the age of 15.Conclusions:If an accurate diagnosis is made, an appropriate conservative rehabilitation program can be implemented to safely return an athlete to participation without permanent deformity following a type I Salter-Harris fracture.


1997 ◽  
Vol 108 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Ying Wang ◽  
Renée Toury ◽  
Michelle Hauchecorne ◽  
N. Balmain

HAND ◽  
1980 ◽  
Vol os-12 (1) ◽  
pp. 51-53 ◽  
Author(s):  
E. Michelinakis ◽  
H. Vourexaki

A case of mallet finger in a child is described. The epiphysis of the terminal phalanx was displaced dorsally with the extensor tendon attached to it, and was first diagnosed two weeks after injury. The treatment was by open reduction. Radiograph three years later showed that a satisfactory position of the epiphysis and normal growth of the terminal phalanx had occurred.


1988 ◽  
Vol 36 (3) ◽  
pp. 987-991
Author(s):  
Shinichi Mishima ◽  
Katsumi Suzuki ◽  
Nario Ihara ◽  
Hiroshi Ojima ◽  
Kenzo Ito

1992 ◽  
Vol 127 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Mimi H Chiang ◽  
Charles S Nicoll

Previous work in our laboratory has shown that the internal environment of rats has reduced growth-promoting activity during the second half of gestation and this condition is associated with resistance to the anabolic effects of GH. The placenta appears to be responsible for this condition but injections of estradiol plus progesterone into virgin females did not mimic it. Accordingly, it seemed worthwhile to test the effects of a placental lactogen (PL) for possible growth inhibitory effects. In the present study the effects of human (h)PL on skeletal growth in young female rats and on the growth of embryonic tissue transplants under their kidney capsules were investigated. Human (h) and bovine (b) GH, and ovine prolactin (oPRL) were also tested to determine whether the results obtained with hPL were specific. Twice daily subcutaneous injections of a high dose of hPL (10mg/day), but not of oPRL (5 mg/day) for 7 days inhibited both host tail growth and tibial epiphyseal plate width, and growth of whole 10-day embryo transplants. Injections of hGH at 1 mg/day for 8 days significantly increased host skeletal growth and growth of 12-day embryonic head transplants; at the same dose, neither bGH nor oPRL affected growth of the embryonic heads or of the host tibial epiphyseal plate width, but the bGH increased host tail growth. By contrast, the 1 mg/day dose of hPL significantly reduced the host's tibial epiphyseal plate width, tail growth, and transplant growth; lower doses of hPL (10 and 100 μg/day) were also inhibitory. Although all the hormone treatments increased total serum IGF-1 levels in the females, none of them had a significant effect when compared to saline injected control animals. Thus, the growth-inhibitory effects of hPL treatment appear to be specific to that hormone and they are not mediated by depression of serum IGF-1 levels. If these effects of hPL are mimicked by one or more of the rodent PLs, then the reduced growth-promoting activity and resistance to GH action that occurs in pregnant rats could be due to the rat PLs. These results indicate that in addition to having glucose-sparing effects in the mother, PLs could promote fetal growth by inhibiting growth of maternal tissues, which would thus spare other metabolites, such as amino acids and vitamins, for the conceptus.


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