Development of Flattening and Apparent Fragmentation Following Ischemic Necrosis of the Capital Femoral Epiphysis in a Piglet Model

Joshi, Atul; Marković, Ljubiša; Hardinge, K.; Murphy, Jimmy

doi:10.2106/00004623-200208000-00007

Cited by 137 publications

(115 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although we have previously observed histological evidence of revascularization and repair as early as 2 weeks following the induction of ischemia in the piglet model [9], none of the infarcted femoral heads in this study showed evidence of revascularization or repair at 2 weeks. The absence of repair process suggests that the decline in the indentation stiffness is related to the ischemic injury, growth arrest of bony epiphysis, and epiphyseal cartilage thickening.…”

Section: Discussioncontrasting

confidence: 79%

Indentation properties of growing femoral head following ischemic necrosis

Pringle

Koob

Kim

2004

Journal Orthopaedic Research

View full text Add to dashboard Cite

Little is known about the mechanical properties of the growing femoral head as it develops deformity following ischemic injury. The purpose of this study was to determine the indentation stiffness of growing femoral head following ischemic injury and to correlate the changes in stiffness with radiographic and histopathologic changes in the femoral head as it develops deformity. Following the induction of ischemia in 24 piglets, indentation testing of whole femoral heads was performed at 2, 4, and 8 weeks, as well as on femoral heads from eight sham operated animals. At 2 weeks, a 52%) reduction of indentation stiffness was observed in the infarcted femoral heads compared to the control heads (p = 0.004). The bony epiphyses in infarcted femoral heads were smaller due to growth arrest but they were not deformed. Histologically, no evidence of repair was seen. At 4 and 8 weeks, the indentation stiffness in the infarcted femoral heads was reduced by 75% (p < 0.000001) and 72% (p = 0.001) respectively compared to the control heads. Variable degree of femoral head deformity and repair was observed at 4 weeks. Severe deformity with extensive revascularization and repair were observed at 8 weeks. Although epiphyseal cartilage was thickened on the infarcted femoral heads only a weak correlation was found between the increase in the cartilage thickness and the decrease in the indentation stiffness (R2 = 0.55). These results indicate that the indentation properties of growing femoral head were significantly affected by ischemic injury, prior to the presence of repair process and deformity. A further decrease in the indentation stiffness was concomitant with repair of the infarcted head. These findings suggest that a reduction in the mechanical properties of the infarcted femoral head include both a cartilage and a bony component, which cannot be differentiated at this point. The study validates early institution of treatments that are aimed at limiting the mechanical loading of the affected hip. The study also suggests that in order to minimize the mechanical compromise of the infxcted femoral head, early institution of treatments aimed at stimulating new bone formation and retarding osteoclastic bone resorption may be beneficial.

show abstract

Section: Discussioncontrasting

confidence: 79%

Indentation properties of growing femoral head following ischemic necrosis

Pringle

Koob

Kim

2004

Journal Orthopaedic Research

View full text Add to dashboard Cite

show abstract

“…With continued walking, there can be flattening of the articular surface. In a piglet model, Kim and Su (2002) observed mild femoral head flattening at 4 weeks after the induction of ischemia, and severe flattening at 8 weeks, but they did not describe changes after 8 weeks and until the full growth of the piglet. We found earlier development of coxa plana: both decrease in epiphyseal height and flattening of the articular surface in 1 of the 6 P2 piglets (i.e.…”

Section: Discussionmentioning

confidence: 87%

“…The interruption of the vascular supply to the capital femoral epiphysis was accomplished by cutting the ligamentum teres and ligating the femoral neck (containing the epiphyseal artery) with a no. 2 Ethibond suture (Babyn et al 1998, Kim andSu 2002).…”

Section: Animals and Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Deformity of the femoral head following vascular infarct in piglets

et al. 2006

View full text Add to dashboard Cite

Background In Legg-Calvé-Perthes disease (LCPD), 4 major patterns (coxa plana, coxa magna, coxa vara, subluxation) of the femoral head are commonly observed. However, direct observation of pathological specimens is rarely possible. An animal model of LCPD may clarify the pathogenesis of femoral head deformity.Animals and methods In 26 piglets, we interrupted the vascular supply to the capital femoral epiphysis by cutting the ligamentum teres and ligating the femoral neck containing the epiphyseal artery. 6-7 piglets in each experimental group were killed at early (2 and 4 weeks: P2 and P4), intermediate (12 weeks: P12), and late (20 weeks: P20) periods. We examined the extracted femoral heads macroscopically and radiographically.Results The mean decrease in epiphyseal height was 1.5 mm, 4.1 mm, 5.0 mm, and 7.5 mm in P2, P4, P12 and P20, respectively (rs = 0.76, p = 0.002). The mean increase of diameter was 4.1 mm, 6.9 mm, and 6.8 mm in P4, P12 and P20, respectively. Decrease of the articulotrochanteric distance was mild in P2 and P4, and severe in P12 and P20. Subluxation of the femoral head was observed only in P12 and P20 piglets.Interpretation The piglet model of LCPD was useful in the early stage of devascularization for investigation of the developmental pattern of femoral head deformity. However, when the piglets had grown to 20 weeks old or more-that is, to full skeletal maturity-the femoral head and acetabulum showed severe deformities that were most likely caused by heavy body weight.

show abstract

“…7,23,24 Miniature swine proximal femoral anatomy closely resembles that of human proximal femoral anatomy, [25][26][27] but to date this model has not been established in studying hypothyroid growth plate changes.…”

mentioning

confidence: 99%

The effects of hypothyroidism on the proximal femoral physis in miniature swine

Tank

Weiner

Jacquet

et al. 2013

Journal Orthopaedic Research

View full text Add to dashboard Cite

As a potential means of comparing hypothyroidism in humans, this work intended to establish a defined hypothyroid state in immature miniature swine and evaluate specific molecular, cellular, and extracellular responses of their growth plates. Two male, 11-week-old Sinclair miniature swine were given 6-propyl-2-thiouracil (PTU) in their water and two other like animals (controls) were provided water without PTU. Blood levels of thyroid stimulating hormone (TSH), triiodothyronine (T3), and thyroxin (T4) were monitored weekly. At 25 weeks of age, the hind limb proximal femoral physes were harvested and divided into portions for histology and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. Compared to controls, swine administered PTU exhibited increased TSH and decreased T3 and T4 serum levels during the study period, features consistent with a hypothyroid state. Compared to controls, hypothyroid swine exhibited structurally altered physes and demonstrated significantly decreased gene expression of aggrecan (p < 0.05) and type X collagen (p 0.1). This is the first hypothyroid model established in miniature swine and represents a potentially important advance for understanding the condition in humans, in which, like this swine model, there are changes critical to growth plate molecular biology, biochemistry and structure. ß 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31:1986Res 31: -1991Res 31: , 2013 Keywords: hypothyroidism; miniature swine; growth plate; slipped capital femoral epiphysis A relationship between endocrine-associated biochemical abnormalities and altered growth plate structure and function has been suggested in multiple pediatric orthopedic pathologies, including hypothyroidism. [1][2][3][4][5][6] The hypothyroid condition has been examined in several studies, but further biochemical and structural information would be beneficial for understanding the pathology more completely in growth plate maturation.Decreases in physeal height or thickness of growth plate cartilage proliferating and hypertrophic zones are reported in hypothyroid rat models, 7 and diminished numbers of hypertrophic chondrocytes and disruption of endochondral bone formation have been identified in hypothyroidism. 8,9 Thyroid hormone has been linked to regulation of type X collagen synthesis, physeal chondrocyte hypertrophy, and terminal chondrocyte differentiation. [10][11][12] Hypothyroid physeal chondrocytes express decreased levels of several genes, including types I and X collagen mRNA, and increased production of parathyroid hormone-related protein. 9,[13][14][15] These numerous biochemical and structural changes suggest that thyroid hormone plays an important role in growth plate maturation and function. Hypothyroidism in children results in short stature and delayed bone age, oftentimes with fragmented secondary centers of their femoral heads resembling those in Legg-Perthes disease. 16 No published data appear to be available concerning size...

show abstract

Development of Flattening and Apparent Fragmentation Following Ischemic Necrosis of the Capital Femoral Epiphysis in a Piglet Model

Cited by 137 publications

References 16 publications

Indentation properties of growing femoral head following ischemic necrosis

Indentation properties of growing femoral head following ischemic necrosis

Deformity of the femoral head following vascular infarct in piglets

The effects of hypothyroidism on the proximal femoral physis in miniature swine

Contact Info

Product

Resources

About