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Basic anatomy of a tibia (1) Apophysis (traction epiphysis) (2) Epiphysis (pressure epiphysis)(3) Epiphyseal plate(4) Metaphysis(5) Diaphy-sis

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OssificationPrimary ossification centres- diaphyseal

Secondary ossification centresepiphyseal

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Components of the Epiphysis and Metaphysis(1) Articular cartilage(2) Epiphyseal cartilage(3) Secondary center of ossification; (4) Epiphyseal plate; (5) Epiphysis; (6) Metaphysis; (7) Fibrous layer of the periosteum; (8) Ringof LaCroix; (9) Groove of Ranvier; (10) Fibrous components of the epiphyseal plate; (11) Cortical bone.

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Zones of the Cartilaginous Component of the Epiphyseal Plate(1)Reserve zone(2) proliferative zone (3) zone of maturation(4) zone of degeneration(5) zone of provisional calcification (6) hypertrophic zone

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Blood supply of the Epiphyseal Plate(1) Epiphyseal artery (2) Epiphyseal Plate (3) Perichondrial Artery (4) Metaphyseal Artery (5) Nutrient Artery

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Physeal fractures30% of all childrens fractures involve the physisClassificationSalter-Harris (1963)I Gentle closed reductionII before 10 days *III Open reductionIV internal fixationVOften retrospective diagnosis Avoid metal across physis if possible* After 10 days accept position and perform osteotomy if required laterSalter RB, Harris WR: J Bone Joint Surg 45A: 587-622, 1963

IIIIIIIVV

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Modifed salterHarris Classifcation of Fractures of the Epiphyseal Plate.Simple fracture through the hypertrophic zone of the epiphyseal plate.

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Fracture through the epiphyseal plate and the metaphysis.

Modifed salterHarris Classifcation of Fractures of the Epiphyseal Plate.

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Fracture through the epiphyseal plate and the epiphysis.

Modifed salterHarris Classifcation of Fractures of the Epiphyseal Plate.

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Fracture through the epiphysis and the metaphysis.

Modifed salterHarris Classifcation of Fractures of the Epiphyseal Plate.

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Compression fracture of the epiphyseal plate.

Modifed salterHarris Classifcation of Fractures of the Epiphyseal Plate.

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lateral bone bridge formation.

Modifed salterHarris Classifcation of Fractures of the Epiphyseal Plate.

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Physeal AnatomyReserve Zone- few cells, high matrix- cells from Groove of Ranvier- cells quiescentProliferative Zone- cellular proliferation / mitosis- columns of cells- longitudinal growth- metaphyseal sideHypertrophic zoneA. Maturation- enlarged, swollen, vacuolatedB. Degeneration- increase Alk Phos- increases phosphate for calcificationC. Provisional calcification- ECM calcify- cell death

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Role of periosteum/ Overgrowth2 layersCambial layer (highly osteogenic)Fibrous layerCircumferential periosteal sectioning stimulates growthHemisectioning produces asymmetrical growth?due to a combination of increased blood flow and release of periosteal tension affecting the whole bone

Shapiro F: Fractures of the femoral shaft in children. The overgrowthphenomenon. Acta Orthop Scand 52:649655, 1981.

Remodeling of angulated fractures in children is a wellrecognized phenomenon (Fig. 321). The site of correction and the mechanism by which remodeling occurs are poorly understood. Remodeling at the fracture site occurs by bone resorption on the convexity and deposition on the concavity of the fracture. This phenomenon of "bone drift" is well recognized clinically, and has been quantified in the rabbit model (10). However, the majority of remodeling occurs by reorientation of the growth plates, with improvement in the overall alignment of the limb. Asymmetric and longitudinal growth of the physis contribute to this remodeling. Therefore, measurement of angular remodeling at the fracture site alone gives an inadequate picture of the overall limb alignment as remodeling occurs (10, 11). Remodeling capacity depends on the number of years of growth remaining, the proximity of the fracture to a rapidly growing physis, the magnitude of angular deformity, and the plane of angulation relative to adjacent joints. Remodeling may continue for 5 to 6 years after fracture, as long as growth occurs during the period of remodeling (11). The rate of remodeling is minimally influenced by age, but the completeness of remodeling may be limited by the number of years of growth remaining (11, 12, 13, 14). Fractures in the plane of joint motion and near a rapidly growing physis have the greatest capacity to remodel. Fractures with smaller degrees of malunion are more likely to remodel completely (15). Remodeling of rotational deformity has also been noted in children, but this is less predictable than angular remodeling (16, 17). It has been postulated that torsional remodeling occurs by helical growth of the physis

Another distinguishing physiologic response to bone healing in children is the potential for growth stimulation after fracture. The age of the patient and the amount of periosteal stripping influence the amount of growth stimulation (7). This phenomenon is most commonly reported after femoral fractures in children between the ages of 3 and 9 years, but it also occurs after other fractures (18, 19, 20, 21). The exact mechanism for growth acceleration is unknown, but increased blood flow to the growth plate and release of periosteal tension after fracture are potential causes. Hyperemia as a cause of overgrowth is supported by the observation that growth acceleration may occur with conditions that cause increased vascularity, such as congenital vascular anomalies, inflammatory conditions, and tumoral disorders (19). Transverse sectioning of the periosteum also produces overgrowth. Periosteal stripping or division close to the growth plate increases the effect of transverse periosteal release, but longitudinal incision of the periosteum does not cause growth acceleration (7, 22). Hemicircumferential release of the periosteum causes asymmetric growth and subsequent angular deformity (23). This phenomenon is most often seen clinically after fracture of the proximal tibial metaphysis in children, when the medial periosteum is torn transversely, while the lateral periosteum remains intact. These findings support the observation that the periosteum acts as a mechanical restraint on epiphyseal growth through its attachments to the perichondrial ring (24). In older children, premature physeal closure has been noted after diaphyseal fracture (25, 26). Perhaps the variable growth responses after fracture can be partially explainedby differences in periosteal damage or asymmetric hyperemic responses after fracture.

7. Jacobsen J. Periosteum: its relation to pediatric fractures. J Pediatr Orthop Br 1997;6:84.8. Lane J. Breakout session 2: fracture repair process. Clin Orthop 1998;355S:S354.9. Einhorn T. The cell and molecular biology of fracture healing. Clin Orthop 1998;355S:S7.10. Murray D, Wilson-MacDonald J, Morscher E, et al. Bone growth and remodelling after fracture. J Bone Joint Surg Br 1996;78:42.11. Wallace M, Hoffman E. Remodelling of angular deformity after femoral shaft fractures in children. J Bone Joint Surg Br 1992;74:765.12. Friberg K. Remodelling after distal forearm fractures in children. I. The effect of residual angulation on the spatial orientation of the epiphyseal plates. Acta Orthop Scand 1979;50:537.13. Friberg K. Remodelling after distal forearm fractures in children. II. The final orientation of the distal and proximal epiphyseal plates of the radius. Acta Orthop Scand 1979;50:731.14. Friberg K. Remodelling after distal forearm fractures in children. III. Correction of residual angulation in fractures of the radius. Acta Orthop Scand 1979;50:741.15. Perona P, Light T. Remodeling of the skeletally immature distal radius. J Orthop Trauma 1990;4:356.16. Benum P, Ertresvag K, Hoisetii K. Torsion deformities after traction treatment of femoral fractures in children. Acta Orthop Scand 1979;50:87.17. Hagglund G, Hansson L, Norman O. Correction by growth of rotational deformity after femoral fracture in children. Acta Orthop Scand 1983;54:858.18. Corry I, Nicol R. Limb length after fracture of the femoral shaft in children. J Pediatr Orthop 1995;15:217.19. Gasco J, dePablos J. Bone remodeling in malunited fractures in children: is it reliable? J Pediatr Orthop Br 1997;6:126.20. Hougaard K. Femoral shaft fractures in children: a prospective study of the overgrowth phenomenon. Injury 1989;20:170.21. Shapiro F. Fractures of the femoral shaft in children: the overgrowth phenomenon. Acta Orthop Scand 1981;52:649.22. Wilde G, Baker G. Circumferential periosteal release in the treatment of children with leg-length inequality. J Bone Joint Surg Br 1987;69:817.23. Carvell J. The relationship of the periosteum to angular deformities of long bones. Clin Orthop 1983;173:262.24. Houghton G, Rooker G. The role of the periosteum in the growth of long bones. J Bone Joint Surg Br 1979;61:218.25. Beals R. Premature closure of the physis following diaphyseal fractures. J Pediatr Orthop 1990;10:717.26. Hresko M, Kasser J. Physeal arrest about the knee associated with non-physeal fractures in the lower extremity. J Bone Joint Surg Am 1989;71:698.

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Perichondral Ring of La Croix & Groove of RanvierSurround the physis circumferentially at its peripheryGroove - resting and proliferating cellsRing - cartilage cells that move towards the metaphysis and become contigous with periosteum

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Salter Harris Classification

I. Whole epiphysis is separated from shaftII. Fracture through metaphysis and physisIII. Separation of part of the epiphysis- fracture through physis and epiphysisIV. Fracture passes vertically through epiphysis / physis / metaphysisV. Crushing of part or all of the epiphysis

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Physeal fracturesThought to occur primarily through hypertrophic zoneReserve zone injury- Increased growth arrest with proximal tibia and distal femur- Because of undulating course of physis- More likely damage to germinal or resting layers

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ManagementDo not remanipulate physeal injuries > 7-10 days- risk injury- exception type 3/4 - in these anatomical reduction more importantMetaphyseal / diaphyseal- can MUA up to 3 weeks after

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Anatomy of the physis and the principle of remodelling in childrens fracturesDominic InmanTrauma term3/3/2008

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Anatomy of the physis2 growth platesSphericalHorizontal3 layers in the physisReserve zoneProliferative zoneHypertrophic zoneMaturation zoneDegenerative zoneZone of provisional calcificaton

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Reserve zoneChondrocytes store lipids, glycogen and proteoglycan aggregatesBlood vessels pass through this layer causing low pO2

Diseases with defects of this layerPseudoachondroplasiaDiastrophic dwarfismKneist syndrome

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Proliferative zoneLongitudinal growth occursGood blood supply inhibits calcification

Diseases with defects in this layerGigantismAchondroplasiaHypochondroplasiaMalnutrition, irradiation injury, glucocorticoid excess

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Hypertrophic zone (1)Maturation zoneDegeneration zoneProvisional calcification zoneChondrocytes increase in size by 5Accumulate calcium in their mitochondriaDie releasing Ca from matrix vesiclesMaturation under hormone controlIndian hedgehog produced by physeal chondrocytes and regulates PTHrP which inhibits maturation

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Hypertrophic zone (2)Osteoblasts use cartilage as a scaffold for bone formationLow pO2 facilitates thisDiseases with defects in this layerMucopolysaccharidosesMorquios, Hurlers, HuntersRickets, osteomalaciaInsufficient Ca2+ / P for normal calcificationPhysis appears widenedEnchondromas originate in this zonePhyseal fractures

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How immature bone differsMore porous, more vascularThicker, stronger periosteumPresence of physisLower Youngs modulusLess energy required to break immature boneFail in tension or compressionComminuted fractures less common as lower energyBone usually fails before soft tissuesHeal quicker as more vascularPhyseal