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CALCIFICATION AND OSSIFICATION I. Calcification in the Callus in Healing Fractures in Normal Rats
MARSHALL R. URIST; FRANKLIN C. McLEAN
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Johns Hopkins Medical School, Baltimore, Maryland; Department of Physiology, University of Chicago, Chicago, Illinois
1941 by The American Orthopaedic Association, Inc.
The Journal of Bone & Joint Surgery.  1941; 23:1-16 
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Abstract

1. The healing process in the fractures observed is essentially one of formation of a fibrocartilaginous callus in and around the defect in the shaft, and the subsequent invasion, removal, and replacement of the fibrocartilaginous mass by new bone arising from the cambium layer of the periosteum and from the endosteum.

2. The progress of calcification in this process has been observed by impregnation of undecalcified sections with silver nitrate. By this method, which is extremely sensitive for bone salt, no deposition of salt is observed in the procallus, or prior to the formation of osseous tissue.

3. Bone matrix is formed subperiosteally and subendosteally, first at some distance from the fracture line, at about the second or third day following a fracture. It is calcified as it is laid down under optimum conditions with no appreciable interval between its formation and the deposition of bone salt within it. As the new bone invades the fibro-cartilaginous callus, it removes the fibrous tissue, fibrocartilage, and hyaline cartilage, replacing them by bone matrix. In this process remnants of the invaded tissue may be utilized and converted into bone matrix by the invading osteogenic cells. In all instances the new matrix is calcifiable as soon as it is recognizable as osseous tissue.

4. A lag in calcification of newly formed osseous tissue may occur. This is attributed to failure in the supply or transport of bone minerals, rather than to lack of calcifiability in the bone matrix.

5. The matrix of hyaline cartilage becomes calcifiable when the adjacent cartilage cells become vesicular or hypertrophic. The calcification of cartilage matrix is further conditioned by its relationship to the bone tissue invading the fibrocartilaginous callus. Only matrix in contact with the invading bone calcifies, and, if the matrix has not been made calcifiable by hypertrophy of the adjacent cells, it calcifies only when converted into bone matrix by the advancing osteogenic process.

6. Only tissues recognizable as bone matrix or cartilage matrix calcify in the callus. There is no random calcification in the fibro-cartilaginous callus, the great mass of which remains completely free from bone salt except where it is invaded and converted into bone from its periphery.

7. Particles of bone, including their bone salt, have been demonstrated in foreign-body giant cells and in macrophages during the resorption of necrotic bone. Fragments of dead cortical bone have been observed to undergo decalcification in advance of the disintegration of the bone matrix. This differs from the process of resorption of living bone, in which the bone mineral and organic matrix are removed simultaneously. No phagocytic activity of osteoclasts, either for particles of bone or for bone salt, has been demonstrated.

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    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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