Bone defects

Bone defects surgically produced in sheep and rabbit models, have been treated with freeze dried methylpyrrohdinone chitosan [334-336]. hi view of improving bone tissue reconstitution with chitosan associated with calcium phosphate. Microscopic and histological analyses showed the presence of an osteogenic reaction moving from the rim of the surgical lesion toward the center. In control lesions, dense fibrous tissue, without the characteristic histoarchitecture of bone was observed. 

Roessler, Wilke A, Griss PM, and Kienapfel H. Missing osteoconductive effect of a resorbable PEO/PBT copolymer in human bone defects A clinically relevant pilot study with contrary results to previous animal studies. Biomed Mater Res (Appl Biomater), 2000, 53, 167-173. 

Antibiotic-loaded composites of poly(DL-lactic acid) and hydroxyapatite have been studied as a filler in the repair of bone defects (106). The drug dideoxykanamycin was formulated at 20% by weight in a 50 50 PL A/hydroxyapatite composite. Cyclindrical composites were implanted into the penetrated tibeas of rats. Antibiotic was present at the implantation site at least 8 weeks postimplantation. 

Bio-nanocomposites based on calcium phosphates can perform other innovative fundions such as acting as a reservoir for the controlled release of bioadive compounds once the material is implanted in the bone defect. For instance, the incorporation of a morphogenetic protein that promotes bone regeneration in an HAP-alginate-collagen system [110] or a vitamin in a Ca-deficient HAP-chitosan nanocomposite [111] are recent examples of this kind of application. 

Fig. 6.11 pCT images of implantation site. Bone defect was filled with newly formed bone after 4 weeks implantation. 

The question of whether the variances are not even wider than this and the compositions (including total ash content) stable enough to be distinctive for each individual is particularly interesting and important from the standpoint of the existence of Osteogenests imperfecta (brittle bones) in its various forms and related congenital bone "defects."... 

Davideau, J. L., Lezot, F., Kato, S., Bailleul-Forestier, 1., and Berdal, A. (2004). Dental alveolar bone defects related to vitamin D and calcium status. /. Steroid Biochem. Mol. Biol. 89-90, 615-618. 

Passi, P., Zadro, A., Marsilio, E, Lora, S., Caliceti, P., and Veronese, F.M. (2000). Plain and drug loaded polyphosphazene membranes and microspheres in the treatment of rabbit bone defects. J. Materials Science-Materials Med., 11, 643-654. 

Copper was recognized as nutritionally essential by 1924 and has since been found to function in many cellular proteins.470-474 Copper is so broadly distributed in foods that a deficiency has only rarely been observed in humans.4743 However, animals may sometimes receive inadequate amounts because absorption of Cu2+ is antagonized by Zn2+ and because copper may be tied up by molybdate as an inert complex. There are copper-deficient desert areas of Australia where neither plants nor animals survive. Copper-deficient animals have bone defects, hair color is lacking, and hemoglobin synthesis is impaired. Cytochrome oxidase activity is low. The protein elastin of arterial walls is poorly crosslinked and the arteries are weak. Genetic defects in copper metabolism can have similar effects. 

Abnormal calcium transport undoubtedly contribute to bone defects but specific examples are poorly described. For the major calcium transporters, significant defects are lethal in embryonic life, such as in the Cavl.2 L-type calcium channel... 

Aho AJ, Rekola J, Matinlinna J, Gunn J, Tirri T, Viitaniemi P, Vallittu P. Natural composite of wood as replacement material for ostechondral bone defects. Journal of Biomedical Materials Research B 2007, 83, 64-71. 

I. Reiche, C. Vignaud, L. Favre-Quattropani, L. Chariet, M. Menu, Diffusion in archaeological bones, Defect and Diffusion Forum Vols. 194-199 (2001) 953-960. 

Meinel, L., Fajardo, R., Hofmann, S., Langer, R., Chen, J., Snyder, B., Vunjak-Novakovic, G., and Kaplan, D. "Silk implants for the healing of critical size bone defects". Bone 37(5), 688-698 (2005). 

Allogeneic bone matrix repair, replacement, and/or reconstruction of bone defects... 

Lithium might be expected to affect bone structure and function because of its chemical similarity to magnesium and calcium. In elderly lithium-treated patients and in animal experiments using weanling and mature rats, lithium was shown to accumulate in bone (204). Further biochemical studies showed no evidence of resulting bone defects (205, 206). Bone density measurements on mature rat bone, and on hand radiographs in lithium patients, failed to show any significant differences attributable to lithium (206). 

Dawson KL,Farnan IE,Constantz BR, Young SW (1991) Sohd-state phosphorus-31 nuclear magnetic resonance differentiation of bone mineral and synthetic apatite used to fill bone defects. Inv Radiol 26 946-950... 

Osteomalacia and rickets are caused by a mineralization defect during bone formation, resulting in an increase in osteoid, the unmineralized organic matrix of bone. Defective mineralization produces rickets in children and osteomalacia in adults. Osteomalacia or rickets is usually due to either vitamin D deficiency or phosphate depletion. 

In bone, a CaBP called osteocalcin contains 49 amino acids (M.W. 5500-6000). Its synthesis is stimulated by 1,25-(0H)2D. Osteocalcin contains four residues of y-carboxyglutamic acid, which require vitamin K for their synthesis and are important as binding sites for calcium (Chapter 36). Although vitamin K deficiency reduces the osteocalcin content of bone, it does not cause functional bone defects. For this reason, osteocalcin may function in calcium mobilization rather than deposition. Alternatively, as an effective inhibitor of hydroxyapatite formation, it may prevent overmineralization of bone. 1,25-(OH)2D increases y-glutamyl carboxylase activity in the renal cortex. The relationship between vitamin D and vitamin K needs clarification. 

Effects of Cadmium tCdi its chemical similarity to zinc (an essential micronutrient for animals, plants and humans) leads to its toxicological properties. Cd once absorbed by an organism remains stocked for many decades. This bio-persistence generates lung diseases, bone defects, renal dysfunction, increases blood pressure etc. 

Copper is a cofactor in several enzymes, including lysyl oxidase and superoxide dismutase. Ceruloplasmin, a deep-blue glycoprotein, is the principal copper-containing protein in blood. It is used to transport Cu2+ and maintain appropriate levels of Cu2+ in the body s tissues. Ceruloplasmin also catalyzes the oxidation of Fe2+ to Fe3+, an important reaction in iron metabolism. Because the metal is widely found in foods, copper deficiency is rare in humans. Deficiency symptoms include anemia, leukopenia (reduction in blood levels of white blood cells), bone defects, and weakened arterial walls. The body is partially protected from exposure to excessive copper (and several other metals) by metal-lothionein, a small, metal-binding protein that possesses a large proportion of cysteine residues. Certain metals (most notably zinc and cadmium) induce the synthesis of metallothionein in the intestine and liver. 

Acampora, D., Merlo, G.R., Paleari, L., Zerega, B., Postiglione, M.P., Mantero, S., Bober, E., Barbieri, O., Simeone, A., Levi, G. 1999. Craniofacial, vestibular and bone defects in mice lacking the Distal-less-related gene Dlx5. Development 126, 3795-3809. 

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