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M Yazdi

Publications and source records attributed to M Yazdi.

8 recordsLinked to original sources
PubMed1994

Effects of lathyritic drugs and lathyritic demineralized bone matrix on induced and sustained osteogenesis.

Demineralized bone matrix was implanted in normal and lathyritic rats. At 2 weeks, the bone that formed in the lathyritic animals had an elevated alkaline phosphatase activity and a reduced calcium content compared with the controls. Four weeks after implantation, these biochemical parameters were reversed, with a decrease in alkaline phosphatase activity and an increase in calcium content to control levels. The histology of the recovered implants revealed new bone formation. Lathyritic demineralized bone matrix was prepared from bones of rats fed beta-aminopropionitrile for 2 weeks (2-week BAPN-DBM) or 4 weeks (4-week BAPN-DBM), and was implanted in normal rats. Two weeks after implantation, both preparations of lathyritic demineralized bone matrix demonstrated early bone formation, although alkaline phosphatase activity and calcium content were reduced. By 4 weeks after implantation, no biochemical or histological evidence of bone formation remained at the site of the 4-week BAPN-DBM implants; continued but reduced bone formation was observed at the site of the 2-week BAPN-DBM implants. Reconstitution of inactivated normal demineralized bone matrix with the guanidine-soluble extracts restored the osteoinductive capacity. However, reconstitution of inactivated lathyritic demineralized bone matrix (4-week BAPN-DBM) failed to restore the osteoinductive capacity. These results indicate that the degree of crosslinking of the collagen matrix that acts as a carrier for osteoinductive proteins plays a key role in inducing and sustaining osteogenesis.

Aminopropionitrile↗
PubMed1992

Demineralized bone matrix polydioxanone composite as a substitute for bone graft: a comparative study in rats.

Demineralized bone matrix (DBM) has been successfully used as a substitute for bone grafting. Autogenous bone grafts (ABG) may cause donor site morbidity and undergo significant resorption. DBM may overcome these problems but is mechanically unstable when originally placed. We explored using a slowly resorbable template, polydioxanone (PDS), in combination with DBM and compared it to ABG in a rat 9 x 9 mm cranial defect model. After both 1 and 3 months, histologically and biochemically well-formed bone was present in ABG/PDS and DBM/PDS-treated defects, but not in control defects (PDS alone). Mechanical push-out tests using a servohydraulic testing frame were conducted. Maximum load before failure of DBM/PDS increased from 65% at 1 month to 100% of that of intact skull at 3 months. In contrast, ABG/PDS was 50% as strong as DBM/PDS and not significantly stronger than PDS alone. ABG/DBM did not significantly increase in strength from 1 to 3 months. We conclude that DBM/PDS is better than ABG/PDS in treating cranial defects in the rat model, and that an absorbable osteoinductive bone substitute with superior mechanical advantage is possible without the disadvantages of ABG.

Animals↗
PubMed1992

Effects of non-steroidal anti-inflammatory drugs on demineralized bone-induced bone formation.

The inhibitory effect of some non-steroidal anti-inflammatory drugs (NSAIDs) on bone resorption is well documented. To explore the effect of NSAIDs on bone formation, we investigated the time course and dose/response characteristics of treatment with various non-steroidal anti-inflammatory drugs (NSAIDs) on ectopic bone formation induced by demineralized bone matrix (DBM) in the rat model. Using biochemical assays, both inhibitory and stimulatory effects on bone formation were found in rats treated with NSAIDs prior to DBM implantation depending on the type and amount of drug administered. There appears to be an enhancement of bone formation for acetaminophen (50 mg/kg), acetylsalicylic acid (50 mg/kg), and ibuprofen (50 mg/kg). Indomethacin (4 mg/kg) and piroxicam (4 mg/kg) had inhibitory effects. Flurbiprofen, on the other hand, did not appear to affect bone formation significantly. In contrast, there was no effect of NSAIDs on bone formation in rats treated with the drugs after implantation of the DBM. It appears that the time course of the drug administration is critical, suggesting that early events in bone formation may be modulated by arachidonic acid metabolites.

Acetaminophen↗
PubMed1991

Effects of indomethacin on demineralized bone-induced heterotopic ossification in the rat.

Indomethacin inhibits bone formation when treatment is initiated before the implantation of demineralized bone matrix (DBM). For the inhibition of bone induction to occur, indomethacin treatment had to be initiated 6 h or more before implantation of DBM. Initiating the drug treatment at or after the time of DBM implantation had no effects on the amounts of new bone formed. The inhibition by indomethacin is dose related over a range between 0.04 and 4 mg/kg body weight. Recovered day-1 DBM implants, transplanted into indomethacin pre- and posttreated syngeneic rats, formed bone at the same rate as controls did. However, recovered day-1 DBM implants lyophilized before transplantation showed decreased bone formation but significant dystrophic calcification as judged by a lower alkaline phosphatase activity and an elevated calcium content.

Alkaline Phosphatase↗
PubMed1991

Postmortem degradation of demineralized bone matrix osteoinductive potential. Effect of time and storage temperature.

The osteoinductive growth factors present in demineralized bone are degraded by tissue enzymes. Storage of rat limbs at low temperature (4 degrees C) before harvesting of bones preserves the osteoinductive potential of such factors. Storage at room temperature for more than 24 hours causes the recovered bone matrix to be biologically inactive, presumably as the result of biodegradation.

Alkaline Phosphatase↗
PubMed1989

Osteogenesis in bone defects in rats: the effects of hydroxyapatite and demineralized bone matrix.

Hydroxyapatite (HA) and Demineralized Bone Matrix (DBM) are being investigated as potential osteogenic agents with hopes that these substances can be used to induce bone formation in non-union fractures. This study was done to determine the relative effects of HA and DBM implanted as moldable phospholipid composites in bone defects that result in non-unions. We studied 22 ten-month-old Long-Evans male rats with 5.0 mm unilateral radial defects implanted with HA, DBM, and a combination of both substances. Control defects were left unfilled. Eight weeks after implantation, the histological sections demonstrated a decrease in bone formation with HA relative to controls. The HA crystals were encapsulated by connective tissue stroma made up of collagenous elements, fibroblasts, and blood vessels. There were no indications of bone formation within the fibrous stroma. 45Calcium, alkaline phosphatase, and bone gla protein (BGP) assays demonstrated a 16% increase in bone formation in rats implanted with DBM, an 80% decrease in groups implanted with HA (p = 0.01) and an 80% decrease with DBM plus HA (p = 0.01). Radiologic analysis corresponds well with histological and biochemical results. We conclude that osteogenesis in non-union defects is enhanced by the implantation of DBM, while HA interferes with bone formation in the rat model. In the presence of both substances, HA appears to impede new bone growth, negating any positive effects seen with DBM.

Alkaline Phosphatase↗