Abstract
Bone tissue is a composite material composed of an inorganic stiff mineral phase embedded in a compliant organic matrix. Similar to other composites, the mechanical properties of bone depend upon the properties, volume fraction, and orientation of its constituents as well as the bonding interactions. Interfacial bonding between the mineral and organic constituents are based, in part, on electrostatic interactions between negatively charged organic domains and positively charged mineral surface. Phosphate and fluoride ions can alter mineral-organic interfacial causing a permutation in the mechanical properties. Partial debonding between the mineral and organic constituents of bone may play an important role in the mechanical properties of aged and diseased bone. The present study examines the effects of phosphate and fluoride ion treatment on the compression properties of cortical bone and the reversibility of the effect.
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Varying the mechanical properties of bone tissue by changing the amount of its structurally effective bone mineral content
The effect of fluoride ions on the mechanical properties of bone tissue in tension was investigated with an in vitro model. Structurally effective Bone Mineral Content (BMC) of bovine bone tissue was changed by fluoride ion treatment. First, bovine cortical bone specimens were treated with a detergent solution in order
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The effect of in vitro fluoride ion treatment on the ultrasonic properties of cortical bone
The mechanical properties of composites are influenced, in part, by the volume fraction, orientation, constituent mechanical properties, and interfacial bonding. Cortical bone tissue represents a short-fibered biological composite where the hydroxyapatite phase is embedded in an organic matrix composed of type I collagen and other noncollagenous proteins. Destructive mechanical testing
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In situ observation of fluoride-ion-induced hydroxyapatite-collagen detachment on bone fracture surfaces by atomic force microscopy
The topography of freshly fractured bovine and human bone surfaces was determined by the use of atomic force microscopy (AFM). Fracture surfaces from both kinds of samples exhibited complex landscapes formed by hydroxyapatite mineral platelets with lateral dimensions ranging from ~90 nm × 60 nm to ~20 nm × 20 nm. Novel AFM techniques
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The effect of fluoride treatment on bone mineral in rabbits
Fluoride therapy has been used clinically for many years, but its use remains controversial and many basic questions remain unanswered. Accordingly, this study returns to an animal model to study the effects of high doses of fluoride on bone mineral in rabbits. Twelve rabbits, aged 3(1/2) months at the start
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Compressive properties of cortical bone: mineral-organic interfacial bonding
Bone tissue is an anisotropic non-homogeneous composite material composed of inorganic, bone mineral fibres (hydroxyapatite) embedded in an organic matrix (type I collagen and non-collagenous proteins). Factors contributing to the overall mechanical behaviour include constituent volume fraction, mechanical properties, orientation and interfacial bonding interactions. Interfacial bonding between the mineral and
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Fluoride & Osteoarthritis
While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.
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"Pre-Skeletal" Fluorosis
As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.
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Skeletal Fluorosis: The Misdiagnosis Problem
It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.
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Mechanisms by which fluoride may reduce bone strength
Based on a large body of animal and human research, it is now known that fluoride ingestion can reduce bone strength and increase the rate of fracture. There are several plausible mechanisms by which fluoride can reduce bone strength. As discussed below, these mechanisms include: Reduction in Cortical Bone Density De-bonding of
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Fluoride Reduces Bone Strength Prior to Onset of Skeletal Fluorosis
The majority of animal studies investigating fluoride's impact on bone strength have found that fluoride has either no effect, or a detrimental effect, on bone strength. Importantly, several of the animal studies that have found fluoride reductes bone strength have reported that this reduction in strength occurs before signs of skeletal fluorosis
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