The Clinician’s Guide to Prevention and Treatment of Osteoporosis was developed by an expert committee of the National Osteoporosis Foundation (NOF) in collaboration with a multispecialty council of medical experts in the field of bone health convened by NOF. Readers are urged to consult current prescribing information on any drug, device, or procedure discussed in this publication.

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Clinician’s Guide to Prevention and Treatment of Osteoporosis

The total antioxidant activity of 12 fruits and 5 commercial fruit juices was measured in this study using automated oxygen radical absorbance capacity (ORAC) assay. On the basis of the wet weight of the fruits (edible portion), strawberry had the highest ORAC activity (micromoles of Trolox equivalents per gram) followed by plum, orange, red grape, kiwi fruit, pink grapefruit, white grape, banana, apple, tomato, pear, and honeydew melon. On the basis of the dry weight of the fruits, strawberry again had the highest ORAC activity followed by plum, orange, pink grapefruit, tomato, kiwi fruit, red grape, white grape, apple, honeydew melon, pear, and banana. Most of the antioxidant capacity of these fruits was from the juice fractions. The contribution of the fruit pulp fraction (extracted with acetone) to the total ORAC activity of a fruit was usually less than 10%. Among the commercial fruit juices, grape juice had the highest ORAC activity followed by grapefruit juice, tomato juice, orange juice, and apple juice.

Total Antioxidant Capacity of Fruits

See related commentary by Kanis, page [1829][1]

Since the publication of the Osteoporosis Canada guidelines in 2002, there has been a paradigm shift in the prevention and treatment of osteoporosis and fractures. [1][2],[2][3] The focus now is on preventing fragility fractures and their negative

/pdf/2010-clinical-practice-guidelines-for-the-diagnosis-and-4ttqfkm9wl.pdf

2010 clinical practice guidelines for the diagnosis and management of osteoporosis in Canada: summary

The global prevalence of dementia is estimated to be as high as 24 million, and is predicted to double every 20 years through to 2040, leading to a costly burden of disease. Alzheimer disease (AD) is the leading cause of dementia and is characterized by a progressive decline in cognitive function, which typically begins with deterioration in memory. Before death, individuals with this disorder have usually become dependent on caregivers. The neuropathological hallmarks of the AD brain are diffuse and neuritic extracellular amyloid plaques-which are frequently surrounded by dystrophic neurites-and intracellular neurofibrillary tangles. These hallmark pathologies are often accompanied by the presence of reactive microgliosis and the loss of neurons, white matter and synapses. The etiological mechanisms underlying the neuropathological changes in AD remain unclear, but are probably affected by both environmental and genetic factors. Here, we provide an overview of the criteria used in the diagnosis of AD, highlighting how this disease is related to, but distinct from, normal aging. We also summarize current information relating to AD prevalence, incidence and risk factors, and review the biomarkers that may be used for risk assessment and in diagnosis.

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Epidemiology of Alzheimer disease

Anthocyanins are natural colorants belonging to the flavonoid family. They are widely distributed among flowers, fruits, and vegetables. Using the automated oxygen radical absorbance capacity (ORAC) assay developed in our laboratory, we determined the antioxidant capacity of 14 anthocyanins including the aglycons delphinidin, cyanindin, pelargonidin, malvidin, peonidin, and their derivatives with different sugar linkages. Among these anthocyanins, kuromanin (cyanidin-3-glucoside) had the highest ORAC activity, which was 3.5 times stronger than Trolox (vitamin E analogue), while pelargonin had the lowest antioxidant activity but was still as potent as Trolox. Different patterns of hydroxylation and glycosylation in anthocyanins appear to modulate their antioxidant properties. Therefore, in addition to their colorful characteristics, anthocyanins possess potent antioxidant properties.

https://www.kuromanin.com/Oxygen%20Radical%20Absorbing%20Capacity%20of%20Anthocyanins.pdf

Oxygen Radical Absorbing Capacity of Anthocyanins

Diphosphonates and inhibition of bone mineralisation

Oral alendronate induces progressive increases in bone mass of the spine, hip, and total body over 3 years in postmenopausal women with osteoporosis

Etidronate and the risk of fractures

The aim of the study was to assess risedronate's effect on bone mineral density in postmenopausal women with rheumatoid arthritis receiving glucocorticoids. We carried out a two center, 2 year, double-masked, placebo-controlled trial with a third year of nontreatment follow-up. We studied 120 women requiring long-term glucocorticoid therapy at > 2.5 mg/day prednisolone randomized to treatment with daily placebo; daily 2.5 mg risedronate; or cyclical 15 mg risedronate (2 out of 12 weeks). At 97 weeks, bone mineral density was maintained at the lumbar spine (+1.4%) and trochanter (+0.4%) in the daily 2.5 mg risedronate group, while significant bone loss occurred in the placebo group (-1.6%, p = 0.03; and 4.0%, p < 0.005, respectively). At the femoral neck, there was a nonsignificant bone loss in the daily 2.5 mg risedronate group (-1.0%) while in the placebo group bone mass decreased significantly (-3.6%, p < 0.001). The difference between placebo and daily 2.5 mg risedronate groups was significant at the lumbar spine (p = 0.009) and trochanter (p = 0.02) but did not reach statistical significance at the femoral neck. Although not significantly different from placebo at the lumbar spine, the overall effect of the cyclical regimen was similar to that of the daily 2.5 mg risedronate regimen. Treatment withdrawal led to bone loss in the risedronate groups that was significant at the lumbar spine. A similar number of patients experienced adverse events (including upper gastrointestinal events) across treatment groups and risedronate was generally well tolerated. Thus risedronate preserves bone mass in postmenopausal women with rheumatoid arthritis receiving glucocorticoids while patients receiving a placebo have significant bone loss.

Prevention of bone loss with risedronate in glucocorticoid-treated rheumatoid arthritis patients.

A 12-year-old female suffering from osteogenesis imperfecta (OI) was treated with 3-amino-1-hydroxypropylidene-1,1-bisphosphonate (APD) orally, 250 mg daily, for periods of 2 months, alternating with periods of 2 months of abstinence. Total duration of therapy was 1 year. Radiological and clinical improvement was striking. Furthermore, X-rays of the bones showed large, parallel radio-opaque striae, corresponding exactly to the periods of therapy. These were present in all metaphyses.

C Nagant de Deuxchaisnes

Papers

Diphosphonates and inhibition of bone mineralisation

Oral alendronate induces progressive increases in bone mass of the spine, hip, and total body over 3 years in postmenopausal women with osteoporosis

Etidronate and the risk of fractures

Prevention of bone loss with risedronate in glucocorticoid-treated rheumatoid arthritis patients.

Radiological manifestations of bisphosphonate treatment with APD in a child suffering from osteogenesis imperfecta.