Osteoporosis and fragility fracture

2018 ◽  
Author(s):  
Kassim Javaid
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Mass ◽  
Fragility Fracture ◽  
Peak Bone Mass ◽  
Early Adulthood ◽  
Multifactorial Disease ◽  
The Uk ◽  
Rate Of Bone Loss

Osteoporosis is defined as a systemic bone disease with reduction in both bone density and microarchitectural integrity, resulting in an increase in fragility fracture risk. It is a multifactorial disease which, through effects on bone formation and resorption, reduces the peak bone mass achieved during early adulthood and increases the rate of bone loss in later adulthood. Osteoporosis is clinically silent until a fragility fracture occurs. There are 3 million patients with osteoporosis in the UK, with over 200 000 fractures per year and 80 000 hip fractures. This chapter addresses the causes, clinical features, diagnosis, and management of osteoporosis.

scholarly journals Investigation of the bone density in multiple sclerosis

2008 ◽  
Vol 7 (2) ◽  
pp. 46-51
Author(s):  
O. S. Dranichnikova ◽  
V. D. Zavadovskaya ◽  
V. M. Alifirova
Keyword(s):  
Physical Activity ◽  
Multiple Sclerosis ◽  
Bone Density ◽  
Bone Formation ◽  
Bone Mass ◽  
Computer Tomography ◽  
Dramatic Decrease ◽  
Disability Status ◽  
Common Opinion ◽  
Therapy Sessions

A number of investigations revealed a problem of osteopenic syndrome in patients with multiple sclerosis but there is no common opinion concerning factors which lead to its development. We observed 65 patients with multiple sclerosis with various type of its course and disability status of several degree based upon EDSS scale. Ultrasound osteometry of the calcaneus, computer tomography of QCT of L1—L3 vertebras were performed, serum crosslaps, N-MID osteocalcin were used. Decreased bone density, injured bone microarchitectonics and suppression of bone formation and resorption, which were correlated EDSS were found. Correlations with other factors (growth, weight, gender, and number of steroid therapy sessions ) for these parameters was not revealed. This allowed to conclude that the main reason of decreased bone mass in patients with multiple sclerosis is the dramatic decrease in physical activity.

scholarly journals Tracking of vitamin D status from childhood to early adulthood and its association with peak bone mass

2017 ◽  
Vol 106 (1) ◽  
pp. 276-283 ◽  
Author(s):  
Kun Zhu ◽  
Wendy H Oddy ◽  
Patrick Holt ◽  
Wendy Chan She Ping-Delfos ◽  
Jenny Mountain ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Mass ◽  
Peak Bone Mass ◽  
Early Adulthood ◽  
Vitamin D Status

scholarly journals Porcupine inhibitors impair trabecular and cortical bone mass and strength in mice

2018 ◽  
Vol 238 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Thomas Funck-Brentano ◽  
Karin H Nilsson ◽  
Robert Brommage ◽  
Petra Henning ◽  
Ulf H Lerner ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Mass ◽  
Trabecular Bone ◽  
Cortical Bone ◽  
Bone Strength ◽  
Bending Test ◽  
Bone Homeostasis ◽  
Mineral Density

WNT signaling is involved in the tumorigenesis of various cancers and regulates bone homeostasis. Palmitoleoylation of WNTs by Porcupine is required for WNT activity. Porcupine inhibitors are under development for cancer therapy. As the possible side effects of Porcupine inhibitors on bone health are unknown, we determined their effects on bone mass and strength. Twelve-week-old C57BL/6N female mice were treated by the Porcupine inhibitors LGK974 (low dose = 3 mg/kg/day; high dose = 6 mg/kg/day) or Wnt-C59 (10 mg/kg/day) or vehicle for 3 weeks. Bone parameters were assessed by serum biomarkers, dual-energy X-ray absorptiometry, µCT and histomorphometry. Bone strength was measured by the 3-point bending test. The Porcupine inhibitors were well tolerated demonstrated by normal body weight. Both doses of LGK974 and Wnt-C59 reduced total body bone mineral density compared with vehicle treatment (P < 0.001). Cortical thickness of the femur shaft (P < 0.001) and trabecular bone volume fraction in the vertebral body (P < 0.001) were reduced by treatment with LGK974 or Wnt-C59. Porcupine inhibition reduced bone strength in the tibia (P < 0.05). The cortical bone loss was the result of impaired periosteal bone formation and increased endocortical bone resorption and the trabecular bone loss was caused by reduced trabecular bone formation and increased bone resorption. Porcupine inhibitors exert deleterious effects on bone mass and strength caused by a combination of reduced bone formation and increased bone resorption. We suggest that cancer targeted therapies using Porcupine inhibitors may increase the risk of fractures.

Peak bone mass and bone loss in postmenopausal osteoporosis: Authors' reply

BMJ ◽  
1991 ◽  
Vol 303 (6816) ◽  
pp. 1548-1548 ◽  
Author(s):  
M A Hansen ◽  
K Overgaard ◽  
B J Riis ◽  
C Christiansen
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Postmenopausal Osteoporosis ◽  
Peak Bone Mass

scholarly journals Sex Steroids and the Construction and Conservation of the Adult Skeleton

2002 ◽  
Vol 23 (3) ◽  
pp. 279-302 ◽  
Author(s):  
B. Lawrence Riggs ◽  
Sundeep Khosla ◽  
L. Joseph Melton
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Cancellous Bone ◽  
Sex Steroids ◽  
Peak Bone Mass ◽  
Dietary Calcium Intake ◽  
Growth Spurt ◽  
Slow Phase ◽  
Age Related ◽  
Aging Men

Abstract Here we review and extend a new unitary model for the pathophysiology of involutional osteoporosis that identifies estrogen (E) as the key hormone for maintaining bone mass and E deficiency as the major cause of age-related bone loss in both sexes. Also, both E and testosterone (T) are key regulators of skeletal growth and maturation, and E, together with GH and IGF-I, initiate a 3- to 4-yr pubertal growth spurt that doubles skeletal mass. Although E is required for the attainment of maximal peak bone mass in both sexes, the additional action of T on stimulating periosteal apposition accounts for the larger size and thicker cortices of the adult male skeleton. Aging women undergo two phases of bone loss, whereas aging men undergo only one. In women, the menopause initiates an accelerated phase of predominantly cancellous bone loss that declines rapidly over 4–8 yr to become asymptotic with a subsequent slow phase that continues indefinitely. The accelerated phase results from the loss of the direct restraining effects of E on bone turnover, an action mediated by E receptors in both osteoblasts and osteoclasts. In the ensuing slow phase, the rate of cancellous bone loss is reduced, but the rate of cortical bone loss is unchanged or increased. This phase is mediated largely by secondary hyperparathyroidism that results from the loss of E actions on extraskeletal calcium metabolism. The resultant external calcium losses increase the level of dietary calcium intake that is required to maintain bone balance. Impaired osteoblast function due to E deficiency, aging, or both also contributes to the slow phase of bone loss. Although both serum bioavailable (Bio) E and Bio T decline in aging men, Bio E is the major predictor of their bone loss. Thus, both sex steroids are important for developing peak bone mass, but E deficiency is the major determinant of age-related bone loss in both sexes.

91313094 Role of peak bone mass and bone loss in postmenopausal osteoporosis: 12 year study

Maturitas ◽  
1992 ◽  
Vol 15 (1) ◽  
pp. 83-84
Author(s):  
M.A Hansen ◽  
K Overgaard ◽  
B.J Riis ◽  
C Christiansen
Keyword(s):  
Bone Loss ◽  
Bone Mass ◽  
Postmenopausal Osteoporosis ◽  
Peak Bone Mass

Low bone mass and fast rate of bone loss at menopause: equal risk factors for future fracture. A 15-year follow-up study

Maturitas ◽  
1997 ◽  
Vol 26 (2) ◽  
pp. 154-155
Author(s):  
B.J. Riis ◽  
M.A. Hansen ◽  
A.M. Jensen ◽  
K. Overgaard ◽  
C. Christiansen
Keyword(s):  
Risk Factors ◽  
Bone Loss ◽  
Bone Mass ◽  
Fast Rate ◽  
Low Bone Mass ◽  
Follow Up Study ◽  
Future Fracture ◽  
Rate Of Bone Loss

scholarly journals Relationship Between Pretreatment Rate of Bone Loss and Bone Density Response to Once-Yearly ZOL: HORIZON-PFT Extension Study

2015 ◽  
Vol 30 (3) ◽  
pp. 570-574 ◽  
Author(s):  
Richard Eastell ◽  
Steven Boonen ◽  
Felicia Cosman ◽  
Ian R Reid ◽  
Lisa Palermo ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Loss ◽  
Extension Study ◽  
Density Response ◽  
Rate Of Bone Loss

Effect of dietary calcium on bone density in growing rabbits

1991 ◽  
Vol 260 (3) ◽  
pp. E471-E476 ◽  
Author(s):  
V. Gilsanz ◽  
T. F. Roe ◽  
J. Antunes ◽  
M. Carlson ◽  
M. L. Duarte ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Mass ◽  
Calcium Intake ◽  
Peak Bone Mass ◽  
Skeletal Maturity ◽  
Dietary Calcium ◽  
Calcium Excretion ◽  
Vertebral Bone ◽  
Epiphyseal Closure ◽  
Renal Calcium Excretion

Reductions in peak bone mass at skeletal maturity may increase the risk for the subsequent development of osteoporosis. Although changes in calcium intake can modify the rate of decline in bone density in the mature skeleton, longitudinal assessments of the effect of dietary calcium supplementation during skeletal growth on peak bone mass have not been done in humans or experimental animals. Thus quantitative computed tomography (QCT) was used to monitor changes in vertebral bone density at 6-wk intervals during growth from 8 wk of age until skeletal maturity at 35 wk in male New Zealand White rabbits maintained on diets containing 0.15% (low Ca), 0.45% (normal Ca), or 1.35% (high Ca) calcium. Serum parathyroid hormone (PTH) and calcitriol levels increased, and renal calcium excretion decreased in low Ca compared with normal Ca; in contrast, serum calcitriol levels decreased and renal calcium excretion increased from control values in high Ca. Vertebral bone density by QCT did not differ during growth between high Ca and normal Ca, and peak values at epiphyseal closure also did not differ in these two groups. Vertebral bone density was lower, however, throughout the study in low Ca, and peak values at epiphyseal closure remained below those in either normal Ca or high Ca. Quantitative bone histology revealed decreases in cortical thickness in the third lumbar vertebra in low Ca, whereas trabecular bone area did not differ among groups; there was no histological evidence of osteomalacia in low Ca. Thus dietary calcium restriction during growth reduces peak bone mass at skeletal maturity, but raising dietary calcium intake above normal levels does not increase peak bone mass in this experimental model.

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