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T-score ≥ −1


T-score between −1 and −2.5


T-score ≤ −2.5


Fractures occur spontaneously or following minimal trauma, defined as falling from a standing height or less. Fractures of the vertebrae, hips, and distal radius (Colles’ fracture) are the most characteristic fragility fracture, but patients with osteoporosis are prone to all types of fractures. Up to 40% of women and 13% of men develop one or more osteoporotic fractures during their lifetime.

Factors that contribute most to the risk of developing an osteoporotic fracture:

  • Low BMD (twofold increased risk for every one standard deviation [SD; T-score] decrease of BMD)
  • Age (twofold increased risk for every decade of age above 60 years)
  • Previous fragility fracture (fivefold increased risk for a subsequent fracture)
  • Frequent falls
  • Corticosteroid use

Complications of osteoporotic fractures

Vertebral fractures cause loss of height, anterior kyphosis (dowager’s hump), reduced pulmonary function (each fracture decreases FVC by 9%), and an increased mortality rate. Approximately one third of all vertebral fractures are painful but two thirds are asymptomatic. Hip fractures are associated with permanent disability in nearly 50% of patients and with a 20% excess mortality rate compared to the age-matched nonfracture population.


Affect both phases of bone remodeling leading to rapid loss of bone. They impair bone formation by promoting apoptosis of existing osteoblasts and reducing the development of new osteoblasts. They increase bone resorption by decreasing the production of sex steroids and osteoprotegerin, an endogenous inhibitor of bone resorption. Osteocytes are also affected and undergo apoptosis.

Pharmacological therapy should be advised for patients who have any one of the following:

• a history of vertebral or hip fragility fracture,

• a T-score < −2.5,

• are drug-naïve and over the age of 40 years with osteopenia, and have a 10-year risk ≥3% for hip fracture or ≥20% for other major osteoporosis fractures according to the FRAX tool.

Vitamin D metabolism and action:

There are two natural forms of vitamin D: cholecalciferol (D3) and ergocalciferol (D2). Humans acquire vitamin D by two routes: endogenous synthesis in the skin during sunlight exposure (D3) and dietary intake (D2 and D3). Vitamin D from either source is converted in the liver by 25-hydroxylase to 25-OH vitamin D and fluticasone propionate - salmeterol xinafoate (Advair) then by 1-alpha-hydroxylase in the kidney to 1,25-dihydroxy (OH)2 vitamin D. The latter binds to intestinal vitamin D receptors to promote calcium and phosphorous absorption. Parathyroid hormone (PTH) and hypophosphatemia are major inducers of 1-alpha-hydroxylase activity. As a patient becomes vitamin D deficient and serum calcium decreases, the PTH level increases inducing the 1-alpha-hydroxylase enzyme to convert 25-OH vitamin D into 1,25 (OH)2 vitamin D. Therefore, the 25-OH vitamin D level will decrease before the 1,25 (OH)2 vitamin D level. For this reason, measuring the 25-OH vitamin D level is the best measure of vitamin D stores.






Das schmeckt: kalziumreiche Nahrungsmittel

Gesunde Knochen und Muskeln Richtig essen – genügend bewegen

The National Osteoporosis Foundation (NOF)

American Society for Bone and Mineral Research

The International Society for Clinical Densitometry (ISCD)

SRG ( (German)



Fracture Risk Assessment Tool (FRAX)

Hip Fracture Risk Calculator

Aktiv gegen Osteoporose - Patientenbroschüre Rheumaliga Schweiz (inkl. PDF) (German)

Osteoporose - Patientenbroschüre Rheumaliga Schweiz (German)