Internal Diseases and Therapy · MU Sofia

55. Osteoporosis

Explains osteoporosis as a skeletal disorder of reduced bone mass and fragility, with its fracture, pain and height-loss consequences. Covers the T-score thresholds against osteopenia, fragility fractures, bone remodelling and the post-menopausal loss of bone, then diagnosis by DXA and the FRAX risk model. Ends with management: lifestyle measures and drug options such as bisphosphonates, SERMs and denosumab.

Inside: 1 section · 2 labelled pictures · 15 flashcards · 4 min

Topic 55 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 579 words (4 min of reading), with 15 flashcards.

In this note

  1. Osteoporosis

Osteoporosis

Osteoporosis is a skeletal disorder characterised by decreased bone mass and structural deterioration of bone with consequent increase in bone fragility and susceptibility to fracture. The permanent clinical consequences of the disease include fractures, bone pain, height loss and physical deformity.

Image: “Osteoporosis -- Smart-Servier” by Laboratoires Servier, CC BY-SA 3.0, via Wikimedia Commons.

Bone density is said to be osteoporotic if it is equal to or greater than 2.5 standard deviations below the mean at peak bone mass (this is in comparison to osteopenia which is between 1 and 2.5 standard deviations below the mean).

Fragility fractures are common in osteoporotic patients, and are defined as fractures caused by mechanical forces that would not ordinarily result in a fracture (so called low-level trauma). In practice these are falls that occur at a standing height or less.

Osteoporosis is common in white women, in fact, half will develop an osteoporotic fracture in their lifetime. Common fractures are the vertebrae, the hip (proximal femur) and the wrist.

To understand pathogenesis, it is important to understand bone remodeling. Osteocytes are the most important cell in the remodelling process, they are derived from osteoblasts and as they mature (during the osteoid-osteocyte phase) there is secretion and calcification of bone matrix material. When bone needs to be resorbed this is done directly through apoptosis proximate to skeletal microcracks or fatigue damage in need of repair and indirectly through enhancement of pre-osteoblast or mesenchymal stromal development.

Physical activity, hormones and genetic factors are all important in the process of achieving peak bone mass by the third decade. Sex hormones in particular play a critical role in growth of the long bones and axial skeleton. Once through childhood, from the age of about 30 onwards, the balance of bone deposition and bone remodeling is about even (or at least it should be).

As we get older, there is naturally some loss of bone (osteopenia), however, for older women especially, there is a marked increase post menopause, with losses of up to 5% of bone density per year. This loss is reduced in obese women, it is thought because of their increased estrogen from adipose tissue. A decline in circulating estrogen is primarily responsible for bone loss following both natural and surgical menopause, which is mediated through upregulation of cytokines and results in increased osteoclast activity.

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