Solar and nutritional Osteomalacia (soft bones at all stages of life) – Jan 2019

Spot the silent sufferers: A call for clinical diagnostic criteria for solar and nutritional osteomalacia.

J Steroid Biochem Mol Biol. 2019 Jan 14. pii: S0960-0760(18)30542-9. doi: 10.1016/j.jsbmb.2019.01.004.
Uday S1, Högler W2.


Overview of Rickets and vitamin D contains the following summary
Rate of rickets is usually < 0.1% of births, unless dark skin, breastfed, preemie, twin, Mongolian, or Russian
Rate of rickets has greatly increased with the drop in vitamin D levels during the past 40 years
400 IU can prevent/treat most rickets Turkey gave vitamin D to EVERY child and eliminated Rickets
Can have rickets without a low serum level of vitamin D (~20% of the time)
Giving enough Vitamin D to the mother (before and after birth) PREVENTS most forms of Rickets
Rate of rickets in some countries varies from 10% to 70% (typically poor health overall)
Rickets has been more than doubling in many countries
Rickets is strongly associated with severe breathing problems (weak ribs)
Bowed legs is not the primary indication of rickets    (3 other indications of rickets are seen more often)
Rickets is typically due to low cellular Vitamin D - April 2024
Some Rickets is due to poor genes - Vitamin D needed lifelong – June 2020
Vitamin D and Rickets consensus took 80 years

Rickets category has 128 items
Image Image

Osteomalacia in children = Rickets

Osteomalacia definitions

  • Osteomalacia Wikipedia
    "Osteomalacia in children is known as rickets, and because of this, use of the term "osteomalacia" is often restricted to the milder, adult form of the disease"
  • Mayo Clinic: Osteomalacia refers to a marked softening of your bones, most often caused by severe vitamin D deficiency
  • Arthritis UK Osteomalacia often develops because of a lack of vitamin D.
    It can cause bone pain and muscle weakness.
    In children it used to be called rickets, but nowadays it more often affects adults

Bone Pain

Magnesium is also needed to build strong bones
Items in both categories Bones and Magnesium are listed here:

 Download the PDF from Sci-Hub via VitaminDWiki

Osteomalacia and rickets result from defective mineralization when the body is deprived of calcium. Globally, the main cause of osteomalacia is a lack of mineral supply for bone modeling and remodeling due to solar vitamin D and/or dietary calcium deficiency. Osteomalacia occurs when existing bone is replaced by unmineralized bone matrix (osteoid) during remodeling in children and adults, or when newly formed bone is not mineralized in time during modeling in children. Rickets occurs when hypomineralization affects the epiphyseal growth plate chondrocytes and adjacent bone metaphysis in growing children. Hence, osteomalacia co-exists with rickets in growing children. Several reports in the last decade highlight the resurgence of so-called "nutritional" rickets in the dark-skinned population living in high-income countries.

However, very few studies have ever explored the hidden iceberg of nutritional osteomalacia in the population.

Rickets presents with hypocalcaemic (seizures, tetany, cardiomyopathy), or hypophosphataemic complications (leg bowing, knock knees, rachitic rosary, muscle weakness) and is diagnosed on radiographs (cupping and fraying of metaphyses).

In contrast, osteomalacia lacks distinctive, non-invasive diagnostic laboratory or imaging criteria and the clinical presentation is non-specific (general fatigue, malaise, muscle weakness and pain). Hence, osteomalacia remains largely undiagnosed, as a hidden disease in millions of dark-skinned people who are at greatest risk. Radiographs may demonstrate Looser's zone fractures in those most severely affected, however to date, osteomalacia remains a histological diagnosis requiring a bone biopsy. Biochemical features of high serum alkaline phosphatase (ALP), high parathyroid hormone (PTH) with or without low 25 hydroxyvitamin D (25OHD) concentrations are common to both rickets and osteomalacia.

Here, we propose non-invasive diagnostic criteria for osteomalacia. We recommend a diagnosis of osteomalacia in the presence of

  • high ALP,
  • high PTH,
  • low dietary calcium intake (<300 mg/day)
  • and/or low serum 25OHD (<30 nmol/L).

Presence of clinical symptoms (as above) or Looser's zone fractures should be used to reaffirm the diagnosis. We call for further studies to explore the true prevalence of nutritional osteomalacia in various populations, specifically the Black and Asian ethnic groups, in order to identify the hidden disease burden and inform public health policies for vitamin D/calcium supplementation and food fortification.

From chart in the PDF

  • Pregnancy/Birth: Obstructed labour, neonatal hypocalcaemia, low birth weight
  • Infant: craniotabes, seizures , dilated cardiomyopathy leading to heart failure and cardiac death, hypotonia, poor feeding, restlessness, irritability, leg bowing
  • Child: muscle weakness, delayed development and dentition, swelling of wrists and ankles, leg bowing deformities
  • Adolescent: Hypocalcaemic seizures, tetany, bone pain, muscle weakness, fractures
  • Young adult/adul: Fatigue, bone pain, muscular pain and weakness, difficulty rising from sitting position, waddling gait
  • Old age: fatigue, malaise, muscle weakness, muscle pain, falls and fractures

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