Overview of Rickets and Vitamin D

Summary of Rickets and Vitamin D


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 127 items


Image



Breathing

History

Turkey

Mongolia

Other countries

Rickets - World

  • Nutritional rickets around the world: an update - 2016
    PDF is available free at Sci-Hub   10.1080/20469047.2016.1248170
    Nigeria 1 in 170; Gambia 1 in 70; Bangladesh 1 in 12

Recent Increase

Prevention and treatment

Shaken-baby syndrome

Associated with Dark skin and breastfed

Animals

Rickets Other

How much Vitamin D needed to stop rickets

Other Vitamin D


PDF Re-emerging Nutriional Rickets - 2005, is attached at the bottom of this page

PDF Rickets in Children is attached at the bottom of this page

PDF History of Rickets before the discovery of vitamin D (Jan 2014) is attached at the bottom of this page
Treating rickets by having children on a veranda - 1923
Image

PDF Good Seminar on Rickets - Lancet May 2014 is attached at the bottom of this page
Need 400 IU


Image Image

Forensic Science, Medicine, and Pathology, January 2015, $40 for PDF
Results
In the case of rickets, there was marked architectural disorganization of endochondral ossification at the costochondral junctions and growth plates of long bones. The child abuse-related fractures showed osteochondral callus at different stages of healing, either centered on a discrete fracture line or at metaphyses (e.g. classical metaphyseal lesions). In many instances, the healing fractures disrupted the line of endochondral ossification. In none of the child abuse-related fractures was there any similarity to the histologic appearance of rickets.
Conclusion
The maturation disturbance in the growth plate that occurs in rickets is a distinctive entity that cannot be confused histologically with healing fractures, including the classical metaphyseal lesion.
Includes 20 references - free


Vitamin D Status in Abused and Nonabused Children Younger Than 2 Years Old With Fractures - 2011

 Download the PDF from VitaminDWiki


See also web


In some regions late-onset Rickets may be due to low Calcium


6 Types of rickets"low vitamin D, poor vitamin D receptor. etc.

Poor vitamin D Receptor limits vitamin D in blood from getting to the bones
Image
 Download the PDF from VitaminDWiki


The RESISTANCE of Vitamin D Resistent Rickets may be due to Vitamin D RECEPTOR - March 2019

Detecting reasons for recurrent deformity in treatment of patients with vitamin D-resistant rickets using diagnostic imaging
J Orthop. 2019 Mar 22;16(4):325-328. doi: 10.1016/j.jor.2019.02.033. eCollection 2019 Jul-Aug.
Diachkova GV1, Novikov KI2, Effatparvar MR3, Chistova EA1, Diachkov KA1, Novikova OS1, Korkin AY4, Shikhaleva NG5.

PURPOSE: To assess age related manifestations of the femur and tibia in patients with vitamin D-resistant rickets (VDR) and explore causes for recurrent deformity using imaging modalities.

METHODS: Computed tomography (CT), magnetic resonance imaging (MRI) and dual energy X-ray densitometry (DEXA) were used to assess conditions of long bones of lower limbs in patients with vitamin D-resistant rickets aged from 4 years to 30 years preoperatively and after limb lengthening.

RESULTS:
Age related MRI findings showed specific structure of the femur and tibia in patients with (VDR) preoperatively and after operative treatment. Abundant irregular osteoid formed in femoral and tibial physes was shown to reveal complicated nature of bone deformity causing recurrence in patients with (VDR) at childhood. CT findings allowed us to detect early cortical injury, measure its length with forming Looser's zones, examine significant differences in density measurements of Looser's zones preoperatively and after deformity correction using transosseous osteosynthesis.

CONCLUSION:
Recurrent deformity can develop in patients with (VDR) due to progression of the disease, irregular osteoid deposited in the medial and lateral metaepiphysis, osteoid area measuring over 50% of epiphyseal cross section, insufficient regenerate mineralization, and formation of Looser's zones.

81742 visitors, last modified 03 Sep, 2024,
Printer Friendly Follow this page for updates