Osteocytes are suggested to play a central role in bone remodeling. Evaluation of iliac crest biopsies is a standard procedure for evaluating bone conditions in the clinical setting. Despite the widespread use of such biopsies, little is known about the population of osteocytes in the iliac crest from normal individuals. Contradicting results have been reported on osteocyte lacunar properties in human bone. Hence, a solid understanding of the osteocyte population in healthy bone and the effect of age and sex is needed as good reference data are lacking. Furthermore, the role of cortical bone in bone quality has recently been suggested to be more important than previously realized. Therefore, the present study assesses osteocyte lacunar properties and cortical microstructure of the iliac crest as a function of age and sex. A total of 88 iliac crest bone samples from healthy individuals (46 women, aged 18.5-96.4years and 42 men, aged 22.6-94.6years) with an even age-distribution were examined using synchrotron radiation μCT and in house μCT, with >5×10(6) osteocyte lacunae measured and analyzed. The study revealed that osteocyte lacunar volumes were unaffected by both age and sex. Osteocyte lacunar density did not differ between women and men, and only showed a significant decrease with age when pooling data from both sexes. Cortical porosity and Haversian canal density increased while cortical thickness decreased with age, with cortical thinning dominating the age-related cortical bone loss. None of the cortical microstructural parameters showed any sex dependency. Only weak links between osteocyte lacunar properties and cortical microstructural properties in iliac crest bone were found. Interestingly, the Haversian canal diameters were significantly but weakly negatively correlated with osteocyte lacunar volumes.
Pain in patients with cerebral palsy (CP) is a major health issue strongly associated with reduced quality of life. In this study, we provide an overview of pain conditions in children with CP using the International Classification of Diseases, 11th Revision (ICD-11), which has been updated with a classification of chronic pain. Common causes of pain in children with CP, including hip displacement, muscle spasms, and procedures, are discussed; less studied pain types including headaches, neuropathic pain, visceral pain, and acute versus chronic pain are also highlighted. The addition of chronic pain to the ICD-11 is an important step forward in optimizing both the registration and assessment of pain conditions. However, a tool designed specifically for the different types of pain in patients with CP is imperative. In this paper, we propose a Cerebral Palsy Pain Classification that is aligned with the underlying mechanisms of pain and the ICD-11 pain classification.
Immobilization causes rapid and massive bone loss. By comparing Botulinum Toxin A (BTX)-induced bone loss in mouse strains with different genetic backgrounds we investigated whether the genetic background had an influence on the severity of the osteopenia. Secondly, we investigated whether BTX had systemic effects on bone. Female mice from four inbred mouse strains (BALB/cJ, C57BL/6 J, DBA/2 J, and C3H/HeN) were injected unilaterally with BTX (n = 10/group) or unilaterally with saline (n = 10/group). Mice were euthanized after 21 days, and the bone properties evaluated using μCT, DXA, bone histomorphometry, and mechanical testing. BTX resulted in substantially lower trabecular bone volume fraction (BV/TV) and trabecular thickness in all mouse strains. The deterioration of BV/TV was significantly greater in C57BL/6 J (− 57%) and DBA/2 J (− 60%) than in BALB/cJ (− 45%) and C3H/HeN (− 34%) mice. The loss of femoral neck fracture strength was significantly greater in C57BL/6 J (− 47%) and DBA/2 J (− 45%) than in C3H (− 25%) mice and likewise the loss of mid-femoral fracture strength was greater in C57BL/6 J (− 17%), DBA/2 J (− 12%), and BALB/cJ (− 9%) than in C3H/HeN (− 1%) mice, which were unaffected. Using high resolution μCT we found no evidence of a systemic effect on any of the microstructural parameters of the contralateral limb. Likewise, there was no evidence of a systemic effect on the bone strength in any mouse strain. We did, however, find a small systemic effect on aBMD in DBA/2 J and C3H/HeN mice. The present study shows that BTX-induced immobilization causes the greatest loss of cortical and trabecular bone in C57BL/6 J and DBA/2 J mice. A smaller loss of bone microstructure and fracture strength was seen in BALB/cJ mice, while the bone microstructure and fracture strength of C3H/HeN mice were markedly less affected. This indicates that BTX-induced loss of bone is mouse strain dependent. We found only minimal systemic effects of BTX.
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