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Simultaneous stimulation/ inhibition of both, bone degradation and bone formation, is not supportive for regeneration.
However, the mechanism for silicate bioceramics stimulating bone formation is not fully understood.
In contrast, new bone formation is not a feature of RA.
However, these data have gained little attention as new bone formation is not a feature of RA.
The detailed mechanism of action of the stimulatory effect of simvastatin on bone formation is not well understood.
Additionally, no differences were observed in trabecular or cortical bone of femurs from 1- and 2-year-old KO and WT mice, indicating intramembranous bone formation is not affected by the lack of ASK1.
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However, new bone formation was not observed (Fig. 3a, b).
In sarcoidosis, well-demarcated cystic lesions are found in the phalanges of the fingers, although bony expansion and periosteal new bone formation are not found [10, 14].
Therefore, quantification of the rate of bone formation was not possible.
Interestingly, this near abolishment of bone formation was not accompanied by changes in the expression of well-established osteoblast differentiation markers, such as Col1a1, Bglap or Ibsp (Figure 6E), which is further underscored by the finding that serum osteocalcin levels and alkaline phosphatase activities were not significantly decreased in 6 weeks old female Col1a1-Krm2 mice (Figure 6F).
No changes were observed on osteoid, indicating that bone formation was not disturbed.
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