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anot all studies reported duration of OA; bone study did not report mean age; NR = not reported.
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Using classical design optimization methods for implant-bone studies does not completely guarantee a safety and satisfactory performance, due in part to the randomness of bone properties and loading.
Although PTH has been shown to promote osteoclastogenesis in certain (but not all) physiological and experimental conditions [20], [23], [43], the numbers of osteoclasts in myelomatous bones in our study did not increase during the experimental period.
Thus, transplanted MSCs are likely to contribute to the regeneration of subchondral bone, although the present study did not address this issue.
Lastly, the measurements recorded from the bone models analyzed in this study did not contain hyaline cartilage.
We could not confirm this as the synovial tissue specimens from the RA patients used in this study did not include bone [ 55, 61].
The biochemical and bone remodeling parameters assessed in this study did not show significant differences in patients with IBD with or without fractures or in healthy subjects.
Medians and arithmetic means calculated for the bone of all goosanders in this study did not exceed 300 and 470 mg/kg dw, respectively, and were lower than the values from other reports.
In order to avoid inaccuracies in tests results, which could be the result of the impact of factors other than the level of sex hormones on bone status, patients that qualified for the study did not differ significantly in terms of age, physical activity, oral hygiene, general health, oral health status, or duration of hormone replacement therapy.
Finally, the current study did not investigate the mechanisms for bone damage in type 1 diabetes.
The study did not demonstrate any correlation between absolute bone density and the relative level of the stress shielding.
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