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A second important turning point in the field, with novel therapeutic implications, is the appreciation that chronicity may emerge from persistent and exacerbated pro-inflammatory signals as well as from the failure of the resolution pathways, a concept now well accepted for example to explain the chronicity of rheumatoid arthritis where aggressive fibroblasts are key players (135)

Bone softening happens because of insufficient key nutrients like calcium, vitamin D and phosphate required for bone architecture

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It scavenges free radicals, mitigates oxidative stress, and suppresses pro-inflammatory mediators like TNF- , IL-6, and COX-2 by inhibiting the NF-B signaling pathway (11, 12, 26, 27)

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