Table 1 OPN involves inflammation activity in OA and OP.

Reference	disease	Subjects	cytokines	Main results
Hannah Slovacek, et al. (49)	OA	Blood samples	MMP-9, ADAMTS-4	OPN and ADAMTS-4 inversely fluctuated post-operatively of total joint arthroplasty upregulation of MMP-9 and OPN results in the downregulation of ADAMTS-4.
Jian Tian, et al. (27)	OA	Chondrocytes	IL-1β, TNF-ɑ, MMP-13, ADAMTS-5	OPN deficiency increased the expressions of COL10A1, IL-1β, TNF-ɑ, MMP-13, and ADAMTS-5, but decreased the expression of COL2A1 in chondrocytes, finally accelerated OA progress.
Qiyuan Wang, et al. (50)	OA	Synoviocytes	MMP-13, IL-6, IL-8	OPN upregulates expression of inflammatory factors MMP-13, IL-6 and IL-8 in OA tissues. Inhibiting OPN expression and synoviocyte proliferation is an efficient strategy for OA treatment.
Shenglong Li, et al. (51)	OA	Rat adipose mesenchymal stem cell	IL-1β	IL-1β treatment significantly inhibites the viability and migration of chondrocytes, enhances cell apoptosis andinduced cartilage damage by upregulating IL-1β, OPN, p53 and decreasing the expression of COL1A1, COL2A1, OCN, RUNX2.
Tsai Sen-Wei, et al. (52)	OA	Sprague-Dawley rats	NO, PGE2, iNOS, COX-2	OPN level was inhibited by isorhamnetin accompanied with the down-regulated level of NO, PGE2, iNOS and COX-2 in MIA-induced OA rats.
Jean Cassuto, et al. (53)	OA	Blood samples	CRP, IL-6	Inflammatory mediators CRP, IL-6 increased significantly on day one after surgery vs preoperative value and returned to baseline at 6 week in arthroplasty patients.
María García-Manrique, et al. (54)	OA	Blood samples and synovial fluid	IL-8, TNF	IL-8 in synovial fluid is related to clinical severity and progression in knee osteoarthritis.
Yuichiro Matsui, et al. (55)	OA	C57BL/6 mice	MMP-13	OPN deficiency leads to the induction of MMP-1, which degrades a major component of the cartilage matrix protein type II collagen in mice.
Bao-Ming Tang, et al. (56)	OP	Sprague-Dawley rats	IL-1β, TNF-α, IL-6	Inflammation mediated osteoporosis presented apparently down-regulated in OPN and OCN levels, higher serum IL-1β, TNF-α, IL-6 levels in ovariectomized rats.
Krzysztof Marycz, et al. (57)	OP	MC3T3-E1 cell lines	iNOS, TNF-α, Il-1β	NHAp/IO@miR-21/124 could enhance osteogenesis through increasing osteogenic markers Runx-2, OPN, Coll-1 level, inhibiting the expression of inflammatory markers TNF-α, iNOs or IL-1β in LPS-stimulated cells.
Xiang Gao, et al. (58)	OP	Lewis rats	TNF-α, IL-6	Salvianolate treatment could increase Osterix, OPN, Runx2 level and decrease TNF-α, IL-6 level in serum and IL-1β protein in TNF-α-induced MC3T3-E1 osteoblasts, finally ameliorate osteopenia and improved bone quality.
Wei-Ming Li, et al. (59)	OP	C57BJ/6 L mice	TNF-α, IL-1β, IL-6, CCL-2	Silenceing angiopoietin-like protein2 (ANGPTL2) reduces nuclear factor of activated T cell c1/4 (NFATC1/4) expressions in macrophage colony-stimulating factor -treated cells, decreases Runx2, OPN and Colla1 level and accompanied with down-regulating level pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 and CCL-2.
Chen Lei, et al. (60)	OP	C57B/L6 mice and osteoclasts	TNF-α, IL-1β, IL-6, and MMP-1	MLN64-knockdown alleviates the severity of osteoporosis, down-regulates specific genes related to osteoclastogenesis including Runx2 and inflammatory factors such as TNF-α, IL-1β, IL-6, and MMP-1.
Yu-Qiong He, et al. (61)	OP	C57/BL6 mice and MC3T3-E1 osteoblast-like cells	IL-6, IL-1β and NO	Monotropein increases the proliferation and activity of ALP, bone matrix mineralization and OPN in osteoblastic MC3T3-E1 cells, decreases the production of IL-6, IL-1β and NO.