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. 2023 Nov 23;24(23):16648. doi: 10.3390/ijms242316648

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Schematic representation of the mechanism of Ptx3 regulation of OB and OC formation and function in homeostatic and inflammatory conditions. Left: In conditions of bone homeostasis, PTX3 is synthesized by pre- and mature OBs (1); the released protein inhibits RANKL production (2) and stimulates OPG release (3). This results in reduced RANKL/OPG ratio, which helps restraining osteoclastogenesis (4). A similar effect might be contributed to by the PTX3-dependent control of CD44 expression on OBs (5). Right: Inflammatory conditions (i.e., TNF-α stimulation) increase PTX3 expression in OBs (6). The newly synthesized protein, possibly via the HA network and the engagement of CD44 (7), stimulates collagen production and deposition by OBs (8). At the same time, TNF-α has direct osteoclastogenic effects on OC precursors (9). Also, PTX3 is required for OBs to make and release inflammatory chemokines like CCL2 and CCL3 (10). Created with BioRender.com.