Fibrosis is a pathological feature of a variety of chronic inflammatory diseases that can affect almost all organs, which can cause severe consequences and even lead to death. Fibrosis is characterized by the excessive accumulation of extracellular matrix (ECM) due to disruption of the balance between ECM production and degradation. Although overabundance of ECM proteins has long been the focus of studies on fibrosis, another facet of the problem—impaired degradation of the ECM—is gaining increasing attention. Matrix metalloproteinase (MMP) and the tissue inhibitor of metalloproteinase (TIMP) system is the main molecular system contributing to ECM degradation, and macrophages are the major regulators of ECM. However, the relationship among macrophages, the MMP/TIMP system and the ECM is not fully understood in the context of fibrosis. Here, we discuss in detail the role played by the ECM in the development of fibrosis and highlight the macrophage-MMP-ECM interaction that is involved in fibrogenesis and may be a potential therapeutic target for fibrosis.

The possibility of spontaneous papillae regeneration after implant treatment and the long-term stability of the regenerated papillae were confirmed. However, recession of the facial soft tissue has been found. The incidence of the recession at thin biotype sites tended to be higher.

Nano-sized magnetic minerals (NSMMs) have been studied extensively due to their capability of carrying stable remanence over billions of years (e.g., Evans et al., 1968;Tarduno et al., 2006), which makes significant contributions to the preservation of paleomagnetic and paleoenvironmental records preserving in sediments (

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