Corrigendum: Nitazoxanide, an antiprotozoal drug, reduces bone loss in ovariectomized mice by inhibition of RANKL-induced osteoclastogenesis.

[This corrects the article DOI: 10.3389/fphar.2021.

Distinct pathological changes of osteochondral units in early OVX-OA involving TGF-β signaling.

Introduction: Different opinions exist about the role of subchondral bone in osteoarthritis (OA), probably because subchondral bone has different effects on cartilage degeneration in OA induced by different pathologies. Animal studies to illustrate the role of subchondral bone in cartilage degeneration were mostly based on post-traumatic OA (PT-OA). Postmenopausal women experience a much higher occurrence of OA than similar-aged men.

Nitazoxanide, an Antiprotozoal Drug, Reduces Bone Loss in Ovariectomized Mice by Inhibition of RANKL-Induced Osteoclastogenesis.

Nitazoxanide (NTZ) is an FDA-approved anti-parasitic drug with broad-spectrum anti-infective, anti-inflammatory, and antineoplastic potential. However, its regulatory effects on osteoclastogenesis and the underlying mechanisms remain unclear. The present study found that NTZ potently inhibited osteoclast formation at the early stage of receptor activator of NF-κB ligand-induced osteoclastogenesis in a concentration-dependent manner at a non-growth inhibitory concentration.

Cellular alterations and crosstalk in the osteochondral joint in osteoarthritis and promising therapeutic strategies.

Osteoarthritis (OA) is a joint disorder involving cartilage degeneration and subchondral bone sclerosis. The bone-cartilage interface is implicated in OA pathogenesis due to its susceptibility to mechanical and biological factors. The crosstalk between cartilage and the underlying subchondral bone is elevated in OA due to multiple factors, such as increased vascularization, porosity, microcracks and fissures.

Macroporous scaffolds developed from CaSiO nanofibers regulating bone regeneration via controlled calcination.

Calcium silicate (CS) is envisioned as a good substrate for bone tissue engineering applications because it can provide bioactive ions like Ca and Si to promote bone regeneration. Calcination temperature is a critical factor in determining the crystallinity of CS ceramic, which subsequently influences its degradation and ion release behaviors. To investigate the effect of calcination temperature on the capacity of CS in inducing bone regeneration, CS nanofibers were fabricated via electrospinning of precursor sol-gel and subsequent sintering at 800 °C, 1000 °C or 1200 °C.

Efficient regeneration of rat calvarial defect with gelatin-hydroxyapatite composite cryogel.

To induce bone regeneration efficiently, a properly designed organic-inorganic composite scaffold is necessary and important. Gelatin-hydroxyapatite (HA) composite is a suitable choice for the purpose because it can resemble the chemical composition of natural bone tissue. The gelatin-HA composite can be implanted into bone defects as a hydrogel or cryogel, however, it is interesting to know the effect of their different morphology on inducing osteogenesis in vivo.

Phenotype changes of subchondral plate osteoblasts based on a rat model of ovariectomy-induced osteoarthritis.

Background: Osteoarthritis (OA) is prevalent in postmenopausal women. Subchondral bone in ovariectomized (OVX) rats might play a more important role in cartilage degeneration compared with other types of OA. How subchondral osteoblast changes in OVX rats is still unclear.

Identification of Candidate Genetic Markers and a Novel 4-genes Diagnostic Model in Osteoarthritis through Integrating Multiple Microarray Data.

Background: Osteoarthritis (OA) is a joint disease that leads to a high disability rate and a low quality of life. With the development of modern molecular biology techniques, some key genes and diagnostic markers have been reported. However, the etiology and pathogenesis of OA are still unknown.

[Fluid-solid coupling numerical simulation on ideal porous structure of rat alveolar bone].

Fluid shear stress (FSS) caused by interstitial fluid flow within trabecular bone cavities under mechanical loading is the key factor of stimulating biological response of bone cells. Therefore, to investigate the FSS distribution within cancellous bone is important for understanding the transduction process of mechanical forces within alveolar bone and the regulatory mechanism at cell level during tooth development and orthodontics. In the present study, the orthodontic tooth movement experiment on rats was first performed.