Arachidonic Acid and Docosahexaenoic Acid Suppress Osteoclast Formation and Activity in Human CD14+ Monocytes, In vitro

Kasonga, Abe; Deepak, V.; Kruger, Marlena C.

doi:10.1371/journal.pone.0125145

Cited by 54 publications

(73 citation statements)

References 53 publications

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“…Previous studies have reported the effects of DHA, but not EPA, to inhibit osteoclastogenesis induced by RANKL at the late stage of differentiation in murine bone marrow‐derived macrophages . DHA added at early stage of differentiation to human primary monocytes was shown to suppress OC formation and activity via M‐CSF‐RANKL . Similar findings of DHA and arachidonic acid (DHA > arachidonic acid) inhibiting osteoclastogenesis were noticed in murine RAW264.7 cells .…”

Section: Discussionsupporting

confidence: 55%

Acute effects of dietary fatty acids on osteclastogenesis via RANKL/RANK/OPG system

Naranjo

Garcia

Bermúdez

et al. 2016

Molecular Nutrition Food Res

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For the first time, we show that postprandial TRLs are metabolic entities with osteoclastogenic activity and that this property is related to the type of dietary fatty acid in the meal. The osteoclastogenic potency was as follows: SFAs >>> MUFAs = PUFAs. These exciting findings open opportunities for developing nutritional strategies with olive oil as the principal dietary source of MUFAs, notably oleic acid, to prevent development and progression of osteoclast-related diseases.

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Section: Discussionsupporting

confidence: 55%

Acute effects of dietary fatty acids on osteclastogenesis via RANKL/RANK/OPG system

Naranjo

Garcia

Bermúdez

et al. 2016

Molecular Nutrition Food Res

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show abstract

“…Cornish et al found that a GPR120/40 agonist mimicked the anti-osteoclastogenic actions of fatty acids, identifying a link between lipid and bone metabolism [41]. More recently, Kasonga et al studied the effects of DHA and ARA on osteoclast formation and activity by isolating CD14+ monocytes [42]. Results from this study revealed that both types of long-chain PUFAs decrease the formation potential of osteoclasts in a dose-dependent manner at early stages of differentiation.…”

Section: Discussionmentioning

confidence: 80%

Effects of dietary omega-3 fatty acids on bones of healthy mice

et al. 2019

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Subtle differences were noted at the bones' microstructural level, however these are likely the result of random effects that do not translate into changes that are biologically relevant. Similarly, differences were not seen at the mechanical level, nor were they reflected in blood-based biomarkers of bone metabolism. Altogether, dietary consumption of PUFA do not seem to affect bone structure or metabolism in a healthy model of growing mice.

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“…21) RAW264.7 macrophages (5×10 3 /well) were exposed to 200 ng/mL of LPS in the presence or absence of carvacrol (15 µg/mL) and were differentiated for 7 d.…”

Section: Methodsmentioning

confidence: 99%

Carvacrol Inhibits Osteoclastogenesis and Negatively Regulates the Survival of Mature Osteoclasts

Deepak

Kasonga

Kruger

et al. 2016

Biological & Pharmaceutical Bulletin

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Bone is a dynamic tissue that undergoes continuous remodeling coupled with the action of osteoblasts and osteoclasts. Osteoclast activity is elevated during osteoporosis and periodontitis resulting in excessive loss of trabecular and alveolar bone. Osteoclasts are formed in an inflammatory response to cytokine production receptor activator of nuclear factor-kappaB (NF-κB) ligand (RANKL) and bacterial challenge lipopolysaccharide (LPS). Carvacrol, a monoterpenic phenol present in Origanum vulgare and Thymus vulgaris, is a natural compound with known medicinal properties. We investigated the effects of carvacrol Key words osteoclast; osteoporosis; periodontitis; receptor activator of nuclear factor-κB ligand (RANKL); lipopolysaccharide (LPS) Bone homeostasis is tightly coupled to the bone-forming activity of osteoblasts and bone-resorbing activity of osteoclasts.1) Osteoclasts are multi-nucleated cells that arise from hematopoietic progenitors of monocyte/macrophage lineage and specialize in bone resorption.2) Bone-loss related diseases such as osteoporosis and periodontitis are associated with increased osteoclast formation and elevated osteoclast activity. [3][4][5] Binding of receptor activator of nuclear factor-κB ligand (RANKL) to its receptor RANK in osteoclast precursors triggers trimerization of the receptor and subsequent activation of downstream signaling pathways that includes inhibitor of kappaB (IκB)-a/b kinase (IKK), nuclear factor kappa-B (NF-κB), mitogen-activated protein kinases (MAPKs)-p38, extracellular-signal-regulated kinase (ERK) and c-Jun Nterminal kinase (JNK).6) Activation of these pathways leads to the formation of tartrate resistant acid phosphatase-positive (TRAP+) osteoclasts and bone resorption.Development of apical periodontitis is associated with the presence of microorganisms in the root canal system. 7) Gramnegative bacteria are the most common causative agents in endodontic infections. 8) Bacterial death causes release of lipopolysaccharide (LPS) in the necrotic pulp and dental wall of periapically affected teeth. 9) LPS elicits alveolar bone loss during periodontitis. 10) LPS stimulates the secretion of cytokines by osteoclast precursors such as monocytes and macrophages, resulting in osteoclast formation and bone resorption in vitro and in vivo.11) Earlier studies have also shown that injection of LPS into mouse gingiva induces alveolar bone resorption. 12)

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Arachidonic Acid and Docosahexaenoic Acid Suppress Osteoclast Formation and Activity in Human CD14+ Monocytes, In vitro

Cited by 54 publications

References 53 publications

Acute effects of dietary fatty acids on osteclastogenesis via RANKL/RANK/OPG system

Acute effects of dietary fatty acids on osteclastogenesis via RANKL/RANK/OPG system

Effects of dietary omega-3 fatty acids on bones of healthy mice

Carvacrol Inhibits Osteoclastogenesis and Negatively Regulates the Survival of Mature Osteoclasts

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