Abstract
Chronic inflammation and oxidative stress are two major mechanisms leading to the imbalance between bone resorption and bone formation rate, and subsequently, bone loss. Thus, functional foods and dietary compounds with antioxidant and anti-inflammatory could protect skeletal health. This review aims to examine the current evidence on the skeletal protective effects of propolis, a resin produced by bees, known to possess antioxidant and anti-inflammatory activities. A literature search was performed using Pubmed, Scopus, and Web of Science to identify studies on the effects of propolis on bone health. The search string used was (i) propolis AND (ii) (bone OR osteoporosis OR osteoblasts OR osteoclasts OR osteocytes). Eighteen studies were included in the current review. The available experimental studies demonstrated that propolis could prevent bone loss due to periodontitis, dental implantitis, and diabetes in animals. Combined with synthetic and natural grafts, it could also promote fracture healing. Propolis protects bone health by inhibiting osteoclastogenesis and promoting osteoblastogenesis, partly through its antioxidant and anti-inflammatory actions. Despite the promising preclinical results, the skeletal protective effects of propolis are yet to be proven in human studies. This research gap should be bridged before nutraceuticals based on propolis with specific health claims can be developed.
Highlights
The skeletal system consisting of dense connective tissues, mainly bone, is metabolically active and functionally diverse
Bone remodelling refers to the skeletal reparative process, whereby small areas of bone are resorbed by osteoclasts and replaced by osteoblasts to prevent the accumulation of microfractures and preserve mineral homeostasis by releasing calcium and phosphorus into the circulation
Oxidative stress favours osteoclast formation and bone resorption while hampering osteoblast formation and bone formation, leading to bone loss [7,8,9]. These skeletal effects are achieved by activating signalling pathways, such as mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERK1/2), c-Jun-N terminal kinase (JNK), and p38 MAPK [10,11,12]
Summary
The skeletal system consisting of dense connective tissues, mainly bone, is metabolically active and functionally diverse It undergoes modelling (construction) and remodelling (reconstruction) process in response to stimuli throughout our lifetime [1,2]. Bone remodelling refers to the skeletal reparative process, whereby small areas of bone are resorbed by osteoclasts and replaced by osteoblasts to prevent the accumulation of microfractures and preserve mineral homeostasis by releasing calcium and phosphorus into the circulation. Oxidative stress favours osteoclast formation (osteoclastogenesis) and bone resorption while hampering osteoblast formation (osteoblastogenesis) and bone formation, leading to bone loss [7,8,9] These skeletal effects are achieved by activating signalling pathways, such as mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERK1/2), c-Jun-N terminal kinase (JNK), and p38 MAPK [10,11,12]. Vitamin C, vitamin E, polyphenols, and other antioxidants have been shown to promote osteoblastogenesis, as well as preventing oxidative stress-induced apoptosis of osteoblasts and osteoclastogenesis [15,16,17,18]
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