PQQ and vascular calcification AI Overview and one or two papers, osteoporosis, Bone Mineral Density, renal health, testosterone, periodontitis
Pyrroloquinoline quinone (PQQ) has been shown to play a role in regulating bone metabolism and preventing calcification, potentially through its antioxidant and mitochondrial enhancing properties. Studies suggest PQQ can inhibit osteoclast activity and promote bone formation, potentially offering protection against age-related osteoporosis and fracture healing delays. Furthermore, PQQ's ability to reduce oxidative stress and apoptosis in vascular smooth muscle cells may also contribute to preventing vascular calcification.
PQQ and Bone Health:
Inhibition of Bone Resorption:
PQQ can suppress osteoclast differentiation and activity, thus reducing bone resorption.
PQQ can stimulate bone formation, potentially through inhibiting osteoblastic DNA damage and promoting fibrillin-1 expression.
PQQ supplementation has been shown to improve fracture healing in estrogen-deficient mice by promoting bone formation and reducing bone resorption.
PQQ may be beneficial in preventing and treating age-related osteoporosis by reducing oxidative stress and promoting a more balanced bone metabolism.
PQQ and Vascular Calcification:
Reduced Oxidative Stress:
PQQ's antioxidant properties can help reduce oxidative stress and apoptosis in vascular smooth muscle cells, which are key factors in vascular calcification.
Potential Protective Effects:
By mitigating oxidative stress and apoptosis, PQQ may help prevent or reduce the progression of vascular calcification.
Overall, PQQ's potential benefits in preventing calcification stem from its antioxidant capacity, its role in regulating bone metabolism, and its ability to protect against oxidative stress-induced damage in cells and tissues involved in calcification processes.
Am J Transl Res
. 2022 Jan 15;14(1):582–593.
Pyrroloquinoline quinone inhibits ligature-induced alveolar bone loss through regulation of redox balance and cell senescence
Genxiong Tang 1,*, Haoran Ma 1,*, Shuying Liu 1, Jun Wu 2, Aixiu Gong 1
Author information
Article notes
Copyright and License information
PMCID: PMC8829629 PMID: 35173876
Abstract
It has been demonstrated that oxidative stress is related to periodontitis, and that pyrroloquinoline quinine (PQQ) acts as a powerful antioxidant. This study aimed to explore the effect of PQQ on ligature-induced alveolar bone loss in experimental periodontitis (EP) mice with/without PQQ in the diet. EP mice received a diet supplemented with PQQ for 2 weeks and were compared with sham (control) mice as well as untreated EP mice. Additionally, human periodontal ligament cells (hPDLCs) were treated with PQQ in the presence or absence of lipopolysaccharide (LPS). We found that the bone volume fraction, alkaline phosphatase activity, and the number of antioxidant cells were significantly decreased in EP mice compared with the sham mice, whereas PQQ administration rescued the above effects. In contrast, alveolar bone loss, osteoclast number, cell senescence-associated cells, and cytokines’ expression were significantly increased in EP mice compared with the sham mice but were significantly decreased with PQQ supplementation in periodontal tissues. Furthermore, we found that antioxidant enzymes and Bmi-1 protein expression levels were downregulated, whereas the protein expression levels of cell senescence-related proteins including γ-H2AX, IL-6, IL-1β, p16, and p21 were significantly up-regulated in LPS-induced hPDLCs compared with the control cells. However, PQQ administration partially prevented these changes. These findings suggest that PQQ may alleviate periodontal damage through regulation of the redox balance and cell senescence.
Keywords: Pyrroloquinoline quinone, periodontitis, alveolar bone resorption, oxidative stress, inflammation
Introduction
Over the past decade, periodontitis has become an alarming concern worldwide due to its high prevalence and the current long life expectancy, and thus is an increasing burden to the healthcare system [1,2]. Several studies have demonstrated the relationship of periodontal pathogens with systemic diseases, such as cardiovascular disease, diabetes, and kidney disease [3,4]. However, besides some surgical measures, there are few other therapeutic approaches that are clinically available for treatment of periodontitis [5]. Therefore, it is imperative to develop effective treatment methods to slow down the progression of periodontitis.
Periodontitis, a chronic destructive disease, is caused by the build-up of dental plaque. Bacterial pathogens cause both immune and inflammatory cells to the periodontal site [6]. These cells can resist the invasion of bacteria by producing reactive oxygen species (ROS), leading to oxidative stress (OS) in the periodontal area [7,8]. Local and systemic changes in the redox balance in the periodontium cause cytotoxic effects and periodontal destruction [9]. If the antioxidant defense system fails to clear out ROS in time, ROS accumulation in the periodontium may contribute to the degradation of the periodontal tissue [10]. Therefore, antioxidant therapy, a ROS antagonist, may help patients with periodontal diseases [11].
Pyrroloquinoline quinone (PQQ), which was originally discovered as a new coenzyme in methylotrophic bacteria in 1979, is ubiquitously found in foods [12,13]. Interestingly, PQQ has gained attention because of its role as an antioxidant and its function as a nutritional growth-promoting factor [14,15]. Several studies have shown the protective effects of PQQ on osteoporosis and neuroinjury, as well as on cardiac and immune events [16,17]. PQQ has been reported to be a promising compound that could improve human health [18].
Recently, PQQ has evoked much interest in terms of bone metabolism. Previous studies have demonstrated that PQQ can suppress osteoclast differentiation and bone resorptive activity, suggesting that it is a potential drug for bone resorption inhibition [19]. PQQ administration alleviated testosterone deficiency-induced osteoporosis through mitigation of ROS production and DNA damage, promotion of osteoblast proliferation and differentiation, as well as reduction in osteoclastic bone resorption [20]. Furthermore, previous studies have reported the benefits of the chondroprotective effect of PQQ during osteoarthritis development [21,22].
These findings indicated that PQQ can decrease bone resorption and promote bone formation. High doses of PQQ in a mouse model protected the mandible from developing osteoporosis [23]. Destructive erosion of bone is a major complication of periodontal diseases [24]. However, it is unclear whether application of PQQ can suppress alveolar bone loss and attenuate periodontitis.
Am J Transl Res
. 2022 Jan 15;14(1):582–593.
Pyrroloquinoline quinone inhibits ligature-induced alveolar bone loss through regulation of redox balance and cell senescence
Genxiong Tang 1,*, Haoran Ma 1,*, Shuying Liu 1, Jun Wu 2, Aixiu Gong 1
Author information
Article notes
Copyright and License information
PMCID: PMC8829629 PMID: 35173876
Abstract
It has been demonstrated that oxidative stress is related to periodontitis, and that pyrroloquinoline quinine (PQQ) acts as a powerful antioxidant. This study aimed to explore the effect of PQQ on ligature-induced alveolar bone loss in experimental periodontitis (EP) mice with/without PQQ in the diet. EP mice received a diet supplemented with PQQ for 2 weeks and were compared with sham (control) mice as well as untreated EP mice. Additionally, human periodontal ligament cells (hPDLCs) were treated with PQQ in the presence or absence of lipopolysaccharide (LPS). We found that the bone volume fraction, alkaline phosphatase activity, and the number of antioxidant cells were significantly decreased in EP mice compared with the sham mice, whereas PQQ administration rescued the above effects. In contrast, alveolar bone loss, osteoclast number, cell senescence-associated cells, and cytokines’ expression were significantly increased in EP mice compared with the sham mice but were significantly decreased with PQQ supplementation in periodontal tissues. Furthermore, we found that antioxidant enzymes and Bmi-1 protein expression levels were downregulated, whereas the protein expression levels of cell senescence-related proteins including γ-H2AX, IL-6, IL-1β, p16, and p21 were significantly up-regulated in LPS-induced hPDLCs compared with the control cells. However, PQQ administration partially prevented these changes. These findings suggest that PQQ may alleviate periodontal damage through regulation of the redox balance and cell senescence.
Keywords: Pyrroloquinoline quinone, periodontitis, alveolar bone resorption, oxidative stress, inflammation
Introduction
Over the past decade, periodontitis has become an alarming concern worldwide due to its high prevalence and the current long life expectancy, and thus is an increasing burden to the healthcare system [1,2]. Several studies have demonstrated the relationship of periodontal pathogens with systemic diseases, such as cardiovascular disease, diabetes, and kidney disease [3,4]. However, besides some surgical measures, there are few other therapeutic approaches that are clinically available for treatment of periodontitis [5]. Therefore, it is imperative to develop effective treatment methods to slow down the progression of periodontitis.
Periodontitis, a chronic destructive disease, is caused by the build-up of dental plaque. Bacterial pathogens cause both immune and inflammatory cells to the periodontal site [6]. These cells can resist the invasion of bacteria by producing reactive oxygen species (ROS), leading to oxidative stress (OS) in the periodontal area [7,8]. Local and systemic changes in the redox balance in the periodontium cause cytotoxic effects and periodontal destruction [9]. If the antioxidant defense system fails to clear out ROS in time, ROS accumulation in the periodontium may contribute to the degradation of the periodontal tissue [10]. Therefore, antioxidant therapy, a ROS antagonist, may help patients with periodontal diseases [11].
Pyrroloquinoline quinone (PQQ), which was originally discovered as a new coenzyme in methylotrophic bacteria in 1979, is ubiquitously found in foods [12,13]. Interestingly, PQQ has gained attention because of its role as an antioxidant and its function as a nutritional growth-promoting factor [14,15]. Several studies have shown the protective effects of PQQ on osteoporosis and neuroinjury, as well as on cardiac and immune events [16,17]. PQQ has been reported to be a promising compound that could improve human health [18].
Recently, PQQ has evoked much interest in terms of bone metabolism. Previous studies have demonstrated that PQQ can suppress osteoclast differentiation and bone resorptive activity, suggesting that it is a potential drug for bone resorption inhibition [19].
PQQ administration alleviated testosterone deficiency-induced osteoporosis through mitigation of ROS production and DNA damage, promotion of osteoblast proliferation and differentiation, as well as reduction in osteoclastic bone resorption [20]. Furthermore, previous studies have reported the benefits of the chondroprotective effect of PQQ during osteoarthritis development [21,22].
These findings indicated that PQQ can decrease bone resorption and promote bone formation. High doses of PQQ in a mouse model protected the mandible from developing osteoporosis [23]. Destructive erosion of bone is a major complication of periodontal diseases [24]. However, it is unclear whether application of PQQ can suppress alveolar bone loss and attenuate periodontitis.