The Crossroads between Infection and Bone Loss

Oliveira, Tiago Carvalho; Gomes, Maria Salomé; Gomes, Ana Cordeiro

doi:10.3390/microorganisms8111765

Cited by 37 publications

(35 citation statements)

References 123 publications

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“…Apoptosis is a critical form of RCD that results in the clearance of unhealthy cells without strong damage (if not always) to surrounding tissues. Bacterial infection is considered an important factor for osteoblast apoptosis (Oliveira et al, 2020). Escherichia coli , P .…”

Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis OG1RF induces apoptosis in MG63 cells via caspase‐3/‐8/‐9 without activation of caspase‐1/GSDMD

Wen

Zhong

et al. 2021

Oral Diseases

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Objective Regulated cell death is key in the pathogenesis of persistent apical periodontitis. Here, we investigated the mechanisms of regulated cell death in osteoblast‐like MG63 cells infected with Enterococcus faecalis OG1RF. Materials and methods MG63 cells were infected with live E. faecalis OG1RF at the indicated multiplicity of infection for the indicated infection time. We evaluated the cells by flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labelling assay and lactate dehydrogenase release analysis; measured the activity of caspase‐1/‐3/‐8/‐9 and the release of interleukin‐1β; and determined the expression of apoptosis‐associated proteins and gasdermin D by apoptosis antibody array and Western blotting. Results Enterococcus faecalis OG1RF reduced the mitochondrial membrane potential of the infected cells, increased the percentage of apoptotic and terminal deoxynucleotidyl transferase dUTP nick end labelling‐positive cells, and enhanced lactate dehydrogenase release. The expression of caspase‐3 and survivin and the activity of caspase‐3/‐8/‐9 were upregulated, while the expression of death receptor 6 was downregulated. The activity of caspase‐1/gasdermin D and the release of interleukin‐1β remained unaltered. Conclusion Enterococcus faecalis OG1RF induced both intrinsic and extrinsic MG63 cell apoptosis via caspase‐3/‐8/‐9 activation but did not activate the pyroptotic pathway regulated by caspase‐1/gasdermin D.

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Section: Discussionmentioning

confidence: 99%

Enterococcus faecalis OG1RF induces apoptosis in MG63 cells via caspase‐3/‐8/‐9 without activation of caspase‐1/GSDMD

Wen

Zhong

et al. 2021

Oral Diseases

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“…In synergy with RANKL, TLR-induced production of TNF-α and IL-6 may also promote functional osteoclast differentiation ( 90 , 91 ). When mature osteoclasts are ready to function, increased size and multinucleation of osteoclasts and polarized organization of the cytoskeleton facilitate their transportation to the microenvironment, where they produce protons (H + ) (for mineral dissolution), cathepsin K, and collagenase (for organic component degradation) using lysosome-derived vesicles from the cytosol to resorptive sites ( 92 , 93 ). RANKL and M-CSF may also play important roles in cytoskeletal reorganization, thereby promoting bone resorption ( 94 ).…”

Section: Mechanisms Of Bone Loss Related To Inflammasomesmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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“…Bony remodelling is driven by counterbalancing activities of osteoclasts, which are responsible for bone resorption, and osteoblasts, which are responsible for bone building (apposition) [28]. Bone plays a complex and important role in immune responses, and local and systemic infections can also cause bone pathology [30][31][32]. Osteoblasts and osteocytes can regulate numbers and differentiation of B-cells and T-cells in bone marrow [33,34], and osteoclasts create the bone marrow cavity required for normal hematopoiesis [35].…”

Section: Rickettsioses Includingmentioning

confidence: 99%

The Impact of Tick-Borne Diseases on the Bone

Farooq

Moriarty

2021

Microorganisms

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Tick-borne infectious diseases can affect many tissues and organs including bone, one of the most multifunctional structures in the human body. There is a scarcity of data regarding the impact of tick-borne pathogens on bone. The aim of this review was to survey existing research literature on this topic. The search was performed using PubMed and Google Scholar search engines. From our search, we were able to find evidence of eight tick-borne diseases (Anaplasmosis, Ehrlichiosis, Babesiosis, Lyme disease, Bourbon virus disease, Colorado tick fever disease, Tick-borne encephalitis, and Crimean–Congo hemorrhagic fever) affecting the bone. Pathological bone effects most commonly associated with tick-borne infections were disruption of bone marrow function and bone loss. Most research to date on the effects of tick-borne pathogen infections on bone has been quite preliminary. Further investigation of this topic is warranted.

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The Crossroads between Infection and Bone Loss

Cited by 37 publications

References 123 publications

Enterococcus faecalis OG1RF induces apoptosis in MG63 cells via caspase‐3/‐8/‐9 without activation of caspase‐1/GSDMD

Enterococcus faecalis OG1RF induces apoptosis in MG63 cells via caspase‐3/‐8/‐9 without activation of caspase‐1/GSDMD

Inflammasomes in Alveolar Bone Loss

The Impact of Tick-Borne Diseases on the Bone

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