Inflammatory Processes Affecting Bone Health and Repair

Torres, Haydee M.; Arnold, Katherine M.; Oviedo, Manuela; Westendorf, Jennifer J.; Weaver, Samantha R.

doi:10.1007/s11914-023-00824-4

Cited by 12 publications

(4 citation statements)

References 178 publications

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“…There are three partially overlapping phases during bone healing, including the in ammatory phase, the endochondral bone formation phase, and the coupled remodeling phase [38]. Growing evidence show that the eventual bone healing may be highly dependent on the initial in ammatory phase, which may be in uenced by both the local and systemic responses to the injurious stimulus [39][40][41]. Necroptosis is one of various ways to the demise of cells distinguished by an unprogrammed and passive mechanism, commonly initiated by external factors such as damage, infection, ischemia, and similar stressors [42,43].…”

Section: Discussionmentioning

confidence: 99%

Osteoking Promotes Bone Formation and Bone Defect Repair through ZBP1-STAT1-PKR-MLKL-mediated Necroptosis

Suya,

Liu,

et al. 2023

Preprint

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Background: Osteoking has been used for fracture therapy with a satisfying clinical efficacy. However, its therapeutic properties and the underlying mechanisms remain elusive. Method: A bone defect rat model was established to evaluate the pharmacological effects of Osteoking by the dynamic observation of X-ray, micro-CT and histopathologic examination. Transcriptome profiling was performed to identify bone defect-related genes and Osteoking effective targets. Then, a "disease-related gene-drug target" interaction network was constructed and a list of key network targets were screened, which were experimentally verified. Results: Osteoking effectively promoted bone defect repair in rats by accelerating the repair of cortical bone and the growth of trabeculae. Histopathologically, the bone defect rats displayed lower histopathologic scores in cortical bone, cancellous bone and bone connection than normal controls, and Osteoking exerted a favorable effect with a dose-dependent manner (all P<0.001). The abnormal serum levels of bone turnover markers, bone growth factors and bone metabolism-related biochemical indexes in bone defect rats were also reversed by Osteoking treatment. Following the transcriptome-based network investigation, we hypothesized that osteoking might attenuate the levels of ZBP1-STAT1-PKR-MLKL-mediated necroptosis involved into bone defect. Experimentally, the expression levels of ZBP1, STAT1, PKR and the hallmark inflammatory cytokines for the end of necroptosis were distinctly elevated in bone defect rats, but were all effectively reversed by Osteoking treatment, which were also suppressed the activities of RIPK1, RIPK3 and MLKL in bone tissue supernatants. Conclusions: Osteoking may promote bone formation and bone defect repair by regulating ZBP1-STAT1-PKR axis, leading to inhibit RIPK1/RIPK3/MLKL activation-mediated necroptosis.

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Section: Discussionmentioning

confidence: 99%

Osteoking Promotes Bone Formation and Bone Defect Repair through ZBP1-STAT1-PKR-MLKL-mediated Necroptosis

Suya,

Liu,

et al. 2023

Preprint

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“…Other co-morbidities such as COPD [27], kidney disease [28], and periodontitis [29] have also been reported to influence OP. While not apparently influencing the incidence of OP but aggravating the condition, the basis may be related to the inflammation associated with such conditions, as inflammation can also affect bone (reviewed [30]). Some of these inflammatory influences may be associated with an age-related low level of chronic inflammation (inflammaging) [31].…”

Section: Variables and Factors Influencing Post-menopause Diseases An...mentioning

confidence: 99%

The Heterogeneity of Post-Menopausal Disease Risk: Could the Basis for Why Only Subsets of Females Are Affected Be Due to a Reversible Epigenetic Modification System Associated with Puberty, Menstrual Cycles, Pregnancy and Lactation, and, Ultimately, Menopause?

Hart

2024

IJMS

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For much of human evolution, the average lifespan was <40 years, due in part to disease, infant mortality, predators, food insecurity, and, for females, complications of childbirth. Thus, for much of evolution, many females did not reach the age of menopause (45–50 years of age) and it is mainly in the past several hundred years that the lifespan has been extended to >75 years, primarily due to public health advances, medical interventions, antibiotics, and nutrition. Therefore, the underlying biological mechanisms responsible for disease risk following menopause must have evolved during the complex processes leading to Homo sapiens to serve functions in the pre-menopausal state. Furthermore, as a primary function for the survival of the species is effective reproduction, it is likely that most of the advantages of having such post-menopausal risks relate to reproduction and the ability to address environmental stresses. This opinion/perspective will be discussed in the context of how such post-menopausal risks could enhance reproduction, with improved survival of offspring, and perhaps why such risks are preserved. Not all post-menopausal females exhibit risk for this set of diseases, and those who do develop such diseases do not have all of the conditions. The diseases of the post-menopausal state do not operate as a unified complex, but as independent variables, with the potential for some overlap. The how and why there would be such heterogeneity if the risk factors serve essential functions during the reproductive years is also discussed and the concept of sets of reversible epigenetic changes associated with puberty, pregnancy, and lactation is offered to explain the observations regarding the distribution of post-menopausal conditions and their potential roles in reproduction. While the involvement of an epigenetic system with a dynamic “modification-demodification-remodification” paradigm contributing to disease risk is a hypothesis at this point, validation of it could lead to a better understanding of post-menopausal disease risk in the context of reproduction with commonalities may also lead to future improved interventions to control such risk after menopause.

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“…The relationship between rheumatic diseases and the development of OP is complex. In this case, it is important to consider that pro-inflammatory cytokines responsible for decreased BMD are also associated with the activity of rheumatic diseases [9]. On one hand, chronic inflammatory processes lead to decreased bone density, while on the other hand, the disease process can also lead to bone remodeling [9].…”

mentioning

confidence: 99%

“…Therapy with GCs is often used in many rheumatic diseases to reduce inflammatory activity. Paradoxically, it can also increase the risk of fractures by stimulating bone resorption, especially with chronic GCs therapy [9].…”

mentioning

confidence: 99%

Dual-energy X-ray absorptiometry – is it the gold standard, or is bone mineral density everything?

Żuchowski,

Jeka

2024

Reumatologia

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Inflammatory Processes Affecting Bone Health and Repair

Cited by 12 publications

References 178 publications

Osteoking Promotes Bone Formation and Bone Defect Repair through ZBP1-STAT1-PKR-MLKL-mediated Necroptosis

Osteoking Promotes Bone Formation and Bone Defect Repair through ZBP1-STAT1-PKR-MLKL-mediated Necroptosis

The Heterogeneity of Post-Menopausal Disease Risk: Could the Basis for Why Only Subsets of Females Are Affected Be Due to a Reversible Epigenetic Modification System Associated with Puberty, Menstrual Cycles, Pregnancy and Lactation, and, Ultimately, Menopause?

Dual-energy X-ray absorptiometry – is it the gold standard, or is bone mineral density everything?

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