Post-Traumatic Osteoarthritis: Inflammatory, Cellular and Biochemical Mechanisms of Disease Progression

TRAUMA ◽  
2016 ◽  
Vol 17 (1) ◽  
pp. 99
Author(s):  
I.Yu. Holovach ◽  
I.M. Zazirnyi ◽  
I.P. Semeniv
Keyword(s):  
Disease Progression ◽  
Post Traumatic ◽  
Biochemical Mechanisms

Challenges of post-traumatic stress disorder (PTSD) in Iraq: biochemical network and methodologies. A brief review

2020 ◽  
Vol 41 (4) ◽  
Author(s):  
Daniele Suzete Persike ◽  
Suad Yousif Al-Kass
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Structural Changes ◽  
Stress Disorder ◽  
Feedback Mechanism ◽  
Biochemical Network ◽  
Response To Treatment ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Biochemical Mechanisms

AbstractPost-traumatic stress disorder (PTSD) is a multifaceted syndrome due to its complex pathophysiology. Signals of illness include alterations in genes, proteins, cells, tissues, and organism-level physiological modifications. Specificity of sensitivity to PTSD suggests that response to trauma depend on gender and type of adverse event being experienced. Individuals diagnosed with PTSD represent a heterogeneous group, as evidenced by differences in symptoms, course, and response to treatment. It is clear that the biochemical mechanisms involved in PTSD need to be elucidated to identify specific biomarkers. A brief review of the recent literature in Pubmed was made to explore the major biochemical mechanisms involved in PTSD and the methodologies applied in the assessment of the disease. PTSD shows pre-exposure vulnerability factors in addition to trauma-induced alterations. The disease was found to be associated with dysfunctions of the hypothalamic–pituitary–adrenal axis (HPA) and hypothalamus–pituitary–thyroid axis. Sympathetic nervous system (SNS) activity play a role in PTSD by releasing norepinephrine and epinephrine. Cortisol release from the adrenal cortex amplifies the SNS response. Cortisol levels in PTSD patients, especially women, are later reduced by a negative feedback mechanism which contributes to neuroendocrine alterations and promotes structural changes in the brain leading to PTSD. Gender differences in normal HPA responsiveness may be due to an increased vulnerability in women to PTSD. Serotonin and dopamine levels were found to be abnormal in the presence of PTSD. Mechanisms such as the induction of neuroinflammation and alterations of mitochondrial energy processing were also associated with PTSD.

Gait Risk Factors for Disease Progression Differ Between Non-traumatic and Post-traumatic Knee Osteoarthritis

2021 ◽  
Author(s):  
Shawn M. Robbins ◽  
Jean-Pierre Pelletier ◽  
François Abram ◽  
Mathieu Boily ◽  
John Antoniou ◽  
...  
Keyword(s):  
Risk Factors ◽  
Knee Osteoarthritis ◽  
Disease Progression ◽  
Post Traumatic

Effects of Bisphosphonate on Long-Term Culture of Cartilage Allografts

2013 ◽  
Author(s):  
Yilu Zhou ◽  
Lauren Resutek ◽  
Liyun Wang ◽  
X. Lucas Lu
Keyword(s):  
Medial Meniscus ◽  
Biomechanical Properties ◽  
Culture Conditions ◽  
Protective Mechanisms ◽  
Post Traumatic ◽  
Biochemical Mechanisms ◽  
Altered Metabolism

Zoledronic acid (ZA), an FDA approved bisphosphonate (BP) medicine, is widely used for the treatment of osteoclast-related bone loss diseases [1]. Our previous study has found that systemic administration of ZA could dramatically suppress the development of post-traumatic osteoarthritis (PTOA) in the DMM (destabilization of the medial meniscus) mouse model, a model recapitulating the altered joint loading associated with PTOA [2]. This finding is consistent with a few similar studies using different animal models [3]. However, little is known about the cellular and biochemical mechanisms of BP mediated chondro-protection in PTOA pathogenesis. Studies have shown that PTOA often initiates from the apoptosis and altered metabolism of cartilage chondrocytes. In this study, we will investigate the direct effects of ZA on the metabolisms of chondrocytes using long-term in vitro culture of cartilage allografts. As one of the earliest responses of chondrocytes to mechanical stimulation, intracellular calcium ([Ca 2+] i) signaling is the upstream of numerous mechanotransduction pathways [4]. We hypothesize that the chondro-protective mechanisms of ZA could be represented by the characteristics of [Ca 2+] i signaling of in situ chondrocytes. Our specific aims were to: (i) compare the in situ spontaneous [Ca 2+] i responses of chondrocytes cultured in non-ZA and ZA supplemented environments, and (ii) compare the biomechanical properties of cartilage allografts under the two culture conditions.

scholarly journals Erythropoietin Protects from Post-Traumatic Edema in the Rat Brain

2007 ◽  
Vol 27 (7) ◽  
pp. 1369-1376 ◽  
Author(s):  
Olivier Verdonck ◽  
Hana Lahrech ◽  
Gilles Francony ◽  
Olivier Carle ◽  
Régine Farion ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Apparent Diffusion Coefficient ◽  
Brain Edema ◽  
Acceleration Model ◽  
Apparent Diffusion ◽  
Post Traumatic ◽  
Biochemical Mechanisms ◽  
Impact Acceleration ◽  
Magnetic Resonance Imaging Mri ◽  
Brain Water

Erythropoietin (Epo) is gaining interest in various neurological insults as a possible neuroprotective agent. We determined the effects of recombinant human Epo (rhEpo, 5000 IU per kg bw) on brain edema induced in rats by traumatic brain injury (TBI; impact-acceleration model; rhEpo administration 30 mins after injury). Magnetic resonance imaging (MRI) and a gravimetric technique were applied. In the MRI experiments, the apparent diffusion coefficient (ADC) and the tissue T1 relaxation time were measured hourly in the neocortex and caudoputamen, during a 6 h time span after TBI. In the gravimetric experiments, brain water content (BWC) was determined in these two regions, 6 h after TBI. Apparent diffusion coefficient measurements showed that rhEpo decreased brain edema early and durably. Gravimetric measurements showed that rhEpo decreased BWC at H6 in the neocortex as well as in the caudoputamen. No significant differences in ADC, in T1, or in BWC were found between rhEpo treated-TBI rats and sham-operated rats. Our findings show that post-traumatic administration of rhEpo can significantly reduce the development of brain edema in a model of diffuse TBI. Further studies should be conducted to identify the biochemical mechanisms involved in these immediate effects and to assess the use of rhEpo as a possible therapy for post-traumatic brain edema.

The effect of post-traumatic stress disorder on HIV disease progression following hurricane Katrina

AIDS Care ◽  
2009 ◽  
Vol 21 (10) ◽  
pp. 1298-1305 ◽  
Author(s):  
Kathleen H. Reilly ◽  
Rebecca A. Clark ◽  
Norine Schmidt ◽  
Charles C. Benight ◽  
Patricia Kissinger
Keyword(s):  
Disease Progression ◽  
Hurricane Katrina ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Hiv Disease ◽  
Post Traumatic Stress ◽  
Post Traumatic

scholarly journals Cyclic loading regime considered beneficial does not protect injured and interleukin-1-inflamed cartilage from post-traumatic osteoarthritis

2021 ◽  
Author(s):  
Atte Seppo Aleksi Eskelinen ◽  
Cristina Florea ◽  
Petri Tanska ◽  
Han-Hwa K Hung ◽  
Eliot H Frank ◽  
...  
Keyword(s):  
Cyclic Loading ◽  
Disease Progression ◽  
Interleukin 1 ◽  
Tissue Level ◽  
Osteoarthritis Progression ◽  
Post Traumatic ◽  
Interleukin 1Α ◽  
Level Loading ◽  
Bovine Cartilage

Post-traumatic osteoarthritis is a degenerative musculoskeletal condition where homeostasis of articular cartilage is perturbated by lesions and inflammation, leading to abnormal tissue-level loading. These mechanisms have rarely been included simultaneously in in vitro osteoarthritis models. We modeled the early disease progression in bovine cartilage regulated by the coaction of (1) mechanical injury, (2) pro-inflammatory interleukin-1α challenge, and (3) cyclic loading mimicking walking and considered beneficial (15% strain, 1 Hz). Surprisingly, cyclic loading did not protect cartilage from accelerated glycosaminoglycan loss over 12 days of interleukin-1-culture despite promoting aggrecan biosynthesis. Our time-dependent data suggest that this loading regime could be beneficial in the first days following injury but later turn detrimental in interleukin-1-inflamed cartilage. Consequently, early anti-catabolic drug intervention may inhibit, whereas cyclic loading during chronic inflammation may promote osteoarthritis progression. Our data on the early stages of post-traumatic osteoarthritis could be utilized in the development of countermeasures for disease progression.

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