Oxidative stress and temporomandibular joint disorders

Kawai, Yosuke; Lee, Masaichi-Chang-il; Kubota, Eiro

doi:10.1016/j.jdsr.2008.08.001

Cited by 21 publications

(18 citation statements)

References 15 publications

(28 reference statements)

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“…[16][17][18] The mechanical stress on the TMJ as well as on masticatory muscles can generate free radicals through some mechanisms, triggering a cascade of reactions that can exacerbate tissue damage, inflammation and pain. 16 The purpose of this study was to determine whether there were changes in the oxidative status in individuals with TMD and pain.…”

Section: Discussionmentioning

confidence: 99%

Changes in the salivary oxidative status in individuals with temporomandibular disorders and pain

Almeida

Amenábar

2016

Journal of Oral Biology and Craniofacial Research

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Section: Discussionmentioning

confidence: 99%

Changes in the salivary oxidative status in individuals with temporomandibular disorders and pain

Almeida

Amenábar

2016

Journal of Oral Biology and Craniofacial Research

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“…The ROS, especially HO • is responsible for lipid peroxidation and disruption of cellular homeostasis. Nitzan reported that lysis of SAPL layer by phospholipase A2 (sPLA2) together with the depolymerization of HA caused by free radicals may result in a deteriorated lubrication of the articular surface, thus further proceeding to the internal derangement (ID) of the TMJ [189]. The HO • also degrades collagen and proteoglycans (Pgs) into low molecular masses, which act as immunogens for synoviocytes or chondrocytes [190].…”

Section: Temporomandibular (Tmb) Joint Disordersmentioning

confidence: 99%

Oxidative stress and human health

Rahman¹,

Hosen²,

Islam³

et al. 2012

ABB

326

214

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Redox degenerative reactions of the biological system inevitably produce reactive oxygen species (ROS) and their derivatives. Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species (ROS), such as hydrogen peroxide, organic hydro peroxides, nitric oxide, superoxide and hydroxyl radicals etc. Information are accumulating steadily, supporting the general importance of oxidative damage of tissue and cellular components as a primary or secondary causative factor in many different human diseases and aging processes. Many of the recent landmarks in scientific research have shown that in human beings, oxidative stress has been implicated in the progression of major health problems by inactivating the metabolic enzymes and damaging important cellular components, oxidizing the nucleic acids, leading to cardiovascular diseases, eye disorders, joint disorders, neurological diseases (Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis), atherosclerosis, lung and kidney disorders, liver and pancreatic diseases, cancer, ageing, disease of the reproductive system including the male and female infertility etc. The advent of a growing number of in vitro and in vivo models for evaluating the human disease pathology is aiding scientists in deciphering the detailed mechanisms of the point of intersection of the oxidative stress with other cellular components or events in the growing roadmap leading to different human disorders. The toxic effect of reactive oxygen and nitrogen species in human is balanced by the antioxidant action of non-enzymatic antioxidants, as well as by antioxidant enzymes. Such antioxidant defences are extremely important as they represent the direct removal of free radicals (prooxidants), thus providing maximal protection for biological sites. These systems not only assert with the problem of oxidative damage, but also play a crucial role in wellness, health maintenance, and prevention of chronic and degenerative diseases. In this review we have tried to generate a gross picture on the critical role of ROS in deteriorating human health and the importance of antioxidative defense system in ameliorating the toxicity of ROS

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“…This inflammatory response could be triggered as result of the tissue breakdown and the consequent release of damageassociated molecular patterns (DAMPs), such as low molecular weight hyaluronan (LMW-HA), high-mobility group protein 1 (HMGB1), and S100 proteins [73,74], activating resident inflammatory cells, including dendritic cells and macrophages [75]. At initial stages of the disease, functional overload induces oxidative stress that initiates cartilage disruption [76,77] and activation of MMPs and aggrecanases, promoting the secretion of DAMPs and the activation of the immune response [75]. During the disease progression, there is a local imbalance between the expression of specific cytokines, their receptors, and regulatory soluble receptors, which may be critical in the biological activity of the cytokine network [35].…”

Section: Role Of the Immuno-inflammatory Response In The Pathogenesismentioning

confidence: 99%

Osteoarthritis of the Temporomandibular Joint: Clinical and Imagenological Diagnosis, Pathogenic Role of the Immuno- Inflammatory Response, and Immunotherapeutic Strategies Based on T Regulatory Lymphocytes

Monasterio¹,

Castillo²,

Betancur³

et al. 2018

Temporomandibular Joint Pathology - Current Approaches and Understanding

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Osteoarthritis is a degenerative disease affecting the TMJ. It is the most common TMJ disorder and shows a higher prevalence in women and older people. TMJ osteoarthritis (TMJ-OA) is characterized by variable degrees of inflammation, destruction of the articular cartilage, and sub-chondral bone resorption. In this context, diverse pro-inflammatory cytokines, chemokines, enzymes, and bone-resorptive associated factors have been considered as possible markers of active TMJ-OA. The molecular balance is determinant not only for initiation and progression, but also for the clinical expression of the disease. Recent advances in the biochemical analysis of synovial fluid from affected patients have provided new insights into the patho-physiology of the TMJ-OA; however, its molecular pathogenesis still remains unclear. Recently, a Th1 and Th17-dominated immune response has been associated with the inflammatory and destructive events characteristic of TMJ-OA and, in particular, the Th17 lymphocyte pathway has a pivotal role in the increased production of RANKL, which is involved in osteoclast activation and subsequent sub-chondral bone resorption. Understanding the TMJ physiology and pathogenesis of the TMJ-OA, together with the key molecular determinants of the TMJ tissue destruction, will enable the development of new chair-side point of care diagnostics and more conservative treatment modalities with minimal complications.

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Oxidative stress and temporomandibular joint disorders

Cited by 21 publications

References 15 publications

Changes in the salivary oxidative status in individuals with temporomandibular disorders and pain

Changes in the salivary oxidative status in individuals with temporomandibular disorders and pain

Oxidative stress and human health

Osteoarthritis of the Temporomandibular Joint: Clinical and Imagenological Diagnosis, Pathogenic Role of the Immuno- Inflammatory Response, and Immunotherapeutic Strategies Based on T Regulatory Lymphocytes

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