Tumor necrosis factor-α as a biochemical marker of pain and outcome in temporomandibular joints with internal derangements

Shafer, David; Assael, Leon A.; White, Lorraine B.; Rossomando, Edward F.

doi:10.1016/0278-2391(94)90217-8

Cited by 168 publications

(84 citation statements)

References 22 publications

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“…This hypothesis is supported by data from several investigations [Shafer et al, 1994;Fu et al, 1995;Kubota et al, Control Inflammation and Bony Changes at the TMJ Cells Tissues Organs 2001;169:257-264 259 1997, 1998Alstergren et al, 1998;Kopp, 1998;Sandler et al, 1998;Takahashi et al, 1998;Fang et al, 1999].…”

Section: Introductionsupporting

confidence: 72%

“…Such observations have led many researchers to believe that knowledge of osteoarthritis (OA), RA, and the associated inflammation of the synovial joints could be applied to the TMJ. Multiple cytokines have been identified in the synovial fluid of patients with temporomandibular disorders (TMD) that resemble those involved in OA and RA in other synovial joints [Holmlund et al, 1991;Shafer et al, 1994;Fu et al, 1995;Kubota et al, 1997Kubota et al, , 1998Alstergren et al, 1998;Kopp, 1998;Sandler et al, 1998;Takahashi et al, 1998;Fang et al, 1999]. It is thought that these cytokines are involved in bony changes, such as osteophyte formation and erosion (resorption), at the TMJ [Takahashi et al, 1998].…”

Section: Introductionmentioning

confidence: 99%

“…Studies evidencing the role of cytokines in the TMJ have primarily focused on tumor necrosis factor-· (TNF·), interleukin-1ß (IL-1ß), IL-6, IL-8, interferon-Á (IFN-Á), interleukin-1 receptor antagonist (IL-1ra), and IL-10 [Shafer et al, 1994;Fu et al, 1995;Kubota et al, 1997Kubota et al, , 1998Alstergren et al, 1998;Kopp, 1998;Sandler et al, 1998;Takahashi et al, 1998;Fang et al, 1999].…”

Section: Introductionmentioning

confidence: 99%

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Inflammation and Bony Changes at the Temporomandibular Joint

Kacena

Merrel

Konda

et al. 2001

Cells Tissues Organs

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Cytokines help mediate the acute and chronic inflammation and associated destruction of connective tissue in arthritic temporomandibular joints (TMJ). The proinflammatory cytokines TNFα, IL-1β, IL-6, IL-8, and IFN-γ are associated with inflammation in synovial joints and connective tissue destruction. Therefore, the increased levels of these cytokines in the synovial fluid of temporomandibular disorder (TMD) patients would be expected. Conversely, IL-1ra and IL-10 acts as inhibitors to these proinflammatory cytokines. Thus, in TMD patients, low levels of IL-1ra and IL-10 might be expected. A review of studies from multiple investigators confirms that proinflammatory cytokine levels increase in TMD patients, IL-1ra levels are also increased, and IL-10 levels remain unchanged. Because IL-10 can inhibit TNFα, IL-1, IL-6, and IL-8, the lack of IL-10 in the TMJ in the face of the other studies showing increases in TNFα, IL-1β, IL-6, and IL-8 could partially explain the exacerbation of the associated osteoarthritis. In addition, although IL-1ra levels are elevated in most of the TMD patients, the increases do not appear to be sufficient to inhibit the inflammation and connective tissue degradation associated with IL-1β. Thus, it appears that treatment of TMD requires a delicate balance between proinflammatory cytokines and cytokine inhibitors such as IL-1ra and IL-10.

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Section: Introductionsupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inflammation and Bony Changes at the Temporomandibular Joint

Kacena

Merrel

Konda

et al. 2001

Cells Tissues Organs

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“…Previous studies have examined whether circulating proinflammatory cytokine levels become elevated in syndromes associated with chronic pain, but mixed results have been reported. [14][15][16][17] The cytokines that could present abnormal levels in blood and cerebrospinal fluid include interleukin-8 (IL-8), interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and soluble TNF receptor (sTNF-R). 18 One challenge in interpreting the cytokine levels reported in many papers has been the limited information on healthy norms and reference values.…”

mentioning

confidence: 99%

Serum cytokine levels in patients with chronic low back pain due to herniated disc: analytical cross-sectional study

et al. 2010

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CONTEXT AND OBJECTIVE: The role of immune response and proinflammatory cytokines in the pathogenesis of chronic pain has been of growing interest. In order to evaluate whether there is any association between disc herniation and elevated cytokine levels, we measured cytokine levels in patients with chronic low back pain and in healthy subjects. DESIGN AND SETTING:Analytical cross-sectional study at the Pain Clinic of Universidade Federal da Bahia (UFBA). METHODS:Cytokine levels were measured using the enzyme-linked immunosorbent assay (ELISA) technique on 23 patients with low back pain (G1) and on 10 healthy subjects (G2). RESULTS:The levels of tumor necrosis factor-alpha [TNF-alpha] (G1 = 5.6 ± 2.3 pg/ml; G2 = 1.6 ± 0.5 pg/ml; P = 0.01) and interleukin-6[IL-6] (G1 = 4.1 ± 3.0 pg/ml; G2 = 0.9 ± 0.4 pg/ml; P = 0.01) were higher in G1. There were no statistically significant differences in relation to interleukin-1 [IL-1] (G1 = 0.5 ± 0.3 pg/ml; G2 = 0.5 ± 0.1 pg/ml; P = 1) or soluble tumor necrosis factor receptor [sTNF-R] (G1 = 572 pg/ml ± 36; G2 = 581 ± 50 pg/ml; P = 0.87). CONCLUSION:The patients with chronic low back pain due to disc herniation presented higher levels of TNF-alpha and IL-6, but not of IL-1 or sTNF-R. RESUMO CONTEXTO E OBJETIVO:A função da resposta imunológica e das citocinas pró-inflamatórias na patogênese da dor crônica tem tido interesse crescente. Para avaliar se há correlação entre hérnia de disco e aumento de citocinas, foi medida a concentração de citocinas em pacientes com lombalgia crônica e em indivíduos sadios. TIPO DE ESTUDO E LOCAL: Estudo transversal analítico realizado na Clínica de Dor da Universidade Federal da Bahia (UFBA).MÉTODO: As concentrações de citocinas foram medidas pela técnica de ELISA (enzyme linked immunosorbent assay) em 23 pacientes com lombalgia (G1) e 10 sadios (G2). RESULTADOS:As concentrações de fator-alfa de necrose tumoral [TNF-alpha] (G1 = 5.6 ± 2.3 pg/ml; G2 = 1.6 ± 0.5 pg/ml; P = 0,01) e interleucina-6 [IL-6] (G1 = 4.1 ± 3.0 pg/ml; G2 = 0.9 ± 0.4 pg/ml; P = 0,01) foram maiores no G1. Não houve diferença estatisticamente significante para interleucina-1 [IL-1] (G1 = 0.5 ± 0.3 pg/ml; G2 = 0.5 ± 0.1 pg/ml; P = 1) e receptor solúvel do factor de necrose tumoral [sTNF-R] (G1 = 572 pg/ml ± 36; G2 = 581 ± 50 pg/ml; P = 0,87).CONCLUSÃO: Os pacientes com lombalgia crônica por hérnia de disco apresentam concentrações maiores de TNF-alpha e IL-6, mas não de IL-1 ou sTNF-R.

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“…High levels of inflammatory mediators in the SF of patients with TMD have been detected, such as disk displacement and OA (Quinn & Bazar, 1990;Shafer et al, 1994;Fu et al, 1995). Among the most recognized inflammatory mediators are arachidonic acid derivatives, related enzymes and some cytokines (Uchôa de Rezende & Constantino de Campos).…”

Section: Characteristics Of the Temporomandibular Jointmentioning

confidence: 99%

Role of Hyaluronic Acid in the Homeostasis and Therapeutics of Temporomandibular Joint Osteoarthritis

et al. 2017

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Morphol., 35(3):870-876, 2017. SUMMARY:The aim of this study was to perform a literature review regarding the role of hyaluronic acid (HA) in the homeostasis and therapeutics of temporomandibular joint (TMJ) osteoarthritis (OA). The TMJ has characteristics that give it special adaptation and recovery abilities, where HA plays a fundamental role in helping to maintain joint homeostasis, which is affected in pathological processes like OA. OA is a chronic degenerative multi-factor disease that can affect all the components of the synovial joints, causing degradation of the articular cartilage, extracellular matrix and breakage in the HA molecules. HA is a non-branched linear polysaccharide with viscosupplementation, anti-inflammatory, lubrication and pain relief effects; it also activates the intrinsic repair processes of the cartilage and normalizes the endogenous production of HA by the synoviocytes. In recent years, the therapeutic use of HA has shown evidence that supports its application in TMJ OA, improving viscosupplementation capacity, acting at the cellular and molecular levels, reducing various inflammatory mediators and improving the reparative characteristics. Its use has been studied in animal models and in humans. However, no consensus has been reached in terms of concentrations, dose, application frequency or molecular weight to be used.

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Tumor necrosis factor-α as a biochemical marker of pain and outcome in temporomandibular joints with internal derangements

Cited by 168 publications

References 22 publications

Inflammation and Bony Changes at the Temporomandibular Joint

Inflammation and Bony Changes at the Temporomandibular Joint

Serum cytokine levels in patients with chronic low back pain due to herniated disc: analytical cross-sectional study

Role of Hyaluronic Acid in the Homeostasis and Therapeutics of Temporomandibular Joint Osteoarthritis

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