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Breivik, Torbjørn; Sluyter, Frans; Hof, M.; Cools, Alexander R.

doi:10.1023/a:1001903221046

Cited by 47 publications

(5 citation statements)

References 38 publications

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“…Our results show significant bone loss induced by bilateral ligature around the first mandibular molars following experimental periodontitis, as described by Klausen [32]. There are Gram-negative bacteria producing lipopolysaccharides and enzymes capable of perturbing the host defense system as well as induction of cytokines involved in the activation of the HPA axis [33]. In our study, there was a highly significant increase in the production of NO, as shown by an increase in total NOS activity in the gingival tissue around the first inferior molars as well as an increase in iNOS mRNA expression.…”

Section: Discussionsupporting

confidence: 62%

Anti-Inflammatory Effect of the Endocannabinoid Anandamide in Experimental Periodontitis and Stress in the Rat

Rettori¹,

Laurentiis

Zubilete

et al. 2012

Neuroimmunomodulation

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Objective: Periodontitis is an infectious disease leading to inflammation and destruction of tissue surrounding and supporting the tooth. The progress of the inflammatory response depends on the host’s immune system and risk factors such as stress. The aim of the present study was to investigate the role of the endocannabinoid anandamide (AEA) in experimental periodontitis with restraint stress, since the endocannabinoid system is known to modulate the hypothalamo-pituitary-adrenal axis as well as immune functions and has been found in human gingival tissues. Methods: Experimental periodontitis was induced by ligature around first inferior molars and immobilization stress for 2 h twice daily for 7 days in a rat model. Results: Corticosterone plasma levels, locomotor activity, adrenal gland weight and bone loss were increased in periodontitis and stress groups, and there was also less weight gain. The inflammatory parameters such as prostaglandin E₂ (radioimmunoassay), nitric oxide (radioconversion of ¹⁴C-arginine), tumor necrosis factor (TNF)-α (ELISA) and interleukin (IL)-1β (Western blot) measured in the gingival tissue were significantly increased in the periodontitis groups compared to the control group. Local injection of AEA (10^–8M, 30 µl) decreased corticosterone plasma levels and the content of the cytokines TNF-α and IL-1β in gingival tissue in periodontitis-stress groups. These AEA-induced inhibitions were mediated by CB₁ and CB₂ cannabinoid receptors since the injection of both antagonists together, AM251 (10^–6M) and AM630 (10^–6M) in 30 µl, prevented these effects. Conclusion: The endocannabinoid AEA diminishes the inflammatory response in periodontitis even during a stressful situation.

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Section: Discussionsupporting

confidence: 62%

Anti-Inflammatory Effect of the Endocannabinoid Anandamide in Experimental Periodontitis and Stress in the Rat

Rettori¹,

Laurentiis

Zubilete

et al. 2012

Neuroimmunomodulation

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show abstract

“…We have shown previously that CCI rats from all behavioural groups have elevated plasma corticosterone levels, peaking on day three [ 41 ]. It is also known that rats with distinct emotional coping responses (proactive versus reactive) show differences in HPA reactivity and helper T lymphocyte polarisation in response to stressors [ 76 , 77 ]. Elevated glucocorticoids are thought to be anti-inflammatory, shifting the balance of helper T lymphocytes towards Th2 [ 78 ].…”

Section: Discussionmentioning

confidence: 99%

Evidence for a distinct neuro-immune signature in rats that develop behavioural disability after nerve injury

Austin

Berglund

Siu

et al. 2015

J Neuroinflammation

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BackgroundChronic neuropathic pain is a neuro-immune disorder, characterised by allodynia, hyperalgesia and spontaneous pain, as well as debilitating affective-motivational disturbances (e.g., reduced social interactions, sleep-wake cycle disruption, anhedonia, and depression). The role of the immune system in altered sensation following nerve injury is well documented. However, its role in the development of affective-motivational disturbances remains largely unknown. Here, we aimed to characterise changes in the immune response at peripheral and spinal sites in a rat model of neuropathic pain and disability.MethodsSixty-two rats underwent sciatic nerve chronic constriction injury (CCI) and were characterised as either Pain and disability, Pain and transient disability or Pain alone on the basis of sensory threshold testing and changes in post-CCI dominance behaviour in resident-intruder interactions. Nerve ultrastructure was assessed and the number of T lymphocytes and macrophages were quantified at the site of injury on day six post-CCI. ATF3 expression was quantified in the dorsal root ganglia (DRG). Using a multiplex assay, eight cytokines were quantified in the sciatic nerve, DRG and spinal cord.ResultsAll CCI rats displayed equal levels of mechanical allodynia, structural nerve damage, and reorganisation. All CCI rats had significant infiltration of macrophages and T lymphocytes to both the injury site and the DRG. Pain and disability rats had significantly greater numbers of T lymphocytes. CCI increased IL-6 and MCP-1 in the sciatic nerve. Examination of disability subgroups revealed increases in IL-6 and MCP-1 were restricted to Pain and disability rats. Conversely, CCI led to a decrease in IL-17, which was restricted to Pain and transient disability and Pain alone rats. CCI significantly increased IL-6 and MCP-1 in the DRG, with IL-6 restricted to Pain and disability rats. CCI rats had increased IL-1β, IL-6 and MCP-1 in the spinal cord. Amongst subgroups, only Pain and disability rats had increased IL-1β.ConclusionsThis study has defined individual differences in the immune response at peripheral and spinal sites following CCI in rats. These changes correlated with the degree of disability. Our data suggest that individual immune signatures play a significant role in the different behavioural trajectories following nerve injury, and in some cases may lead to persistent affective-motivational disturbances.

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“…Breivik et al . [25] demonstrated that periodontal disease susceptibility and progression could be explained, at least in part by brain-neuroendocrine – immune regulatory mechanisms. Genetically determined hypothalamus-pituitary- adrenal axis (HPA) reactivity seems to play a vital role, and a possible feedback is likely to occur from periodontal disease.…”

Section: Discussionmentioning

confidence: 99%

Chromogranin A: Novel biomarker between periodontal disease and psychosocial stress

Reshma¹,

Arunachalam²,

Pillai³

et al. 2013

J Indian Soc Periodontol

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Context:The psychosocial stress has long been regarded as a significant pre-disposing factor for periodontal disease. The association between the periodontal disease and the neuroendocrine hormones has been observed. Chromogranin A (CgA) is supposed to link the activity of the neuroendocrine system to local and systemic immune functions and to be related to periodontitis.Aims:The aim of this study was to determine the CgA levels in saliva and plasma in periodontal health and disease and to assess their potential relationship to periodontitis.Settings and Designs:In this case-control study, the association between periodontal disease and stress marker has been assessed.Materials and Methods:Sixty subjects were chosen for this study: With case group comprising of 30 subjects with chronic periodontitis and control group comprising of 30 healthy subjects. Salivary and plasma CgA levels were determined by ELISA technique. Clinical parameters included were plaque index, papillary bleeding index and clinical attachment loss and probing depth. Correlation analysis was calculated by independent sample t-test.Results:Significantly higher CgA levels were found in saliva and plasma of patients with chronic periodontitis compared with healthy individuals (P < 0.05). No significant difference were observed between salivary and plasma CgA levels.Conclusions:The elevated level CgA in the plasma and saliva of subjects with stress induced chronic periodontitis has yielded insights into biological plausible association between the psychosocial stress and chronic periodontitis. Thus, our results suggest that CgA is a useful biomarker for evaluating at least in part the etiopathogenesis of periodontitis.

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Cited by 47 publications

References 38 publications

Anti-Inflammatory Effect of the Endocannabinoid Anandamide in Experimental Periodontitis and Stress in the Rat

Anti-Inflammatory Effect of the Endocannabinoid Anandamide in Experimental Periodontitis and Stress in the Rat

Evidence for a distinct neuro-immune signature in rats that develop behavioural disability after nerve injury

Chromogranin A: Novel biomarker between periodontal disease and psychosocial stress

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