Self-reported periodontitis and C-reactive protein in Parkinson’s disease: a cross-sectional study of two American cohorts

Lyra, Patrícia; Botelho, João; Machado, Vanessa; Rota, Silvia; Walker, R. T.; Staunton, Juliet; Proença, Luís; Mendes, José João

doi:10.1038/s41531-022-00302-1

Cited by 14 publications

(8 citation statements)

References 55 publications

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“…P-values for the presence of Porphyromonas gingivalis were statistically significant in all PK biospecimens (serum, saliva, and RNA; −0.141, −0.141, and −0.103, respectively). This may indicate a special role for this known keystone pathogen, LPS, and gingipains in amplifying systemic inflammation for PK pathogenesis (Adams et al, 2019;Olsen et al, 2020;Jasemi et al, 2022;Lyra et al, 2022). NHANES data have shown that periodontitis is associated with leukocytosis in PK patients (Botelho et al, 2020) underlining an inflammatory context as a well-accepted part of the pathology (Hirsch et al, 2005;Lee et al, 2009).…”

Section: Discussionmentioning

confidence: 98%

Glucose-6-Phosphatase-Dehydrogenase activity as modulative association between Parkinson’s disease and periodontitis

Laugisch,

Ruppert-Jungck,

Auschill

et al. 2024

Front. Cell. Infect. Microbiol.

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The association between periodontitis (PD) and Parkinson’s disease (PK) is discussed due to the inflammatory component of neurodegenerative processes. PK severity and affected areas were determined using the following neuropsychological tests: Unified Parkinson’s Disease Rating Score (UPDRS) and Hoehn and Yahr; non-motoric symptoms by Non-Motor Symptoms Scale (NMSS), and cognitive involvement by Mini-Mental State Examination (MMSE). Neuroinflammation and the resulting Glucose-6-Phosphatase-Dehydrogenase (G6PD) dysfunction are part of the pathophysiology of PK. This study aimed to evaluate these associations in periodontal inflammation. Clinical data and saliva-, serum-, and RNA-biobank samples of 50 well-characterized diametric patients with PK and five age- and sex-matched neurologically healthy participants were analyzed for G6PD function, periodontal pathogens (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Prevotella intermedia, Campylobacter rectus, Fusobacterium nucleatum, and Filifactor alocis), monocyte chemoattractant protein (MCP) 1, and interleukin (IL) 1-beta. Regression analysis was used to identify associations between clinical and behavioral data, and t-tests were used to compare health and disease. Compared with PK, no pathogens and lower inflammatory markers (p < 0.001) were detectible in healthy saliva and serum, PK-severity/UPDRS interrelated with the occurrence of Prevotella intermedia in serum as well as IL1-beta levels in serum and saliva (p = 0.006, 0.019, 0.034), Hoehn and Yahr correlated with Porphyromonas gingivalis, Prevotella intermedia, RNA IL1-beta regulation, serum, and saliva IL1-beta levels, with p-values of 0.038, 0.011, 0.008, <0.001, and 0.010, while MMSE was associated with Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, serum MCP 1 levels, RNA IL1-beta regulation and G6PD serum activity (p = 0.036, 0.003, 0.045, <0.001, and 0.021). Cognitive and motor skills seem to be important as representative tests are associated with periodontal pathogens and oral/general inflammation, wherein G6PD-saliva dysfunction might be involved.Clinical trial registrationhttps://www.bfarm.de/DE/Das-BfArM/Aufgaben/Deutsches-Register-Klinischer-Studien/_node.html, identifier DRKS00005388.

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Section: Discussionmentioning

confidence: 98%

Glucose-6-Phosphatase-Dehydrogenase activity as modulative association between Parkinson’s disease and periodontitis

Laugisch,

Ruppert-Jungck,

Auschill

et al. 2024

Front. Cell. Infect. Microbiol.

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“…We have recently demonstrated a higher prevalence of periodontitis in PD patients [ 103 ] and possible systemic repercussions with the elevation of circulating white blood cell counts [ 106 ] and c-reactive protein [ 107 ]. In fact, systemic inflammation caused by periodontitis has been hypothesized to develop chronic neuroinflammation and ultimately interfere with PD pathogenesis [ 104 ].…”

Section: Microbial Dysbiosis and α-Synmentioning

confidence: 99%

Revisiting Alpha-Synuclein Pathways to Inflammation

Lyra

Machado

Rota

et al. 2023

IJMS

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Alpha-synuclein (α-Syn) is a short presynaptic protein with an active role on synaptic vesicle traffic and the neurotransmitter release and reuptake cycle. The α-Syn pathology intertwines with the formation of Lewy Bodies (multiprotein intraneuronal aggregations), which, combined with inflammatory events, define various α-synucleinopathies, such as Parkinson’s Disease (PD). In this review, we summarize the current knowledge on α-Syn mechanistic pathways to inflammation, as well as the eventual role of microbial dysbiosis on α-Syn. Furthermore, we explore the possible influence of inflammatory mitigation on α-Syn. In conclusion, and given the rising burden of neurodegenerative disorders, it is pressing to clarify the pathophysiological processes underlying α-synucleinopathies, in order to consider the mitigation of existing low-grade chronic inflammatory states as a potential pathway toward the management and prevention of such conditions, with the aim of starting to search for concrete clinical recommendations in this particular population.

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“…Systemic inflammatory markers, such as CRP, might have a role in early detection of inflammatory oral conditions in PD, together with other systemic inflammatory markers, e.g., WBC, IL-1alpha, IL-1beta, IL-17A and TNF-alpha ( 118–120 ).…”

Section: Dashboard Vital: Nonmotormentioning

confidence: 99%

Chaudhuri’s Dashboard of Vitals in Parkinson’s syndrome: an unmet need underpinned by real life clinical tests

Qamar,

Rota,

Batzu

et al. 2023

Front. Neurol.

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We have recently published the notion of the “vitals” of Parkinson’s, a conglomeration of signs and symptoms, largely nonmotor, that must not be missed and yet often not considered in neurological consultations, with considerable societal and personal detrimental consequences. This “dashboard,” termed the Chaudhuri’s vitals of Parkinson’s, are summarized as 5 key vital symptoms or signs and comprise of (a) motor, (b) nonmotor, (c) visual, gut, and oral health, (d) bone health and falls, and finally (e) comorbidities, comedication, and dopamine agonist side effects, such as impulse control disorders. Additionally, not addressing the vitals also may reflect inadequate management strategies, leading to worsening quality of life and diminished wellness, a new concept for people with Parkinson’s. In this paper, we discuss possible, simple to use, and clinically relevant tests that can be used to monitor the status of these vitals, so that these can be incorporated into clinical practice. We also use the term Parkinson’s syndrome to describe Parkinson’s disease, as the term “disease” is now abandoned in many countries, such as the U.K., reflecting the heterogeneity of Parkinson’s, which is now considered by many as a syndrome.

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Self-reported periodontitis and C-reactive protein in Parkinson’s disease: a cross-sectional study of two American cohorts

Cited by 14 publications

References 55 publications

Glucose-6-Phosphatase-Dehydrogenase activity as modulative association between Parkinson’s disease and periodontitis

Glucose-6-Phosphatase-Dehydrogenase activity as modulative association between Parkinson’s disease and periodontitis

Revisiting Alpha-Synuclein Pathways to Inflammation

Chaudhuri’s Dashboard of Vitals in Parkinson’s syndrome: an unmet need underpinned by real life clinical tests

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