During the past 25 years, there has been an explosion of information regarding the occurrence of gastrointestinal dysfunction in Parkinson’s disease. In this review, the clinical features of gastrointestinal dysfunction in Parkinson’s disease will be described and information regarding the potential role of the enteric nervous system and the gut microbiome in the genesis of Parkinson’s disease will be addressed. Recognition is growing regarding the role that gastroparesis and small intestinal dysfunction may play in Parkinson’s disease, especially with regard to erratic responses to anti-Parkinson medication. The presence of enteric nervous system involvement in Parkinson’s disease is now well established, but whether the enteric nervous system is the starting point for Parkinson’s disease pathology remains a source of debate. The potential role of the gut microbiome also is beginning to emerge. Gastrointestinal dysfunction is a prominent nonmotor feature of Parkinson’s disease and dysfunction can be found along the entire length of the gastrointestinal tract. The enteric nervous system is clearly involved in Parkinson’s disease. Whether it is the initial source of pathology is still a source of controversy. There also is growing recognition of the role that the gut microbiome may play in Parkinson’s disease, but much more research is needed to fully assess this aspect of the disorder.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(15)00007-1.pdf

Gastrointestinal Dysfunction in Parkinson’s Disease

Increasing evidence has suggested an independent association between periodontitis and a range of comorbidities, for example cardiovascular disease, type 2 diabetes, rheumatoid arthritis, osteoporosis, Parkinson’s disease, Alzheimer’s disease, psoriasis, and respiratory infections. Shared inflammatory pathways are likely to contribute to this association, but distinct causal mechanisms remain to be defined. Some of these comorbid conditions may improve by periodontal treatment, and a bidirectional relationship may exist, where, for example, treatment of diabetes can improve periodontal status. The present article presents an overview of the evidence linking periodontitis with selected systemic diseases and calls for increased cooperation between dentists and medical doctors to provide optimal screening, treatment, and prevention of both periodontitis and its comorbidities.

https://tandfonline.com/doi/pdf/10.1080/20002297.2017.1332710

Comorbidity of periodontal disease : two sides of the same coin? An introduction for the clinician

Early involvement of gut is observed in Parkinson’s disease (PD) and symptoms such as constipation may precede motor symptoms. α-Synuclein pathology is extensively evident in the gut and appears to follow a rostrocaudal gradient. The gut may act as the starting point of PD pathology with spread toward the central nervous system. This spread of the synuclein pathology raises the possibility of prion-like propagation in PD pathogenesis. Recently, the role of gut microbiota in PD pathogenesis has received attention and some phenotypic correlation has also been shown. The extensive involvement of the gut in PD even in its early stages has led to the evaluation of enteric α-synuclein as a possible biomarker of early PD. The clinical manifestations of gastrointestinal dysfunction in PD include malnutrition, oral and dental disorders, sialorrhea, dysphagia, gastroparesis, constipation, and defecatory dysfunction. These conditions are quite distressing for the patients and require relevant investigations and adequate management. Treatment usually involves both pharmacological and non-pharmacological measures. One important aspect of gut dysfunction is its contribution to the clinical fluctuations in PD. Dysphagia and gastroparesis lead to inadequate absorption of oral anti-PD medications. These lead to response fluctuations, particularly delayed-on and no-on, and there is significant relationship between levodopa pharmacokinetics and gastric emptying in patients with PD. Therefore, in such cases, alternative routes of administration or drug delivery systems may be required.

Gut dysfunction in Parkinson's disease.

No comprehensive study has previously been published on orofacial function in patients with well-defined Parkinson's disease (PD). Therefore, the aim of this study was to perform an overall assessment of orofacial function and oral health in patients, and to compare the findings with matched control subjects. Fifteen outpatients (nine women and six men, 61-82 yr of age; Hoehn & Yahr Stages 2-4; and with motor impairment ranging from 17 to 61 according to the Unified Parkinson's Disease Rating Scale, Objective Motor Part III) were examined in their 'on' state together with 15 age- and gender-matched controls. Orofacial function and oral health were assessed using the Nordic Orofacial Test, masticatory ability, performance and efficiency, oral stereognosis, jaw opening, jaw muscle tenderness, the Oral Health Impact Profile-49, number of natural teeth, and oral hygiene. Orofacial dysfunction was more prevalent, mastication and jaw opening poorer, and impact of oral health on daily life more negative, in patients with PD than in controls. The results indicate that mastication and orofacial function are impaired in moderate to advanced PD, and with progression of the disease both orofacial and dental problems become more marked. It is suggested that greater awareness of the special needs in PD patients and frequent dental visits are desirable to prevent dental diseases and decay and to support masticatory function.

Orofacial function and oral health in patients with Parkinson’s disease

The diagnoses of periodontal diseases (PD) are primarily based on clinical examination and radiographic parameters. In this pilot exploration we want to supply some evidence whether metabonomic profiling of saliva samples can provide a signature of the disease. Saliva samples were analyzed by Nuclear Magnetic Resonance (NMR) metabonomics from 22 healthy subjects (HS) and 32 patients with clinic and radiographic diagnosis of different PD: Gingivitis (G), Localized Chronic Periodontitis (LCP), Generalized Chronic Periodontitis (GCP), Localized Aggressive Periodontitis (LAP), and Generalized Aggressive Periodontitis (GAP). Pattern recognition analysis of NMR profiles can discriminate GCP patients (n = 21) from HS (n = 22) with an accuracy of 84.1%. Metabolic profiles of GCP patients exhibited higher concentrations of acetate, γ-aminobutyrate, n-butyrate, succinate, trimethylamine, propionate, phenylalanine and valine, and decreased concentrations of pyruvate and N-acetyl groups compared with controls. Our results can provide a contribution to the understanding of the biochemical network and pathway in the GCP and other PD, however at this stage the method can not be extended to the general population as a ready-to-use clinical tool, due to the limited cohort recruited and the exploratory nature of this work. Anyway, a further validation of the statistical model on a larger cohort is in progress with the aim to demonstrate the potential impact in clinical practice of our findings.

Kenichi Kashihara

Papers

Increased Frequencies of Caries, Periodontal Disease and Tooth Loss in Patients With Parkinson's Disease