There has been recent groundbreaking news that there is a causal link between Peridontal Disease and Alzheimer's Disease. Alzheimer's patients have peridontal disease but peridontal disease doesn't necessarily lead to Alzheimer's Disease. The message to all my readers and friends, brush when you wake up, brush after meals, floss 2 times a day. There is no time to waste. You can potentially add 10 good quality of life years to your health !
As a person who has initial stages of peridontal disease, I am very cognizant of the fact that I must regularly see my dentist to manage the condition, and this additional risk is another reason for me to see him at least 4 times a year. Below is an extract from the National Institute of Health's website :
Periodontal disease (PD) is an inflammatory oral disease that affects the supporting structures of the teeth (periodontium), including gingiva, periodontal ligament, cementum, and alveolar bone [1]. The disease results from complex interactions between the dental biofilm and host defense mechanisms. Bacteria and their components like lipopolysaccharides present in the biofilm induce an intensified host inflammatory response. This cascade of inflammatory response damages periodontal structures and leads ultimately to bone loss [1]. Being responsible for disability, speech impairment, low self-esteem, and reduced quality of life, PD has become a major public health concern that burdens the global healthcare system [2].
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a prevalence increasing exponentially with age [3,4]. It is characterized by an irreversible degeneration of neurons and neural connections beginning in the hippocampus and extending to the rest of the brain. People affected by Alzheimer's gradually lose cognitive abilities and autonomy. These symptoms consequently lead to advanced dementia and eventually to death. The cognitive decline that leads to AD has been related to two cardinal neuropathological features, beta-amyloid plaques (Aβ) and neurofibrillary tangles [5,6]. The amyloid plaques consist of deteriorating neuronal processes or neuritis, surrounding deposits of a central core protein called amyloid beta (or beta-amyloid). This protein is derived from a larger molecule called amyloid precursor protein, which is a normal component of nerve cells. The neurofibrillary tangle consists of abnormal accumulations of phosphorylated protein, called tau located within nerve cells. This protein is normally present in neurons. Abnormal chemical changes cause tau molecules to form tangles inside neurons.
There is a growing body of evidence in the literature suggesting a potential association between PDs and systemic diseases, particularly atherosclerotic vascular disease, pulmonary disease, diabetes, pregnancy-related complications, osteoporosis, and kidney disease as well as AD [2]. The periodontal medicine concept has been proposed to study the interrelationship between oral and systemic health. The presence of periodontal pathogens and their metabolic by-products may contribute to the body’s overall inflammatory burden, thus promoting the development of systemic conditions [2,7,8]. It has been suggested that periodontal pathogens could promote initiation or exacerbation of systemic diseases either by entering the bloodstream (bacteremia) or by stimulating an immuno-inflammatory response through the systemic release of toxins and local inflammatory mediators such as cytokines, prostaglandins, and serum antibodies into the bloodstream [2,7,8].
Most studies have indicated that Alzheimer's patients suffer from impaired oral health, a high incidence of PD, and an affected quality of life. These oral manifestations have been justified by the cognitive and motor deficits related to AD, compromising dental care and the maintenance of proper dental hygiene [9-18].
Authors have also suggested that PD may be a risk factor for AD. Hypotheses are mainly based on the involvement of periodontal pathogens and their virulence factors in the pathogenesis and progression of Alzheimer's, either by direct invasion of brain tissue or by indirect action of the bacterial load and pro-inflammatory mediators in systemic circulation [19-22]. Thus, following the elevation of the systemic inflammatory response, periodontal infection would contribute to cerebral and vascular pathologies by altering brain function and, as a result, worsen the neurodegenerative process characterizing AD [19-29].
The purpose of our systematic review was to evaluate how is PD related to the onset and progression of AD and to determine whether patients with PD would be at greater risk of developing AD compared to periodontally healthy subjects.
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