Abstract
Many neurodegenerative diseases cause progressive deterioration in specific areas of the nervous system. This affects both the structure and function of neural tissues. Two of the most common neurodegenerative diseases are Alzheimer disease (AD) and Parkinson disease (PD). AD initially affects cognitive function, wherease PD commonly begins by affecting motor function, although later in the PD trajectory cognitive impairment often ensues. Both conditions are chronic, debilitating and progressively limit the individual’s ability to function independently. As the likelihood of developing neurodegenerative diseases increases with age, the global burden of both AD and PD is set to rise steeply. Between 1980 and 2015, average age at death increased from 73.1 to 81.6 years in the UK and 73.7 to 78.7 years in the USA, a trend seen in most countries with an inverted population age pyramid1. The 2016 worldwide estimates of those living with AD or PD are 44 million and 6 million, respectively2. In the UK alone, the number of people with PD is approximately 16,000. For AD, this is 500,000, representing 62% of those with dementia. In 95% of cases the age of diagnosis is over 65 years; prevalence of dementia rises from 7% over the age of 65, to 13% over the age of 75, and approximately 60% of those affected overall are female3. The annual cost of dementia in the UK is approximately £26.3 billion3, and the annual financial impact of living with PD in the UK has been estimated to be over £16,500 for each individual household affected, costing the UK economy between £450 million and £3 billion per year4. There is also a high social cost, as these diseases often affect the quality of life of carers and loved ones as well as the individuals affected. Periodontitis has for some time been associated with neurodegenerative diseases, largely because of the obvious related decline in ability to provide self-care for the teeth and surrounding tissues. However, it is now being recognised that the relationship might be bi-directional5. There is a growing body of evidence suggesting a potentially proactive role for periodontal pathogens and the periodontal chronic low grade inflammatory response in the development of some types of neurodegenerative diseases. Like many chronic inflammatory diseases, periodontitis is similarly age-related, with onset commonly occurring in mid-life.
Currently there is no cure for AD or PD; treatment of neurodegenerative conditions is limited to, at best, delaying the worsening symptoms. This is in some ways similar to the goal of conventional periodontal treatment, which is to slow the progression of periodontal destruction, ideally reaching a state of periodontal stability. The key to developing improved treatment modalities is likely to be found in discoveries relating to the pathogenesis of these conditions. Whilst the causes of the neuropathology of AD and PD remain somewhat elusive, they are likely to be multifactorial. It has been known for some time that peripheral infection is a strong risk factor for the development and progression of AD in elderly populations. Peripheral infection is a common cause of delirium in the elderly, and delirium has been shown to increase the risk of developing dementia eight-fold over the following 10 years6. Cognitive decline has also been shown to occur at a more rapid rate following a period of delirium in those already diagnosed with AD7. With increased age, and in AD and PD, the blood–brain barrier (BBB) can have increased permeability8,9. However, it is likely that the initiating factors associated with AD or PD occur in mid-life and may be low level, chronic infections. It has recently been suggested that periodontal pathogens and/or the peripheral inflammatory state seen in periodontitis could be implicated in neurodegeneration10,11. These pathogens may slowly increase the permeability of the BBB and produce pro-inflammatory proteins resulting in peripheral and neural inflammation, ultimately leading to neurodegeneration. Thus both AD and PD may be driven by neuroinflammation; this chapter seeks to examine its origin and to discuss its association with periodontitis and its possible role in these two neurodegenerative diseases.
Currently there is no cure for AD or PD; treatment of neurodegenerative conditions is limited to, at best, delaying the worsening symptoms. This is in some ways similar to the goal of conventional periodontal treatment, which is to slow the progression of periodontal destruction, ideally reaching a state of periodontal stability. The key to developing improved treatment modalities is likely to be found in discoveries relating to the pathogenesis of these conditions. Whilst the causes of the neuropathology of AD and PD remain somewhat elusive, they are likely to be multifactorial. It has been known for some time that peripheral infection is a strong risk factor for the development and progression of AD in elderly populations. Peripheral infection is a common cause of delirium in the elderly, and delirium has been shown to increase the risk of developing dementia eight-fold over the following 10 years6. Cognitive decline has also been shown to occur at a more rapid rate following a period of delirium in those already diagnosed with AD7. With increased age, and in AD and PD, the blood–brain barrier (BBB) can have increased permeability8,9. However, it is likely that the initiating factors associated with AD or PD occur in mid-life and may be low level, chronic infections. It has recently been suggested that periodontal pathogens and/or the peripheral inflammatory state seen in periodontitis could be implicated in neurodegeneration10,11. These pathogens may slowly increase the permeability of the BBB and produce pro-inflammatory proteins resulting in peripheral and neural inflammation, ultimately leading to neurodegeneration. Thus both AD and PD may be driven by neuroinflammation; this chapter seeks to examine its origin and to discuss its association with periodontitis and its possible role in these two neurodegenerative diseases.
Original language | English |
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Title of host publication | Periodontitis and systemic diseases |
Subtitle of host publication | Clinical evidence and biological plausibility |
Editors | Josefine Hirschfeld, Iain Chapple |
Place of Publication | Germany |
Chapter | 9 |
Number of pages | 44 |
Edition | 1st |
Publication status | Accepted/In press - 1 Apr 2021 |
Research Groups and Themes
- Cerebrovascular and Dementia Research Group
Keywords
- peridontics
- general dentistry