An article by Victoria Eugenia Criado Montoya,
Dentist-Periodontist and professor of the Periodontics Chair of the Faculty of Dentistry of the Central University of Venezuela
Periodontal disease: periodontitis
The Periodontal disease (PD) is an inflammatory disease that affects the supporting structures of the teeth (periodontium).made up of the gum, the periodontal ligament, the root cementum and the alveolar bone.1 When it affects only the gum it is called gingivitis and if the inflammation extends beyond this, it is called periodontitiswhich is the result of complex interactions between dental biofilm and host defense mechanisms; Bacteria and their products such as lipopolysaccharides induce an intensified host inflammatory response, which destroys the periodontium and ultimately leads to tooth lossl.
Being responsible for developing disability, speech impairment, low self-esteem and decreased quality of life, P has become a major public health problem that overloads the global healthcare system.1
Periodontitis (P) has traditionally been considered a chronic inflammatory pathology of multifactorial originwhich has as its primary etiological factor a highly organized biofilm of bacterial origin in a favorable ecological niche for its growth and development.2
The breakdown of the balance (dysbiosis) between bacterial aggression, of fundamentally anaerobic origin, and the host’s defenses, added to the presence of various risk factors (genetics, tobacco, certain systemic conditions such as diabetes), a inadequate oral hygiene and/or lack of regular visits to the dentistallow the development of periodontitis.2
This is the most common non-communicable inflammatory disease in humans worldwide, affecting only 8% of the adult population in its most serious form.3 In 2010, 3.9 billion people worldwide were reported to have periodontal disease, with a prevalence of mild periodontitis of 35%, and moderate to severe periodontitis of 11%.4 According to the US Centers for Disease Control and Prevention (CDC), periodontitis is considered a global pandemic.5
Neurodegenerative diseases
We understand neurodegenerative diseases to be the set of diseases and disorders characterized by dprogressive degradation of the neurons that are part of our nervous system until they die, causing a series of effects or repercussions of varying severity; which, in turn, can generate advanced loss of mental and/or physical faculties to cope with the demands of daily life and even lead to death due to cardiorespiratory arrest (one of the most frequent causes of death in this type of conditions), requiring external support and different degrees of help.6
The causes of this type of disorders or diseases can be multiple, with a large number of factors that can influence their appearance. Its origin will depend largely on the neurodegenerative disease we are talking about; However, in most cases, The specific causes of the appearance of these pathologies are unknown..
Among the possible etiologies that are suspected for some of them are: viral diseases not yet curable, that affect the nervous system, as well as the presence of alterations in the autoimmune system that attack the body’s own cells, trauma and/or stroke (in the case of vascular dementia). An excess of some elements such as Lewy bodies, beta-amyloid plaques or neurofibrillary tangles is also observed in some dementias.
In this sense, within this type of diseases, the best known are those that are included within the group of dementias such as Alzheimer’s Disease. Alzheimer’s (AD), or the pathologies that cause them such as: Parkinson’s Disease, Multiple Sclerosis, Huntington’s Korea, Friedreich’s Ataxia, and Creutzfeldt-Jakob disease. It is estimated that By 2050 more than thirteen million people will suffer from AD in the world; This means that the death rate from this condition will increase.6
Relationship between periodontitis and neurodegenerative diseases
Different mechanisms have been described to explain the interaction between periodontitis and some neurodegenerative diseases, especially Alzheimer’s:
- Bacteremia produced by the passage of subgingival bacteria into the systemic circulation, through the ulcerated epithelium of the periodontal sac, which can cause infections in other parts of the body.
- Dissemination of inflammatory mediators and bacterial products into the systemic circulation, through the ulcerated wall of the periodontal pockets, triggering an inflammatory response at the systemic level.
- Colonization and infection of the respiratory tract lower in individuals with predisposing factors, mainly due to direct aspiration.7
A recent study showed that people with brain injuries had a higher prevalence of poor oral health parameters and periodontitis.8 The brain, which was thought to have no immune responses, or to be diminished due to its state of “immune privilege”can suffer different inflammatory processes that contribute to the development of Alzheimer’s disease, such as complement activation and the expression of cytokines and chemokines.9
In fact, Inflammation is considered the link between periodontitis and Alzheimer’s disease. Likewise, the presence of activated glial cells that produce significant levels of inflammatory cytokines is a hallmark of Alzheimer’s disease.10
In addition to the direct damage caused by b-amyloid plaques and tau aggregates, the innate immune response attempts to clear these aggregates from the brain, but instead, aggravates neurodegeneration.11 12 At the same time, it has been detected a increased proinflammatory cytokines in older adult patients with Alzheimer’s disease and periodontitis.13
Even, periodontopathogenic bacteria as: T. denticola and C. pneumoniae were detected in brains with Alzheimer’s disease post mortemsuggesting that, in addition to inflammatory mediators, some periodontal pathogens can invade the brain by crossing the blood-brain barrier.14
After a review of the current literature, studies showed that Individuals with cognitive impairment and other types of dementia had increased clinical parameters of periodontitis. In this way, the possible relationship between P and EA is considered, as a result of the high incidence of periodontopathogenic bacteria causing a chronic inflammatory state low grade (neuroinflammation).
Therefore, more studies are required to support the bidirectional link between P and EAespecially cases and controls and cohorts, given the impossibility of conducting clinical trials due to ethical considerations. In addition, health professionals are urged to consider the association of these pathologies, and become increasingly involved in preventive oral health care.15 16 17
Conclusions
The Periodontitis is defined as a chronic inflammatory disease multifactorial associated with dysbiosis of the oral microbiota, and is characterized by the progressive destruction of the periodontium, leading to tooth loss. On the other hand, the Alzheimer’s is a chronic, progressive and irreversible neurodegenerative disease.considered the most common cause of dementia; a term that describes memory loss and other impairments in cognitive ability.
Patients with P have a higher risk of AD compared to periodontally healthy individuals, since it has been determined that AD leads to the loss of self-care and, in the later stages, can lead to a decrease in motor function, generating oral hygiene difficulties; collaborating with the onset of periodontitis. However, the results should be interpreted with caution given the methodological limitations found.
understand the contribution of P to the etiopathogenesis of AD would be of great benefit to the elderly population from all over the world. For future research, epidemiological studies with a better methodological design are needed, such as prospective ones that use the new classification of periodontitis, which evaluates its severity, to associate it with the different degrees of AD in long-term longitudinal studies.
Despite the lack of solid evidence on the effect of P on AD, it is vital importance to improve the oral health of subjects with ADand provide regular dental and periodontal care. Teamwork and cooperation between dentists and neurologists is also necessary to ensure better patient care.
Literature:
1.- Papapanou PN, Sanz M, Buduneli N, Dietrich T, Feres M, Fine DH, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions: Classification and case definitions for periodontitis. J Clin Periodontol 2018;45 Suppl 20:S162–70.
2. -Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases. Lancet. 2005;366:1809—20, http://dx.doi.org/10. 1016/S0140-6736(05)67728-8.
3.- Kassebaum NJ, Bernabe E, Dahiya M, Bhandari B, Murray CJ, Marcenes W. Global burden of severe periodontitis in 1990-2010: A systematic review and meta-regression. J Dent Res. 2014;93:1045—53, http://dx.doi.org/10.1177/ 0022034514552491.
4.- Richards D. Oral diseases affect some 3.9 billion people. Evid Based Dent 2013;14:35.
5.- CDC researchers find close to half of American adults have periodontitis. J Can Dent Assoc 2012;78:c136.
6.- Oscar Castillero Mimenza. Neurodegenerative diseases: types, symptoms and treatments. Psychology and Mind Portal. https://psicologiaymente.com/clinica/enfermedades-neurodegenerativas. Reviewed in February 2018.
7.- Armstrong R. Risk factors for Alzheimer’s disease. Folia Neuropathol 2019;57:87–105.
8.- Kothari M, Spin-Neto R, Nielsen JF. Comprehensive oral health assessment of individuals with acquired brain-injury in neuro-rehabilitation setting. Brain Inj 2016; 30:1103e8.
9.- Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer’s disease. Neurobiol Aging 2000; 21:383e421.
10.- Kamer AR, Craig RG, Dasanayake AP, Brys M, Glodzik Sobanska L, de Leon MJ. Inflammation and Alzheimer’s disease: possible role of periodontal diseases. Alzheimers Dement 2008; 4:242e50.
11.- Gaur S, Agnihotri R. Alzheimer’s disease and chronic periodontitis: is there an association? Geriatr Gerontol Int 2015; 15:391e404.
12.- McGeer PL, McGeer EG. Inflammation, autotoxicity and Alzheimer disease. Neurobiol Aging 2001; 22:799e809.
13.-Cestari JA, Fabri GM, Kalil J, Nitrini R, Jacob-Filho W, de Siqueira JT, etal. Oralinfections and cytokine levels in patients with Alzheimer’s disease and mild cognitive impairment compared with controls. J Alzheimers Dis 2016; 52:1479e85.
14.- Poole S, Singhrao SK, Kesavalu L, Curtis MA, Crean S. Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer’s disease brain tissue. J Alzheimers Dis 2013; 36:665e77.
15.-García Vásquez A., Vidal Chávez S., Anccasi Zevallos M., Franco Quispe G., Ramos Perfecto D., and Mattos Vela,M. Association between periodontal disease and Alzheimer’s disease. Bionatura 2023, 10.21931/RB/CSS.2023.08.04.26Available from: http://dx.doi.org/10.21931/RB/2023.08.04.26.
16.- Desta N. Pathophysiological association between periodontal disease and Alzheimer’s disease: Im portance of periodontal health in the elderly. J Oral Biosci. 1 Dec 2021;63(4):351-9.
17.- Aragón, F., Zea-Sevilla, MA, Montero, J. et al. Oral health in Alzheimer’s disease: a multicenter case-control study. Clin Oral Invest 223061–3070 (2018). https://doi.org/10.1007/s00784-018-2396-z.