Periodontium is a specialized tissue in the oral cavity that surrounds the teeth and acts as a supporting tissue for the teeth. It is made of different components (alveolar bone proper, periodontal ligament, cementum and gingiva). All these components are made up of the basic tissue that build up the human body such as epithelium and connective tissue. The human body undergoes a process called aging which could be defined as the collection of changes in a human being over time. Not only the human body undergoes changes in the process of aging, the microbiota that make up 1-3% of the human body (NIH Human Microbiome Project, 2009) (for every human cell there are 10 microorganisms, the percentage is so small due to light weight) also undergo alterations in the composition and proportion such as decreased diversity and increase of the enteropathogens that increase the risk factor of chronic inflammation (Carmen Garcia Pena, 2017). Since birth, human infant is exposed and colonised by a large amount of microorganisms, mostly from the mother of the infant, the properties of the habitat is what determines which microorganisms can colonise and grow further which give the result of different microbiota at different sites (Phil D. Marsh, 2015). The oral cavity contains a large amount of these microbes, over 700 species or phylotypes (Jorn A. Aas, 2005) have been detected and over 50% have yet not been cultivated. Those microorganisms as mentioned before colonise different sites of the oral cavity and their composition depends on the properties of the site they are invading. The most interesting site that the microorganism are colonising that affect the health of periodontium is the dental plaque.
This review will be discussing the effect of aging on periodontium. Both parts of periodontium, soft and hard tissue, how aging affect them as a unit and also how it affects them individually. Biologic and microbiologic alterations will be reviewed. The paper will review the effect of aging on the gingival epithelium, gingival connective tissue, periodontal ligament, cementum, alveolar bone and cementum, bacterial plaque, immune and inflammatory response. It will also engage in aging effect on progression of periodontal diseases and response to treatment of the periodontium
An electronic literature search was made using PubMed abstract, clinical key, Ebsco host with the keywords such as “periodontology”, “aging”, “alveolar bone”,” periodontal ligament”,” microorganisms”,” oral cavity”, “immune OR inflammatory response” Etc. The words ‘OR’ and ‘AND’ were incorporated in different ways to reach the results wanted. No specific restrictions for the date or the the type of literature was made. In order to find relevant literature for this review the abstracts were read and based on that the relevancy of the article was determined. Irrelevant articles were excluded. Not only relevancy was taken in consideration but the reliability of the sources was also observed.
2. Gingiva and aging
Gingiva is the tissue that is exposed to the oral cavity. Its histological components are gingival epithelium and gingival connective tissue. This chapter will discuss the aging effects on gingival epithelium, gingival connective tissue individually and the tissue interference.
1.3 Gingival epithelium
Gingival epithelium is made up of several part. It covers the underlying connective tissue. There is both keratinized and non-keratinized epithelium in the gingival epithelium. It is made up of junctional epithelium (2), sulcular epithelium (1) and oral epithelium covering the free and attached gingiva
Figure 1Tooth: incisor and surrounding structure, Shu-Xin Zhang, 1999
The differences between these different epithelial parts that make up the gingival epithelium is just some structural differences. Epithelial tissue acts as a barrier, as it does in the entire body. Gingival epithelium does the same, but its role as a barrier get compromised with age (Shklar G., 1966). This will be followed by higher permeability for bacterial antigens and lower resistance to functional trauma. A change of the cell density and thinning of the epithelial tissue is also seen. A flattening of the rete pegs and higher epithelial ridges were also documented (Carranza, 2015). According to a study done by Anja Ainamo, 1981, the width of attached gingiva would increase with age which might be confusing due to the fact that recessions are more seen in elderly patients Although the recessions are not due to a physiologic process of age but could be explained by the cumulative trauma or periodontal inflammation (Carranza, 2015)
1.4 Gingival connective tissue
Gingival connective tissue or lamina propriety which is underlying the gingival epithelial tissue is mostly composed of fibres such as collagen, elastic and reticular, fibroblasts, blood vessels, nervous tissue and extra cellular matrix which is mostly water and contains glycoprotein and proteoglycans. It is divided in two two layers, papillary layer which is the closest has the junction with the epithelial tissue and the reticular layer which has the junction of the periosteum. There are collagen fibre bundles called gingival fibres aad they are concentrated in the marginal gingiva which have the function of bracing marginal gingiva firmly and provide rigidity and unite free gingiva with cementum (Carranza, 2015).
Figure 2: Gingival biopsy, Fermin A. Carranzas, 2015
The older gingival connective tissue demonstrates structural and functional changes. It is very coarse and very dense and has higher mechanical strength and also higher denaturing temperature, these macromolecular changes appear to improve the stability of the collagen (Mackenzie, 1996). Aged fibroblast appears to have a higher degree of intracellular collagen phagocytosis and lower rate of collagen synthesis which would normally result to a lower amount of collagen but due to the macromolecular changes mentioned above, the collagen has more stability which explains the increased amount of collagen in aged gingival connective tissue (Carranza, 2015). Gingival fibres are always affected by oral microorganisms and the products they produce. For example, the LPS (lipopolysaccharides) that are located on bacterial cells cell wall induce secretion of inflammatory mediators which also have some effects on the fibroblasts. Alterations in ECM proteoglycans are also observed.
1.5 Interference between the connective and epithelial tissue
In the the interference between the gingival epithelium and connective tissue there is the epithelial rete pegs and connective tissue ridges as seen in figure 2. With age the rete pegs become flatter and the connective tissue papillae dominates (Carranza, 2015).
3. Periodontal ligament and aging
The periodontal ligament which is an extremely vascular and complicated cellular connective tissue has the role of anchoring the teeth into the alveolar bone, it also has other functions. The width of the periodontal ligament space is on average 0.2 mm, it could decrease if the tooth loses its functionality and increase in theses teeth that have an increased functionality. The periodontal ligament is composed of collagen periodontal fibres, connective tissue cells such as fibroblasts which are the most common, cementoblast and osteoblast. It also has epithelial rests of Malassez. Immune cells and neurovascular cells are also present in the periodontal ligament. Ground substance is also seen in the spaces between the fibres and cells which is composed of mainly water, glycoaminoglycans, proteoglycans and glycoproteins (Carranza, 2015).
Reduction in the number of fibroblasts, irregularity in the structure and reduced organic matrix production are changes seen in the aged periodontal ligament which are similar to the changes seen in the gingival connective tissue. Increase in elastic fibres and decreased number of epithelial cells rests is also present which decreases by degradation and disappearing or by calcification and becoming cementicles. There have been conflicting variable results about width of periodontal ligament space in aged human beings, but the functional status of teeth plays a role, width will decrease if tooth is unopposed and has decreased functionality and increase with increased functionality, both these situation are due to loss of teeth which explain the confliction because the results will be depending on the functionality of the tooth. Age has shown to have negative effects on the chemotaxis, motility and proliferation rate of the cells of the periodontal ligament such as osteoblasts (Groessner-Schreiber B
,1992) (Nishimura F,1997).
Figure 3 periodontal ligament, with its many blood vessels (Anthony L. Mescher,2013)
4. Cementum and ageing
Cementum is calcified, avascularised connective tissue that covers the roots of the teeth. The formation process is continuous thought the life. The width of cementum increases with age. collagen fibres are embedded in the cementum during its formation Cementum also exhibits collagen fibres and calcified interfibrillar matrix. There are two types of cementum, cellular and acellular The classification is according to the presences of cells. Collagen fibres are also present and classifies as intrinsic which are produced by the cementoblasts and extrinsic which are embedded in the cementum from the periodontal ligament. Acellular cementum is the first to be formed, before the tooth reaches the occlusal plane with thickness raging from 50 to 200 ?m. The secondary cementum is formed after the tooth reaches the occlusal plane contains more irregularities (Yamamoto, hasegawa)
Death of cells is common in the lifecycle of the cementocysts and it could be explained by the rapid reduction in the accessibility of nutrition and the poor elimination of waste products of the cementocytes. With age, acellular cementum dominates. Remodelling of the cementum occurs but also resorption is also observed which with age result in irregularities in the surface of the cementum (Carranza, 2015)
5. Alveolar bone and ageing
The alveolar bone consists of osteoblasts that produce matrix vesicles right before mineralisation, theses enzyme filled vesicles help to catalyse the nucleation of hydroxyapatite crystals. When these crystals grow and develop they form bone nodules. The process of bone deposition and remodelling and secretion of collagen comes later which then forms the matured lamellar bone (Carranza, 2015). The alveolar bone, just like the periodontal ligament, acts as a support for the teeth. In general, bone formation gets less with age which leads to a decrease in bone mass (Inoue, et Al., 1997).
Physiologically, the alveolar bone is in balance between osteoblastic and osteoclastic activity, which give it its plasticity property. These cells are affected by hormones such as the parathyroid hormone, calcitonin, oestrogen, and vitamin D, concentration of calcium and phosphate in plasma, neurotransmitters, growth factors and local cytokines (Sodek J, 2000).
Reduction of osteoblast-proliferating precursors or decreased synthesis and secretion of essentiell bone matrix protein may explain the reduction in bone formation (Inoue, et Al., 1997). in the alveolar bone the osteoblasts are surrounded by extra cellular matrix which plays a major role in bone metabolism, there is a possibility that this matrix gets dysfunctional with age (Hebling, 2012).
Cellular damage may also be due to the oxygen-free radicals that also grant the ageing process. An in vitro study has showed that the oxygen radical treated fibronectin inhibits bone nodule formation by osteoblasts in comparison with normal fibronectin. This shows that fibronectin has an important role in the activity of osteoblasts and the damage by oxygen radical that comes with age may explain the age related reduction in bone formation (Hebling, 2012).
Physiologic migration of teeth occurs because the teeth movement doesn’t stop when the eruption is completed, it instead continues. Time and wear leads to flatter proximal contact points and the teeth tend to move mesially which leads to decrease in the length of the alveolar arch by 0,5 cm at the age of 40 (Carranza, 2015).
6. Bacterial plaque and ageing
The amount of bacterial plaque has been suggested to change with age. Studies have shown an increase of the bacterial plaque in elderly but it could also be due to the increase of hard tissue surfaces due to recessions and also because exposed root surface is not as as smooth as enamel so it is a retentive surface for plaque. Although there have been other studies that doesn’t confirm that the bacterial plaque increase with age (Carranza, 2015). There has been discussion about the change of the composition of the microflora with age but to be able to differentiate age related differences from differences due to a shift in the ecology is difficult. (Mombelli A, 2011)
7. Immunosenescene and periodontal cells interaction
Immunosenescene is the negative effect of natural ageing on the immune system. The immune system goes through changes whilst ageing, structural and morphological changes. The most noticeable changes are in thymus which is a primary lymphoid organ that also is an endocrine gland. The thymus is responsible of T-cells production and maturation (Aspinall R, 2000). The thymus is declines in activity by early teens, the stroma of it begins slowly to be replaced by adipose tissue. Thymus shrinkage continues until the of 70 years (Tosi P,1982). There is still a discussion whether the total number of T-cells are getting affected by the thymus shrinkage. T-lymphocytes plays a major role in immune response.
Age related changes in leukocytes and lymphocytes subpopulations have been reported have been (Pawelec G, 2014). A faster and more severe development of gingivitis and an altered inflammatory response induced by gingivitis have also been reported. An increase of antibodies and B-lymphocytes was found in crevicular fluid and a decrease in polymorphonucelar leukocytes (Hebling, 2012).
A study was done on patients in menopause to analyse the secretion of interleukin 1beta and interleukin 6 (Reinhardt RA, 1998). The results showed that menopausal patients that were not undergoing hormone therapy have higher rate of interleukin 1beta and interleukin 6 compared to patients that were undergoing hormonal treatment. Interleukin 6 is responsible for the bone dectruction in periodontitis, its stimulate the osteoclasts precursors (Hebling, 2012). According to another study, there were a greater concentration pf interleukin 1 beta and interleukin 8 in patients that have oestrogen deficiency compared to those with no oestrogen deficiency (Reinhardt RA, 1998). The hypothesis is the older periodontal ligament cells secretes more interleukin 1 beta for a higher rate of alveolar bone resorption in elderly (Hebling, 2012)
8. Ageing as a risk factor for development of periodontal disease
The changes to the periodontal tissue that are related to age could serve as a risk factor for periodontal disease. Moderate loss of periodontal attachment and alveolar bone is associated with age, age by itself doesn’t lead to critical loss of a periodontal support loss in a healthy individual, severe periodontitis is not a caused by age (Huttner EA, 2009).
There are differences between different older age groups in attachment loss and alveolar bone loss which was shown in cross-sectional studies measuring disease experience (Hebling, 2012)
Other longitudinal studies discussing the relation between age and attachment loss or bone loss showed important correlation between age and risk of periodontal disease (Ismail AI,1959) Some studies show no significant contrast within age groups above 65 years, which leads to the conclusion of the age as a risk factor for development of periodontal disease may not be linear (Helbing, 2012)
An odds ratio of 10.4 was reported by A 28-year follow-up study for people between 36-50 years old in comparison with people between 5-15 years. It is possible to compare these result in general with other clinically significant risk factors such as smoking that had an odds ratio of 14. it although comes to a mean increase in clinical attachment level of only 1.34 mm over 28 years 85, which is not enough alone to cause tooth loss (Ismail AI,1959).
9. Ageing and the response to periodontal treatment
For a periodontal treatment to show positive effects there are some requirements from both the patients side and the practitioner. For instance, a thorough supra and subgingival cleaning is required from the practitioner and a maintenance of good oral hygiene and plaque control is required from the patient at home. If one of these requirements are not achieved, the loss of attachment might continue which means that the periodontal therapy was not effective which leads to faster progression with increasing age. According to Carranza’s clinical periodontology, there is not many studies that have directly compared the responsiveness to periodontal treatment in different aging. Even though presence of some histologic differences in aged periodontium, no difference in responsiveness to nonsurgical or surgical treatment for periodontitis have been demonstrated.
There are histologic changes to all component of periodontium but no strong evidence of changes in microbiology of the oral microflora to the adult patient. Some inferior changes in gingival epithelium like thinning and higher permeability for microbial antigen, also for connective tissue –epithelium interference, the rete-pegs become flatter which allows worse barrier for the underlying connective tissue. Age has also shown lower rate of alveolar bone formation and that is due to the Reduction of osteoblast-proliferating precursors or decreased synthesis and secretion of essential bone matrix protein.
Age has negative effects on the immune system which could lead to faster and more severe development of gingivitis and an altered inflammatory response induced by gingivitis.
The conclusion that is obtained from this review is that ageing as a risk factor by itself cannot lead to the severe loss of periodontal attachment in healthy individuals. even though there are some differences to the periodontium with age, it is just not enough for example tooth loss. The main changes to the tissue are changes in the cells. Ageing alone leads to no critical loss of the periodontal attachment in the healthy elderly.
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