The document discusses aging changes that occur in periodontal tissues. It notes that aging leads to intrinsic, stochastic, functional, and clinical changes in tissues. Specifically, it outlines changes seen in the gingiva like thinning epithelium, denser connective tissue, and reduced cellularity. The periodontal ligament sees decreased collagen fibers and reduced elasticity. Cementum increases in width and alveolar bone has reduced density and increased resorption. Systemic factors like reduced bone formation and immune senescence also influence the periodontium with age. Overall, aging is associated with structural and functional alterations in oral tissues that must be differentiated from pathological conditions.

1. AGING IN
PERIODONTIUM
D R M A N I S H A S I N H A
I S T Y E A R P G
RAJARAJESWARI DENTAL COLLEGE AND HOSPITAL

2. 1 .INTRODUCTION
2 .CELLULAR AGING
3. GENERAL FEATURES OFAGING
4. EFFECTS OFAGING ON PERIODONTIUM
Gingival epithelium
Gingival connective tissue
Periodontal ligament
Cementum
Alveolar bone
Bacterial plaque
5. SYSTEMIC AGING AND PERIODONTIUM
6. IMMUNE SENSECENCE AND PERIODONTAL CELL INTERACTION
7. EFFECT OFAGING ON PROGRESSION OF PERIODONTAL DISEASE
8. AGING AND RESPONSE TO TREATMENT ON PERIODONTIUM
9. EFFECT ON WOUND HEALING AND PROGNOSIS
10. CONCLUSION

4. DEFINITION
• Aging is a complex, continuous, and slow process
• that gradually involves most, if not all, organs of the
• organism, causing abnormal functioning both in
• qualitative and quantitative terms as well as
• morphological or structural changes.

5. Comfort (1956) Gottlieb & Orban

6. • Improvement in both social living conditions and health care has
led to a greater life span for people across the globe, resulting in an
increase in periodontal disease expectancy among the dentate elderly people.
• Some loss of periodontal attachment and alveolar bone may be expected in
older persons, but age alone in a healthy adult does not lead to a critical loss
of periodontal support.

7. • Alterations in oral tissues do occur with age. These histophysiological and clinical
alterations in the oral cavity associated with age must be differentiated from
pathological conditions.
• Although the severity of periodontal disease is known to be associated with age,
functional changes in periodontal tissue cells during the aging process have not been
well characterized.

8. CELLULAR AGING
• Cellular aging is the result of a progressive decline in the
proliferative capacity and life span of cells and the effects of
continuous exposure to exogenous influences that result in the
progressive accumulation of cellular and molecular damage.

9. GENERAL FEATURES OF AGING
FOUND IN ALL TISSUES
Tissue desiccation.
Diminished reparative ability.
Reduced elasticity.
Altered cell permeability

10. STRUCTURAL AND BIOCHEMICAL CHANGES WITH
CELLULAR AGING
• A number of cell functions decline progressively with age and there are morphologic alterations
in aging cells.
• Human ageing induces histophysiological and clinical alterations in oral tissues.
Oxidative phosphorylation by mitochondria is reduced as is synthesis of nucleic acids and
structural and enzymatic proteins, cell receptors, and transcription factors.
Cells have a decreased capacity for uptake of nutrients and for repair of chromosomal damage;

11. • Concomitantly , there is a steady accumulation of lipofuscin pigment, indicating past
membrane injury and lipid peroxidation.

12. EFFECTS OF AGING
• The effects of human aging on periodontal tissues are based on biomolecular changes
of the cells of periodontium that exacerbate bone loss in elderly patients with
periodontitis.
• These effects may be associated with
(1) alterations in differentiation and proliferation of osteoblasts and osteoclasts;
(2) an increase in periodontal cell response to the oral microbiota and mechanical stress
leading to the secretion of cytokines involved in osseous reabsorption; and
(3) systemic endocrine alterations in elderly persons.

13. TYPE OF CHANGES IN PERIODONTIUM
WITH AGE
INTRINSIC
STOCHASTIC
FUNCTIONAL
PHYSIOLOGIC
CLINICAL

14. INTRINSIC CHANGES
• In epithelium, a progenitor population of cells (stem cells), situated in the basal layer, provides
new cells of the oral epithelium.
• In the aging process, cell renewal takes place at a slower rate with fewer cells, so the effect is to
slow down the regenerative processes.

15. STOCHASTIC CHANGES
• Stochastic changes occurring in the cells also affect tissue; for example, glycosylation and
cross-linking produce morphologic changes and physiologic changes.
• Structures become stiffer, with loss of elasticity and increased mineralization. With a loss of
regenerative power, structures become less soluble and more thermally stable.
• Somatic mutations lead to decreased protein synthesis and structurally altered proteins.
• Free radicals contribute to the accumulation of waste in the cell.

16. PHYSIOLOGIC CHANGES
• In the periodontal ligament , a decrease in the number of collagen fibres , leads to a reduction or
loss in tissue elasticity.
• With aging ,the alveolar bone shows a decrease in bone density and increase in bone resorption.

17. FUNCTIONAL CHANGES
• With aging , the cells of the oral epithelium and periodontal ligament have reduced mitotic
activity and all cells experience a reduction in metabolic rate.
• There is reduction in healing capacity and rate.

18. CLINICAL CHANGES
• Attrition is a compensatory change that acts as a stabilizer between loss of bony support and
excessive leveraging from occusal forces imposed on the teeth.
• Gingival recession and reductions in bone height.
• A reduction in “overjet” of the teeth is seen ,manifesting as an increase in edge to edge contact
of the anterior teeth.

19. CHANGES IN PERIODONTAL
TISSUES ASSOCIATED WITH
AGING
• The periodontium—the tissues that support the teeth—consists of gingiva, periodontal
ligament, cementum, and alveolar bone.
• Anatomical and functional changes in periodontal tissues have been reported as being
associated with the aging process.

20. AGE CHANGES IN GINGIVA
Changes in the gingiva caused by aging can be observed in
1.Epithelium.
2.Epithelium-connective tissue interface.
3.Connective tissue.

21. EPITHELIUM
• Thinning and decreased keratinization of the gingival epithelium which leads to, an increase in
permeability to bacterial antigens and decreased resistance to functional trauma or both.
• Migration of junctional epithelium to more apical position.
• Increased amount of attached gingiva.
• Shape of the rete pegs – Flattening of the rete pegs
• Increase in the height of epithelial ridge,

22. EPITHELIUM CONNECTIVE
TISSUE INTERFACE
• In this interface, connective tissue ridges will be more prevalent in younger individuals whereas
connective tissue papillae will be more prominent in older individuals.
• The change from ridges to papillae involves the formation of epithelial cross-ridges
with increasing age.

23. CONNECTIVE TISSUE
• Irregular to finely textured prepubertal connective tissue
shows a gradual transition with age to a more dense,
coarsely textured tissue in the higher age groups.
• Decreased connective tissue cellularity.
• Reduction in organic matrix production with
advancing age.

24. EFFECTS ON GINGIVAL FIBROBLASTS
In vivo and in vitro studies, have shown functional and structural alterations in fibroblasts
associated with aging.
• Gingival fibroblasts (GFs) may be constantly affected by oral bacteria and its products,
such as the lipopolysaccharides (LPS), present in their cell walls.
• The LPS induces GF to release some inflammatory cytokines such as prostaglandin E2
(PGE2), interleukin (IL)-1, and plasminogen activator (PA).
• The influence of these inflammatory mediators on both GF and periodontal ligament
fibroblasts (PLFs) may be an important factor in the severity of periodontal disease.

25. CHANGES IN GROUND SUBSTANCE
• Quantitative differences in protein synthesis were found in young and old GFs in vitro
• Old fibroblasts also presented an increased rate of collagen intracellular phagocytosis,
which can affect the balance between synthesis and degradation of collagen in the
connective tissue.
• The aging process in GF causes an increase in DNA structure methylation of collagen
alpha-1 gene, followed by a reduction in mRNA levels and collagen type I synthesis.
• Alterations in the composition of extracellular matrix proteoglycans secreted by GF were
also observed.

26. • The proteoglycans secreted by old fibroblasts presented an increase in the rates of
heparan sulfate and a reduction in chondroitin sulfate in relation to young fibroblasts.

27. EFFECT ON COLLAGEN
• Decreased rate of collagen synthesis
• The rate of maturation of the synthesized collagen changes with age.
• The rate of conversion of salt soluble to salt-insoluble collagen increased with age (Seheir et al.
1976)
• The relative amount of soluble collagen decreases with age.
• The thermal contraction temperature increases with the age

28. CHANGES IN PROPERTIES OF COLLAGEN
• Increase in tensile strength of collagen fibrils.
• decrease in extensibility.
• Increase in thermal conduction.
• Decrease in ratio of ground substance to collagen.
• Decrease in collagen turnover.
• Decrease in water content.
• Increase resistance to proteolytic enzymes.

29. AGE CHANGES IN PERIODONTAL
LIGAMENT
The periodontal ligament ages as in all other tissues of the body.
The fiber and cellular contents decrease.
The structure of the periodontal ligament becomes irregular with age.
Collagen synthesis decreases more than five fold with increasing age.

30. PLFs [periodontal ligament fibroblast] are constantly subjected to mechanical stress
caused by mastication or occlusal forces. Cultured PLFs were observed to produce a
large amount of PGE2, IL-1, and PA in response to mechanical stress.
The aging process may induce a significant reduction in chemotaxis, motility, and
proliferation rates of periodontal ligament cells.

31. Old fibroblasts present an increased rate of collagen intracellular phagocytosis affecting the
balance between synthesis and degradation of collagen in the connective tissue.
The periodontal ligament width shows a progressive decrease in thickness with age.
The bone surface of the periodontal ligament is often irregular in outline in contrast to that in
young adults.

32. • The cells of the periodontal ligament from elderly persons had lower rates of
chemotaxis and proliferation than the cells of the periodontal ligament from young
patients.
• The reduced ability of senescent cells to express the c-fos ligand may be associated
with the low rates of chemotaxis and proliferation of these cells.
• The expression of osteocalcin in fibroblasts from the periodontal ligament is either
reduced or ceased in senescent fibroblasts.
• This reduction may be directly related to the cell’s difficulty in progressing in the
cellular cycle (G1-S) and accomplishing cell respiration.

33. • Jagged in appearance with spicules of both lamellar and non lamellar bone typically projecting
into bundles of suspensory fibers.
• In histologic sections, fibers interrupted by large interstitial spaces appeared to lack either
osseous or cemental attachments.

34. WIDTH OF THE PERIODONTAL
LIGAMENT SPACE
• It is well known that the width of the periodontal ligament space
of nonfunctioning teeth is narrower than that of functioning teeth.
• It has also been noted that the masticatory forces decrease with age.
This could explain decrease in the periodontal ligament space
with age.

35. CEMENTUM
• With age, the cementum increases in width.
• There is a tendency toward greater cemental apposition in
the apical region of the teeth.
• Aging and cell death is a normal characteristic of the life cycle
of the cementocytes. This may be due to a rapid reduction in the
accessibility of nutritive substances together with poor elimination
of waste products of cementocytes.

36. • In general, cementum is acellular except at the root apices and in the furcation areas of
multirooted teeth.
• With increasing age, the process of cementum formation becomes acellular.
• Although remodeling of cementum does not normally take place, local resorption at
the cementum surface followed by cementum apposition is often observed.
• Resorption and apposition of cementum increased with age and may also be
responsible for an increased irregularity of the cemental surface.

37.  CEMENTICLES
- Calcified bodies called cementicles are found in PDL
in older individuals.
- They may lie freely in the connective tissue, may fuse
into large calcified masses or may be joined with cementum.
 EXCEMENTOSIS
- As cementum thickens with age, it envelops these masses
(cementicles) and are called as excementosis.

38. AGE CHANGES IN ALVEOLAR BONE
• Bone formation steadily declines with age, resulting in
significant loss of bone mass.
• Reduction in bone metabolism.
• Decreased vascularity.
• Decreased healing capacity.
• A more irregular periodontal surface of bone and less
regular insertion of collagen fibers.

39. ALVELOAR BONE
osteoblastic and osteoclastic cells are directly or indirectly influenced by the action of
parathyroid hormone (PTH), vitamin D metabolites, calcitonin, estrogen, plasmatic
concentration of calcium and phosphates, neurotransmitters, growth factors, and local
cytokines.
The reduction in bone formation may be due to a decrease in osteoblast proliferating
precursors or to decreases synthesis and secretion of essential bone matrix proteins.
The extracellular matrix surrounding osteoblasts has been shown to play an important
role in bone metabolism. Possible dysfunction of this matrix may occur concomitantly
with the aging process.

40.  One hypothesis of aging postulates that the oxygen-free radical
is a major contributor to the aging process.
 An in vitro study showed that oxygen radical treated fibronectin
(FN) as substratum diminished bone nodule formation by osteoblasts when
compared to intact FN.
 This finding suggested that FN plays an important role in osteoblast activity
and that FN damaged by oxygen radicals during the aging
process may be related to less bone formation.

41. EFFECTS ON BACTERIAL PLAQUE
• Dentogingival plaque accumulation has been suggested to increase with age.
Bacterial composition
Socransky et al (1963) reported the prevalence of spirochetes
increases with age and fall in number of streptococci. Plaque of
young patients contains more viable microorganisms per mg than
plaque from elderly persons.
Greater plaque accumulation in older age group may be possibly due to more recession of gingiva in
the older age group or due to physiologic age change in salivary composition and flow rate.

42. • For supragingival plaque, no real qualitative differences have been shown for plaque
composition.
• Studies suggest increase in number of enteric rods and pseudomonas in older adults particularly
in subgingival plaque.
• There is shift in certain pathogens:
• a)  role of Porphyromonas gingivalis.
• b)  role of Aggregactibacter actinomycetemcomitans.

43. • Immune factors
IgA, IgM and C3 specific immune factors and nonspecific immune factors such as lactoferrin,
lysozyme and lactoperoxidase were higher in plaque of older age group.
• Enzymatic change
Levan hydrolase activity is lower in the plaque in the older age group. This may be due to low level of
streptococci in plaque of older individuals.

44. SYSTEMIC AGING
AND PERIODONTIUM
• Some alterations in the endocrine profile that influences
osseous metabolism occur with age.
• Vitamin D deficiency is a common phenomenon observed in
community- dwelling elderly persons.
• The low levels of calcium resulting from vitamin D deficiency associated
with renal insufficiency might lead to secondary hyperparathyroidism.
• The high levels of PTH resulting from secondary hyperparathyroidism act
in the mobilization of osseous calcium and can cause mineralization problems,
such as bone fractures, and a reduction in osseous density.
• Osteopenia and osteoporosis are considered important risk factors for alveolar
bone loss in the presence of periodontal disease.

45. IMMUNE SENESCENCE
AND PERIODONTAL CELLS INTERACTION
• Aging-related immunological alterations in leukocyte subpopulations
have been reported.
• Reductions in peripheral blood T-lymphocytes, mitotic agents, anti-CD3,
and monoclonal antibodies are the main alterations in the senescent phenotypes
of T-lymphocytes.
• The proliferative phase alterations in T-lymphocytes may be induced by the reduced
secretion of IL-2 and reduced expression of its high affinity receptors.
• The reduced expression patterns of IL-2 and IL-2R in peripheral monocytes of elderly
patients have been reported as influencing the proliferative response of T-lymphocytes.
• IL-2 is produced by helper T-cells and plays an important role in the proliferation and
differentiation of virgin T-cells into effector T-cells.

46. • Alterations in B-lymphocyte subpopulations have been observed in the elderly people.
• The reduction in the peripheral blood population of B lymphocytes is associated with
the decrease in the production of high specificity antibodies as well as in the avidity of
antigen-antibody complexes.
• Other changes in immune senescence include a decline in macrophage, neutrophil,
and natural killer cell function with aging.

47. • Elderly subjects, developed more gingivitis than young subjects.
• The gingival lesion which formed in the older individuals was more pronounced and
contained more inflammatory cells than the corresponding lesion in the younger
subject sample.
• Higher levels of alpha 2-macroglobulin, IgG3, and B-lymphocytes in the crevicular fluid
and a reduction in polymorphonuclear leukocytes (PMN) have also been observed in
the elderly people.

48. • Periodontal ligament cells from the elderly people showed an increase in the
production of PA,47 PGE2, IL-1,6,48 and IL-649 when compared to younger cells,
similar to that described for stimulation with LPS.
• PA is a serine protease that acts in the activation of plasmatic plasminogen into
plasmin and is secreted by many cell types, including periodontal fibroblasts.
• The cells from elderly individuals showed greater activity of PA and greater expression
of tPA mRNA when compared to those from young individuals.

49. • A greater release of PA induced by aging might affect GFs and the periodontal
ligament, and aggravate the inflammatory process and the degradation of the
extracellular matrix in in periodontal tissues of the elderly people.
• The greater production of PGE2 in periodontal ligament cells from older persons might
account for the greater rate of alveolar bone resorption in elderly patients.

50. • Age is associated with some moderate loss of periodontal attachment and alveolar
bone, but age alone in a healthy adult does not lead to a critical loss of periodontal
support.
• Although moderate loss of alveolar bone and periodontal attachment is common in
the elderly people, severe periodontitis is not a natural consequence of aging.
• Cross-sectional studies measuring disease experience demonstrated more attachment
loss and alveolar bone loss among older age groups, since clinical attachment level
and bone loss are irreversible measures of prior disease experience.

51. • Longitudinal studies addressing potential relationships between age and attachment
loss or bone loss showed a statistically significant relationship between age and
incidence of periodontal disease.

52. AGING AND GINGIVAL
RECESSION
The phenomenon that in general the degree of recession increases
with age is well known. However, this is not necessarily the result
of aging since mechanical trauma, e.g., tooth brushing can cause recession.
It has been determined through studies that with age, physiological
apical migration of the epithelium can occur.

53.  This hypothesis also fits with the continuous passive eruption theory by Gottlieb and Orban
1936. It is postulated that as age advances a gradual physiological recession of the gingiva
occurs concomitantly with an apical migration of the epithelium.
 The recession of the gingiva is the result of occlusal migration of teeth compensating for
occlusal wear and a stable location of the gingival margin.
 It seems probable that periodontal destruction will occur by mechanical trauma in the presence
of plaque and consequent inflammation of the periodontium.

55. EFFECTS OF AGING ON THE
PROGRESSION OF PERIODONDAL
DISEASES
One theory is that many sites of advanced periodontal disease
have resulted in tooth loss earlier in life, suggesting that older
age is not a risk factor for periodontal disease .
Thus, age has been suggested to be not a risk factor but a
background or an associated factor for periodontitis.

56.  Advanced age does not decrease plaque control, however, older adults
may
 have difficulty performing adequate oral hygiene because of
compromised
 health, mental status, medications, altered mobility and dexterity.
 Older adults may change toothbrush habits due to disabilities such as
 hemiplegia, visual difficulties, dementia, and arthritis.
 The newer, lightweight, electric-powered toothbrushes may be more
beneficial
 than a manual toothbrush for older adults with physical and sensory

57. • In the older age group (65-80 years), the findings included a
greater size of infiltrated connective tissue, increased gingival
crevicular fluid flow, and increased gingival index.
• age is inevitably associated with an increased loss of connective
tissue attachment.

58. AGING AS A RISK FACTOR FOR
PERIODONTAL DISEASE
• A“risk factor” is defined as ‘any characteristic, behaviour, or exposure with an association to a
particular disease’. Some risk factors like smoking, can be modified to reduce one’s risk of
initiation or progression of disease; while other factors cannot be modified such as genetic
factors.
• Studies show that the effect of age either is non-existent or provides a small and
clinically insignificant increased risk of loss of periodontal support.
• Therefore, age has been suggested to be not a true risk factor but a background or an associated
factor for periodontitis.

59. • Susceptibility to periodontal disease is more significant for the
rate of periodontal destruction than the length of time the
plaque is present.

60. • This level of increased risk probably is not sufficient alone to cause tooth loss. Consequently,
periodontal disease may be considered as time associated and aging itself appears to be
responsible for some attachment and bone loss, which is of a magnitude that is unlikely to have
any clinical significance. This fact is influenced by multiple factors that have been found to be
associated with the prevalence and incidence of the periodontal disease.

61. AGING AND THE RESPONSE TO
TREATMENT OF THE
PERIODONTIUM
• The successful treatment of periodontitis requires both meticulous
home-care plaque control by the patient and meticulous supragingival
and subgingival debridement by the therapist. If plaque control is not
ideal, continued loss of attachment is inevitable. Furthermore, without
effective periodontal therapy, progression of diseases might be faster
with increasing age.

62. few studies clearly demonstrate that despite the histologic changes in the
periodontium with aging, no differences in response to nonsurgical or surgical
treatment have been shown for periodontitis.
A purely biologic or physiologic review indicates that the effects of aging on the
structure of the periodontium, the function of the immune response, and the nature of
either supragingival or subgingival plaque have a negligible impact on an individual's
experience with periodontal disease.

63. WOUND HEALING
• Studies in man and animals suggested that the rate of healing of skin wound decreased with
increasing age.
• Cell migration, myofibroblastic differentiation, collagen remodeling, and proliferation are
decreased in aged fibroblasts. In addition, altered cell migration in wound-healing may be
attributable not only to cellular defects but also to changes in serum factors associated with the
senescence process.
• The tensile strength development of skin incision wounds seemed to be retarded in older
individuals. This was attributed to slower restitution of the microvascular system and an altered
fibroblastic function.

64. • The concept that younger individual with moderate to advance periodontal disease has a worse
prognosis than in older individuals with similar level of disease is probably less related to the
healing capacity of this individual than the risk of re-infection over a longer lifespan.

65. • Abbas et al 1984 concluded that “the time span for wound healing is longer in patients who are
more susceptible to periodontal disease (younger) than in those who are less susceptible”. They
noticed that sites with more loss of attachments had slow rate of wound healing.

66. Patients with same amount of periodontal destruction ,
the rule holds “older the patient, the better the prognosis
in terms of no recurrence of the disease.
In two patients with comparable levels of remaining connective
tissue attachment and alveolar bone, the prognosis is better in
the older of the two

68. REFERENCES
• Clinical Periodontology-Carranza 10th edition.
• Hebling E. Effects of human ageing on periodontal tissues. In Periodontal diseases-a clinician's
guide 2012. InTech.
• Effects of human aging on periodontal tissues-Huttner-22 June 2009-volume 29,issue 4,-American
Academy of Periodontology.
• Effect of age on healing following periodontal therapy lindhe et al j clin periodont 1985;12:774-787.
• Robbins general pathology- Kumar/Cotran.
• Periodontics revisited- Shalu Bathla.
• Cáceres M, Oyarzun A, Smith PC. Defective wound-healing in aging gingival tissue. Journal
of dental research. 2014 Jul;93(7):691-7.