1. Presented By – Dr. Shivesh Mishra
July 29th , 2014
Department of Periodontics
I.T.S. Dental College, Hospital & Research Center
Greater Noida
Moderator- Dr. Shivjot Chhina
Perceptor-Dr. Saurav Kumar

2.  Introduction to Aging
 General Effects of aging
 Effect of aging on peridontium
o Gingival epithelium
o Gingival connective tissue
o Periodontal ligament
o Cementum
o Alveolar Bone
o Bacterial plaque
o Immune response
 Systemic diseases & Periodontal health
 Conclusion

3.  The process of becoming older, a process that is genetically
determined and environmentally modulated.1
 It includes the complex interaction of biologic, psychologic,
and sociologic process over time.
 Thus, in contrast to the chronological milestones which mark
life stages in the developed world, old age in many developing
countries is seen to begin at the point when active
contribution is no longer possible." (Gorman, 2000)

4.  The geriatric population has been growing fast over the last
decades all over the world, changing demographics.
 Changes in biochemical and physiological processes occur
with aging in all body tissues, including the peridontium.
 Human ageing induces histophysiological and clinical
alterations in oral tissues.2
 These alterations must be understood to differentiate
pathological conditions from the altered physiology of oral
tissues resulting from ageing .3

5. External
Hair Brittle, Less Abundant, Gray
Skin Dehydration, Decreased Elasticity, Thermo
Sensitive
Eyes Diminished Vision, Enopthalmos
Nose Diminished Sense Of Smell
Secretory
Glands
Diminished Epithelial Activity

6. Internal
Renal Decreased renal blood flow  Leading to water
retention, Difficulty in removing waste products
Vascular Rise in systolic blood pressure
GIT Constipation and gas accumulation due to
hypotonic musculature
Gonads Decrease estrogen and androgen secretion
Liver Decrease hepatic function
Pancreas Decrease function (diabetes)

7. Alternations in oral motor functions
Lip posture Drooling, angular cheilosis
Muscles of
mastication
Efficiency of Mastication decreases
Tongue Speech, dysphagia, traumatic bite injury
Swallowing Dysphagia
Taste Loss of sensation or decreased sensation

8.  The tissues that support the teeth are called the
periodontium, which consists of gingiva, periodontal
ligament, cementum, and alveolar bone.
 Anatomical and functional changes in periodontal tissues
have been reported as being associated with the ageing
process.4

9.  Thining of epithelium & diminished keratinization.5
 Increased epithelial permeability to pathogens
 Decreased resistance to functional trauma.
 Conflicting results have been reported regarding the shape of
the retepegs.
 A flattening of retepegs and an increase in the height of the
epithelial ridges associated with ageing were both
demonstrated.

10. Gingival sample obtained
from a 25-year-old healthy
subject. Normal aspect of
epithelium layers, dermal
papillae and connective
tissue, without signs of
proliferation (HE staining,
×10).
Gingival sample obtained from
a 66-year-old subject.
Thickening of epithelium due
to acanthosis (HE staining,
×10).
Rom J Morphol Embryol 2013, 54(3 Suppl):811–815

11.  In a morphological 3-dimensional study of the epithelium-connective
tissue interface, connective tissue ridges were
observed to be more prevalent in young individuals whereas
connective tissue papillae were predominant in old
individuals.
 The change from ridges to papillae involves the formation of
epithelial cross-ridges with advanced age.4

12.  Number of cellular elements decreases as age increases.
 The fibroblasts are the main cells in the synthesis of
periodontal connective tissue.
 In vivo and in vitro studies have shown functional and
structural alterations in fibroblasts associated with ageing.6-8

13.  Gingival fibroblasts (GF) may be constantly affected by oral
bacteria and their 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) 6, 14.
 The influence of these inflammatory mediators on both GF
and periodontal ligament fibroblasts (PLF) might account for
the severity of periodontal disease.6

14.  The effect of aging on location of junctional epithelium has
been the subject of much speculation.
 The apical migration of the junctional epithelium, with
consequent gingival recession, has been discussed.
 Although such a migration is associated with aging, the loss
of insertion caused by aging alone may not seem to have
clinical significance.9

15.  Gingival recession progression may occur due to several
factors, such as passive eruption caused by physiological wear
of teeth, a consequence of anatomically thin tissues and
toothbrushing trauma.
 Apparently, gingival recession is not an avoidable
physiological process caused by aging, but a cumulative and
progressive effect from periodontal disease or trauma over
time.5

16. Carranza’s clinical periodontology 10th edition Chapter -6 ,Page No. 94

17.  Coarser and denser gingival connective tissue
 Qualitative and quantitative changes to collagen
include;
◊ increased rate of conversion of soluble to insoluble
collagen.
◊ increased mechanical strength
◊ increased denaturing temperature
 These results indicate increased collagen stabilization
caused by the changes in the macromolecular
conformation

18.  There is also a reduction in the organic matrix production and
in vascularization, and an increase in the number of elastic
fibers.

19.  Decreased number of fibroblasts
 Decreased organic matrix production
 Decreased epithelial cell rests
 Decreased number of collagen fibers
↓
reduction or loss in tissue elasticity

20.  Cells of PDL have reduced mitotic activity
 Thickness of the periodontal ligament varies and may reduce
due to the reduction in the force applied by masticatory
muscles along the time in subjects with complete dentition or
having dental elements with no antagonist.10
 On the other hand, when several elements are missing, there
might be an overload on the existing remaining teeth, with
consequent periodontal ligament thickening.11

21.  Increase in cemental width is a common finding.
 Increase may be 5 to 10 times with increasing age.12
 Increase in width is greater apically and lingually.13
 Deposition takes place mainly in apical region to compensate
for the physiological wear of teeth.

23.  Reduction of bone mass.
 More irregular periodontal surface of bone.
 Less regular insertion of collagen fibers.
 Increased bone resorption.

24.  The reduction in bone formation might be due to a decrease
in osteoblast-proliferating precursors or to decreased
synthesis and secretion of essential bone matrix proteins.6
 The extracellular matrix surrounding osteoblasts has been
shown to play an important role in bone metabolism.
 A possible dysfunction of this matrix might occur
concomitantly with the ageing process.14

25.  Oxygen-free radicals have been reported to cause cellular
damage and, consequently, contribute to the ageing
process.15,16
 In an in vitro study, oxygen radical-treated fibronectin (FN)
was found to inhibit bone nodule formation by osteoblasts
when compared to intact FN.
 This finding suggested that intact FN plays an important role
in osteoblast activity .
 FN damaged by oxygen radicals during the ageing process
might be related to less bone formation

26.  Although age is a risk factor for the reduction of the bone
mass in osteoporosis,it is not causative and therefore
distinguished from physiologic aging process.

27.  Age has been recognized as having much less effect
in altering the host response
 Difference between younger and older individuals
can be demonstrated for T and B cells, cytokines,and
natural killer cells,but not polymorphonuclear cells
and macrophages activity.

28.  McArthur 17 concludes that “measurement of indicators of
immune & inflammatory competency suggested that ,within
the parametes tested ,there was no evidence for age related
changes in host defences correlating with periodontitis in an
elederly group of individuals ,with and without disease.”

29. NUTRIENT INCREASED
FUNCTION
DECREASED FUNCTION
VITAMIN A Bacterial adhesion
Salivary Antimicrobial
Properities,immunoglobulin And
Lymphocytes Production
VITAMIN E ----------------
--------------
Antibody Synthesis,response Of
Lymphocytes,phagocytic Action
VITAMIN C
----------------
--------------
Phagocytic Action Of Neutrophils
And Macrophages,antibody
Response
ZINC
----------------
---------------
Antibody Response,phagocytic
Function Of Macrophages

30. RIBOFLAVIN,VIT
B6,PANTHOTENIC ACID
--------------------
------------
Antibody
synthesis,cytotxic T-cell
toxicity,
lymphocyte response
FOLIC ACID AND
VITAMIN B 12
--------------------
------------
Cytotoxic T cell
toxicity,lymphocyte
production,phagocytic
function of neutrophils
IRON
--------------------
------------
Lymphocytic
proliferation,neutrophil
cytotoxic
activity,antibody
response

31.  Loss of tooth substance – Attrition
 Degree of attrition is influenced by
◦ Musculature
◦ Consistency of food
◦ Tooth hardness
◦ Occupational factors
◦ Habits like bruxism
◦ Continuous tooth eruption
 Gingival recession

32.  Dentogingival plaque accumulation increases with
increase in age:
• with Increase in hard tissue surface area resulting from
gingival recession
• The surface characteristics of the exposed root
surfaceas a substrate for plaque formation

33.  For sub gingival plaque ,increased number of entric
rods and pseudomonads in older adults.
 Periodontal pathogens specifically including an
increased role for P. gingivalis and decreased role for
A. actinomycetemcomitans

34.  Infectious diseases, such as periodontitis, cause inflammation
and contribute to levels of overall infection and inflammation
in the body and may trigger the beginning and/or the
progression of other diseases such as diabetes and
arteriosclerosis.18
 There are two mechanisms through which infection and
inflammation apparently located in periodontal pockets may
harm general health:19
The passage of periodontal
pathogens and their products
into circulation (bacteremia)
The passage of locally
produced inflammatory
mediators into circulation

35. JADA 2006;137(10 supplement):26S-31S.

36.  It is suggested that the potential interactions between
diabetes and periodontitis seem to enhance the
morbidity of these two diseases.20
 The chronic hyperglycemic condition of diabetes is
associated with damage, dysfunction, or failure of
various organs and tissues, including the periodontium.
 It is due to the increased risk for infections in patients
with diabetes, impairment of the synthesis of collagen
and glycosaminoglycans by gingival fibroblasts, and
increased crevicular fluid collagenolytic activity, Altered
wound healing.21

37.  It has been demonstrated by a meta-analysis study that
patients with types 1 and 2 diabetes had worse oral hygiene
and higher severity of gingival and periodontal diseases,
compared to nondiabetic subjects.22
 A multivariate risk analysis showed that subjects with type 2
diabetes had approximately threefold increased odds of
having periodontitis compared with subjects without
diabetes, after adjusting for confounding variables including
age, sex and oral hygiene measures.23

38.  Periodontal and cardiovascular diseases are common
inflammatory conditions in the human population,
atherosclerosis being the major component of the latter.
 Loesche et al did a study on association between periodontal
disease and coronary heart disease.
 They found that in patients with periodntal diseases there are
1.84 times more CHD

39. Subgingival plaque flora
Increased access to flora (compared to supra gingival plaque)
Via ulcerated epithelial lining of the pocket
Underlying connective tissue
Antimicrobial
potential in
tissues
Cellular debris
Systemic circulation
Alterations in serum components of
clotting mechanisms
Elevated levels of fibrinogen
Risk of future coronary heart disease
Destroyed

40.  A meta-analysis study indicated that individuals with
periodontitis had 1.14 times higher risk of developing
coronary heart disease.24
 The more severe the periodontal disease the easier the
periodontal pathogens could enter the circulation, reaching
blood vessels and atherosclerotic lesions.

41.  Another linkage between periodontal disease and CHD is the
level of C-reactive protein, which is an acute-phase reactant
in response to infection or trauma and its high sustained level
was associated with advanced periodontitis.25
 Ridker et al. demonstrated that C-reactive protein levels
predict the risk of coronary events.26

42. Goal of periodontal treatment is to preserve function and
prevent the progression of inflammatory disease
- Factors must be considered in treatment planning
Patients
- Medical and health status
- Medications
- Life style behaviors
- Ability to perform oral hygiene procedures
- Ability to tolerate treatment
- Amount of remaining periodontal support, tooth type

43. Operator side
- Decrease the length of surgical time
- Maintain open communication
- Minimize trauma
- Recalculate medication dosages
- Schedule morning appointment
- Non surgical approach – first treatment of choice
- Surgical approach – depends on nature and extent of disease
- Palliative supportive periodontal care – patients who are not
comply with treatment, have poor oral hygiene, medically or
mentally compromised, functionally impaired.

44. XEROSTOMIA
 Fluoride rinses and dentifrices
 Reduced consumption of alcohol, tobacco, spicy and acidic
foods
 Frequent water in take
 Artificial salivary substitutes
Burning mouth
 Salivary substitutes
 Diphenhydramine, koalin, lidocaine mouth wash

45.  Aging dental patients have particular oral and general health
conditions that dentists should be familiar with detecting,
consulting, and treating.
 Medical diseases and conditions that occur more often with
age may require modification to periodontal preventive tools
as well as the planning and treatment phases of periodontal
care.

46. 1. Webster's New World™ Medical Dictionary, 3rd Edition.
2. Mombelli A. Ageing and the periodontal and peri-implant microbiota.
Periodontol 2000. 1998; 16: 44-52.
3. Savitt ED, Kent RL. Distribution of Actinobacillus actinomycetemcomitans and
Porphyromonas gingivalis by subject age. J Periodontol. 1991; 62: 490-494.
4. Van der Velden U. Effect of age on the periodontium. J Clin Periodontol. 1984; 11:
281 -294.
5. Needleman I. Envelhecimento e o periodonto. In: Newman MG, Takei HH,
Carranza FA. Periodontia clínica. 9.ed. Rio de Janeiro: Guanabara Koogan; 2004.
p.51-5.
6. Abiko Y, Shimizu N, Yamaguchi M, Suzuki H, Takiguchi H. Effect of ageing
on functional changes of periodontal tissue cells. Ann Periodontol. 1998; 3:
350-369.
7. Dumas M, Chaudagne C, Bont F, Meybeck A. In vitro biosynthesis of type I
and III collagens human dermal fibroblasts from donors of increasing age.
Mech AgeingDev. 1994; 73: 179-187.

47. 8. Lee W, McCulloch CA. Deregulation of collagen phagocytosis in ageing
human fibroblasts: effects of integrin expression and cell cycle. Exp Cell
Res. 1997; 237: 383-393.
9. Locker D, Slade GD, Murray H. Epidemiology of periodontal disease among
older adults: a review. Periodontol 2000. 1998; 16: 16-33.
10. Marsillac MWS, Mello HSA. Doença periodontal em idosos. In: Mello HSA.
Odontogriatria. São Paulo: Santos; 2005. p.107-14.
11. Zenóbio EG, Toledo BEC, Zuza EP. Fisiologia, patologia e tratamento das
doenças do periodonto do paciente geriátrico. In: Campostrini E.
Odontogeriatria. Rio de Janeiro: Revinter; 2004. p.184-98.
12. Berglundh T. Clinical & structural characteristics of periodontal tissues in
young & old dogs. J Clin Periodontol 18:616;1991.
13. Van der Velden u. Effect of age on periodontium. J Clin Periodontol
11:81;1984.
14. Roholl PJM, Blauw E, Zurcher C, Dormans J, Theuns HM. Evidence for a
diminished maturation of pre-osteoblasts into osteoblast during ageing in
rats: an ultrastructural analysis. J Bone Miner Res. 1994; 9: 355-366.

48. 15. Selkoe DJ. Deciphering Alzheimer’s disease: the amyloid precursor protein yields new
clues. Science 1990; 248: 1058-1060.
16. McCord JM. Free radicals and inflammation:protection of synovial fluid by superoxide
dismutase. Science 1974; 185: 529-531.
17. McArthur WP. Effect of aging on immunocompetent and inflammatory cells . Periodontol
2000, 1999 : 16-53.
18. Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K. Relatioship between
periodontal infections and systemic disease. Clin Microbiol Infect. 2007; 13: 3-10.
19. Williams RC, Barnett AH, Claffey N, Davis M, Gadsby R, Kellet M et al.The potential impact
of periodontal disease on general health: a consensus view. Curr Med Res Opin. 2008; 24:
1635-43.
20. Novak MJ, Potter RM, Blodgett J, Ebersole JL. Periodontal disease in hispanic Americans
with type 2 diabetes. J Periodontol. 2008; 79: 629-36.
21. Nishimura F, Takahashi K, Kurihara M, Takashiba S, Murayama Y. Periodontal disease as a
complication of diabetes mellitus. Ann Periodontol.1998; 3: 20-9.
22. Khader YS, Dauod AS, El-Qaderi SS, Alkafajei A, Batayha WQ. Periodontalstatus of
diabetics compared with non-diabetics: a meta-analysis. J Diabetes Complication. 2006;
20: 59-68.

49. 23. Shlossman M, Knowler WC, Pettitt DJ, Genco RJ. Type 2 diabetes mellitus and periodontal
disease. JADA 1990;121(4):532-6.
24. Bahekar AA, Singh S, Saha S, Molnar J, Arora R. The prevalence and incidence of coronary
heart disease is significantly increased in periodontitis: a meta-analysis. Am Heart J. 2007;
154: 830-7.
25. Linden GJ, McClean K, Young I, Evans A, Kee F. Persistently raised
Creactive protein levels are associated with advanced periodontal disease.J
Clin Periodontol. 2008; 35: 741-7.
26. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other
markers of inflammation in the prediction of cardiovascular disease in
women. N Engl J Med. 2000; 342: 836-43.