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AGES CHANGES IN
PERIODONTIUM
Dr.Pradnya Wagh
Contents
 Aging is slowing of natural function, disintegration
of the balanced control and organization that characterize
the young adults (Little C.c. 1947)
 Aging of an organ is defined as post maturational
deteriorative changes that with time, lead to an increased
vulnerability to challenges, there by decreasing the
functional ability of the organ.
 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)
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
GENERAL EFFECTS
OF AGING
External
Hair - Brittle, Less abundant, gray
Skin - Dehydration, decreased elasticity,
thermo sensitive
Eyes - Diminished vision, enopthalmos
Nose - Diminished sense of smell
Secretary glands - Diminished epithelial activity
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
Effects of aging on
periodontium
 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
Changeswithingingivalepithelium
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
 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
 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
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) .
The influence of these inflammatory mediators on both GF
and periodontal ligament fibroblasts (PLF) might account for
the severity of periodontal disease.
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
 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
Carranza’s clinical periodontology 10th edition Chapter -6
,Page No. 94
Changeswithingingivalconnectivetissue
 There is also a reduction in the organic matrix production
and in vascularization, and an increase in the number of
elastic fibers.
ChangeswithinPeriodontalLigament
Greater no of elastic fibers.
Decrease in vascularity.
Decrease in mitotic activity.
Decrease in fibroplasia.
Decrease in number of collagen fibers.
Width of periodontal ligament increased or decreased.
Changeswithincementum
changeswithinAlveolarbone
Changes occurring in alveolar bone are similar to remainder of
skeletal system
Increased osteoporosis
Decreased vascularity
Bone resorption increased (or) decreased.
Greater irregularity in the surfaces of alveolar bone facing periodontal
ligament.
Healing rate of bone in extraction sockets appears to be unaffected.
Recent observations with bone graft preparations from donars more
than 50 yrs old possess less osteogenic potential than younger donars.
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
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
fibronectin.
 This finding suggested that intact fibronectin plays an important role in
osteoblast activity .
Fibronectin damaged by oxygen radicals during the ageing process
might be related to less bone formation.
 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.
Immuneresponse
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.
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 defenses correlating with periodontitis in an
elderly group of individuals ,with and without disease.”
Nutritionaleffectonimmuneresponse
Toothperiodontiumrelationship
Bacterialplaque
 For sub gingival plaque ,increased number of enteric
rods and pseudomonads in older adults.
 Periodontal pathogens specifically including an increased
role for P.gingivalis and decreased role for
A.actinomycetemcomitans.
ORALMUCOUSMEMBRANE
Thinning of the oral epithelium or no change
Increased keratinization of lip and cheek mucosa- it may be related to
smoking
Atrophy of connective tissue with loss of elasticity
Increased in number of mast cells.
SALIVARY GLANDS
There is no reduction in potential of salivary gland function.
Association between
periodontium and systemic
diseases
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
DiabetesMellitus
JADA 2006;137(10 supplement):26S-31S.
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
 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
Coronaryheartdisease
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.
PERIODONTALDISEASEANDASPIRATIONPNEUMONIA
Aspiration pneumonia caused by infection of anaerobic organism
usually occurs in patient with periodontal disease.
Aspiration pneumonia results when oropharyngeal secretions, food,
gastric contents are aspirated into the lungs and causes infection
Commonly seen in elderly patients.
Salivary duct as a medium of delivery of organism from the oral cavity
into the lungs.
P.gingivals, pseudomonas A.eruginaso capnocytophaga species
fusobacterium nucleatum are commonly isolated species.
 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.
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
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, kaolin, lidocaine mouth wash
Subgingivalplaqueflora
Increased access to flora (compared to supra gingival plaque)
Via ulcerated epithelial lining of the pocket
Underlying connective tissue
Antimicrobial potential in
tissues
Destroyed
Cellular debris
Systemic circulation
Alterations in serum components of clotting mechanisms
Elevated levels of fibrinogen
Risk of future coronary heart disease
AGING AND SUBGINGIVAL MICROBIOLOGY
COMPOSITION OF SUBGINGIVAL MICROBIOTA
Rodenburg et al (1990) Actinobacillus actinomycetum
slots et al comitance  with age
Savitt of Kent (1991) Porphyromonas
gingivalis –  with age & blacks
Gingival recession
ORAL HYGIENE INSTRUCTIONS
Establish daily routine of brushing
Fluoride dentifrices
Instruments can be adapted as
◦ Handles can be customized
◦ Electrical (or) interproximal brushes
Goal of periodontal treatment is 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
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.
ROOT CARIES
• Root caries – slow progress, rare pulp involvement, painless
• To arrest caries – single topical fluoride and daily use of
fluoride tooth paste
• In high incidence – Daily brushing with fluoride tooth paste
of caries or 0.4% fluoride gel
• APF rinse followed by 1.64% stannous
fluoride rinse once weekly
 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, koaline, lidocaine mouth wash
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.
References
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 Ageing
Dev. 1994; 73: 179-187.
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 treatamento 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.
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.
THANK YOU

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"AGE CHANGES IN PERIODONTIUM"

  • 3.
  • 4.  Aging is slowing of natural function, disintegration of the balanced control and organization that characterize the young adults (Little C.c. 1947)  Aging of an organ is defined as post maturational deteriorative changes that with time, lead to an increased vulnerability to challenges, there by decreasing the functional ability of the organ.
  • 5.  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)
  • 6. 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
  • 8. External Hair - Brittle, Less abundant, gray Skin - Dehydration, decreased elasticity, thermo sensitive Eyes - Diminished vision, enopthalmos Nose - Diminished sense of smell Secretary glands - Diminished epithelial activity 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
  • 9.
  • 10.
  • 11. Effects of aging on periodontium
  • 12.  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
  • 14. 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
  • 15.  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
  • 16.  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
  • 17. 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) . The influence of these inflammatory mediators on both GF and periodontal ligament fibroblasts (PLF) might account for the severity of periodontal disease.
  • 18. 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
  • 19.  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
  • 20. Carranza’s clinical periodontology 10th edition Chapter -6 ,Page No. 94
  • 22.  There is also a reduction in the organic matrix production and in vascularization, and an increase in the number of elastic fibers.
  • 23. ChangeswithinPeriodontalLigament Greater no of elastic fibers. Decrease in vascularity. Decrease in mitotic activity. Decrease in fibroplasia. Decrease in number of collagen fibers. Width of periodontal ligament increased or decreased.
  • 24.
  • 26.
  • 27. changeswithinAlveolarbone Changes occurring in alveolar bone are similar to remainder of skeletal system Increased osteoporosis Decreased vascularity Bone resorption increased (or) decreased. Greater irregularity in the surfaces of alveolar bone facing periodontal ligament. Healing rate of bone in extraction sockets appears to be unaffected. Recent observations with bone graft preparations from donars more than 50 yrs old possess less osteogenic potential than younger donars.
  • 28. 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
  • 29. 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 fibronectin.  This finding suggested that intact fibronectin plays an important role in osteoblast activity . Fibronectin damaged by oxygen radicals during the ageing process might be related to less bone formation.
  • 30.  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.
  • 31. Immuneresponse 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.
  • 32. 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 defenses correlating with periodontitis in an elderly group of individuals ,with and without disease.”
  • 34.
  • 37.  For sub gingival plaque ,increased number of enteric rods and pseudomonads in older adults.  Periodontal pathogens specifically including an increased role for P.gingivalis and decreased role for A.actinomycetemcomitans.
  • 38. ORALMUCOUSMEMBRANE Thinning of the oral epithelium or no change Increased keratinization of lip and cheek mucosa- it may be related to smoking Atrophy of connective tissue with loss of elasticity Increased in number of mast cells. SALIVARY GLANDS There is no reduction in potential of salivary gland function.
  • 40. 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
  • 42. 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
  • 43.  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
  • 44. Coronaryheartdisease 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.
  • 45. PERIODONTALDISEASEANDASPIRATIONPNEUMONIA Aspiration pneumonia caused by infection of anaerobic organism usually occurs in patient with periodontal disease. Aspiration pneumonia results when oropharyngeal secretions, food, gastric contents are aspirated into the lungs and causes infection Commonly seen in elderly patients. Salivary duct as a medium of delivery of organism from the oral cavity into the lungs. P.gingivals, pseudomonas A.eruginaso capnocytophaga species fusobacterium nucleatum are commonly isolated species.
  • 46.  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.
  • 47. 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
  • 48. 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, kaolin, lidocaine mouth wash
  • 49. Subgingivalplaqueflora Increased access to flora (compared to supra gingival plaque) Via ulcerated epithelial lining of the pocket Underlying connective tissue Antimicrobial potential in tissues Destroyed Cellular debris Systemic circulation Alterations in serum components of clotting mechanisms Elevated levels of fibrinogen Risk of future coronary heart disease AGING AND SUBGINGIVAL MICROBIOLOGY
  • 50. COMPOSITION OF SUBGINGIVAL MICROBIOTA Rodenburg et al (1990) Actinobacillus actinomycetum slots et al comitance  with age Savitt of Kent (1991) Porphyromonas gingivalis –  with age & blacks
  • 52. ORAL HYGIENE INSTRUCTIONS Establish daily routine of brushing Fluoride dentifrices Instruments can be adapted as ◦ Handles can be customized ◦ Electrical (or) interproximal brushes
  • 53. Goal of periodontal treatment is 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 Operator side - Decrease the length of surgical time - Maintain open communication - Minimize trauma - Recalculate medication dosages - Schedule morning appointment
  • 54. • 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. ROOT CARIES • Root caries – slow progress, rare pulp involvement, painless • To arrest caries – single topical fluoride and daily use of fluoride tooth paste • In high incidence – Daily brushing with fluoride tooth paste of caries or 0.4% fluoride gel • APF rinse followed by 1.64% stannous fluoride rinse once weekly
  • 55.  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, koaline, lidocaine mouth wash
  • 56.
  • 57. 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.
  • 58. References 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 Ageing Dev. 1994; 73: 179-187.
  • 59. 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 treatamento 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.
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