The document discusses the effects of aging on the periodontium. As people age, the periodontal tissues experience thinning of the gingival epithelium and decreased vascularization. The number of fibroblasts and collagen fibers in the periodontal ligament and gingiva decreases with age. Cementum width increases with age through continued deposition. Alveolar bone mass is reduced and bone formation decreases in older individuals. While the immune response is generally maintained with age, plaque accumulation and pathogens shift. Systemic conditions like diabetes can further impact the aging periodontium.

1. Ageing & the
Periodontium
Presented By – Dr. Jignesh Tate
1st Year Post- Graduate
Department of Periodontics
4/30/2018 1

2. Contents
Introduction to Aging
General Effects of aging
Effect of aging on periodontium
• Gingival epithelium
• Gingival connective tissue
• Periodontal ligament
• Cementum
• Alveolar Bone
• Bacterial plaque
• Immune response
Systemic diseases & Periodontal health
Conclusion
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3. Introduction
• 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)
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1. Webster's New World™ Medical Dictionary, 3rd Edition.

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 periodontium.
• Human ageing induces histo-physiological and clinical
alterations in oral tissues.2 (Mombelli A. 1998)
• These alterations must be understood to differentiate
pathological conditions from the altered physiology of oral
tissues resulting from ageing .3
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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.

5. General effects of aging
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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)
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7. Alternations in oral motor functions
Lip posture Drooling, angular cheilitis.
Muscles of
mastication
Efficiency of Mastication decreases.
Tongue Speech, dysphagia, traumatic bite injury.
Swallowing Dysphagia
Taste Loss of sensation or decreased sensation.
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8. Age dependent changes in periodontal tissues
• 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 (Van
der Velden, 1984)
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9. Changes within gingival epithelium
• Thining of epithelium & diminished keratinization.5
• Increased epithelial permeability to pathogens.
• Decreased resistance to functional trauma.
• Rate of cell division in the basal layer of gingival epithelium has
not been shown to alter with increasing age.
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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

10. • Cellular turnover rate slows down, leading to decline in the
production of both young cells and fibers in the gingiva.
• Epithelial density has been shown to be increased with age.
(Ryan 1974)
• Conflicting results have been reported regarding the shape of
the retepegs.
• A flattening of rete pegs and an increase in the height of the
epithelial ridges associated with ageing were both
demonstrated.
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11. Gingival sample obtained
from a 25-year-old healthy
subject. Normal aspect of
epithelium layers, rete ridges
and connective tissue, (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
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12. • 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
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4. Van der Velden U. Effect of age on the periodontium. J Clin Periodontol. 1984; 11:
281 -294.

13. • 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.
• 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 tooth brushing
trauma.
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14. 4/30/2018 14
Carranza’s clinical periodontology 10th edition Chapter-6, Page No. 94.

15. • 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
(Needleman 2004)
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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

16. Changes within gingival connective tissue
• 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 denaturation temperature.
• These results indicate increased collagen stabilization caused by
the changes in the macromolecular conformation.
• There is also a reduction in the organic matrix production and in
vascularization, and an increase in the number of elastic fibers.
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17. • Connective tissue - 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
• Reduction in the number of fibroblasts in the periodontal
ligament and also in its functional activity.
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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.
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.

18. • Gingival fibroblasts (GF) are 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
• The influence of these inflammatory mediators - both GF and
periodontal ligament fibroblasts (PLF) - the severity of
periodontal disease.6
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19. Changes in Periodontal Ligament
• Decreased number of fibroblasts.
• Decreased organic matrix production.
• Decreased epithelial cell rests.
• Decreased number of collagen fibers.
↓
reduction or loss in tissue elasticity
• Vascularity reduces with age.
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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 (Marsillac M, 2005)
• 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 (Zenobio EG,
2004)
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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.

21. Changes within the cementum
• Increase in cemental width is a common finding.
• Berglundh T. - study on dogs - Increase may be 5 to 10 times
with increasing age.12
• Van der Velden - Increase in width is greater apically and
lingually.13
• Deposition takes place mainly in apical region to compensate
for the physiological wear of teeth.
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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.

22. 4/30/2018 22
• Saverson et al. (1958) – Greater
cemental apposition in the apical region
is a response to the passive eruption of
the tooth.
• According to Ive et al. (1980), passive
eruption and migration of teeth involves
re- attachment of fibers between the
cementum and the periodontal ligament.
Increased cemental deposition might be
required to fulfil this.
• With advancing age, areas of cementum resorption followed by new
cemental apposition may be observed.
• This may result in irregular surface of cementum.

23. Changes in Alveolar bone
• Reduction of bone mass.
• More irregular periodontal surface of
bone.
• Less regular insertion of collagen
fibers.
• Increased bone resorption.
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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
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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.
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.

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.
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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.

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.
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27. Immune response
• 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.
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28. • McArthur17 concluded 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 elderly
group of individuals, with and without disease.”
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17. McArthur WP. Effect of aging on immunocompetent and inflammatory cells . Periodontol 2000, 1999 : 16-
53.

29. Bacterial Plaque
• 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 surface as a
substrate for plaque formation.
• Exposed cementum of the root surface and dental enamel
constitute two unlike types of hard dental tissues with distinct
surface characteristics, which may influence the plaque
formation rate differently.
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30. • For sub gingival plaque, increased number of entric rods and
pseudomonads in older adults. (Slots 1990)
• Periodontal pathogens specifically including an increased role
for P. gingivalis and decreased role for A.
actinomycetemcomitans.
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31. 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
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The passage of periodontal
pathogens and their products
into circulation (bacteremia).
The passage of locally
produced inflammatory
mediators into circulation.

32. Diabetes Mellitus
4/30/2018 32JADA 2006;137(10 supplement):26S-31S.
Food Consumption
Breakdown of carbohydrates in
GIT and absorption of sugars
in bloodstream
Increased blood glucose
levels
Secretion of ꞵ- cells in
the pancreas
Insulin binds to target cell
receptors and allows entry of
glucose into the cell (used for
cellular energy)
Decreased blood
glucose levels
Type 1 Diabetes destroys ꞵ- cells
Type 2 Diabetes causes insulin
resistance at receptor and post
receptor levels

33. •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
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34. • 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 (Khader YS. Et al. 2006)
• 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 (Shlossman M. 2010)
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35. Coronary heart disease (CHD)
• Periodontal and cardiovascular diseases are common
inflammatory conditions in the human population,
atherosclerosis being the major component of the latter.
• Loesche et al. 2001 conducted a study on association between
periodontal disease and coronary heart disease.
• It was found that in patients with periodntal diseases there are
1.84 times more CHD.
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36. ROLE OF SUBGINGIVAL PLAQUE
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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

37. • A meta-analysis study indicated that individuals with
periodontitis had 1.14 times higher risk of developing coronary
heart disease.24 (Bahekar AA 2007)
• The more severe the periodontal disease the easier the
periodontal pathogens could enter the circulation, reaching
blood vessels and atherosclerotic lesions.
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38. • 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 (Linden GJ 2008)
• Ridker et al. 2009 demonstrated that C-reactive protein levels
predict the risk of coronary events.26
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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. 2009; 342: 836-43.

39. PERIODONTAL TREATMENT PLANNING IN OLDER INDIVIDUALS
‘Goal of periodontal treatment is to preserve function and
prevent the progression of inflammatory disease’
- Factors must be considered in treatment planning
Patients
- General health status
- Medications
- Life style behaviors
- Ability to perform oral hygiene procedures
- Ability to tolerate treatment
- Amount of remaining periodontal support
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40. 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.
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41. Conclusion
• 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.
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42. 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: 490-94.
4. Van der Velden U. Effect of age on the periodontium. J Clin Periodontol. 1984;
11: 281-94.
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: 350-69.
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: 179-87.
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: 383-93.
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.
4/30/2018 42

43. 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.
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.
4/30/2018 43

44. 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.
23. Shlossman M, Knowler WC, Pettitt DJ, Genco RJ. Type 2 diabetes mellitus and
periodontal disease. JADA 2010;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. 2009;
342: 836-43.
4/30/2018 44