Aging and smoking effect on
Yousefimanesh H , DDS,MSc
• Increased health awareness and improvements
in preventive dentistry have led to decreasing
tooth loss for all age groups.
• Normal aging of the periodontium is a result
of cellular aging.
• The aging process does not affect every tissue
in the same way.
• Thinning and decreased keratinization of the
• An increase in epithelial permeability to
• A decreased resistance to functional trauma
• The flattening of rete pegs
• Altered cell density
• The consensus is that gingival recession is
not an inevitable physiologic process of
aging but is explained by cumulative effects
of inflammation or trauma on the
Gingival Connective Tissue
• Coarser and denser gingival connective
• An increased rate of conversion of soluble to
• Increased mechanical strength
• Increased denaturing temperature.
• Increased collagen stabilization caused by
changes in the macromolecular conformation
• Greater collagen content has been found in
the gingivae of older
• Decreased numbers of fibroblasts
• Irregular structure, paralleling the changes in
the gingival connective tissues.
• Decreased organic matrix production and
epithelial cell rests
• Increased amounts of elastic fiber.
• Width of the space will decrease if the tooth
is unopposed (hypofunction) or will increase
with excessive occlusal loading.
• An increase in cemental width is a common
• This increase may be 5 to 10 times with
• The increase in width is greater apically and
• A more irregular periodontal surface of bone and
less regular insertion of collagen fibers.
• The healing rate of bone in extraction sockets
appears to be unaffected by increasing age.
• The success of osseointegrated dental implants does
not appear to be age related.
• Bone graft preparations from donors more than 50
years old possessed significantly less osteogenic
potential than graft material from younger donors.
• Dentogingival plaque accumulation has been
suggested to increase with age.
• This might be explained by the increase in hard
tissue surface area resulting from gingival
recession and the surface characteristics of the
exposed root surface.
• Studies have shown no difference in plaque
quantity with age.
• The supragingival plaque, no real qualitative
differences have been shown for plaque
• For subgingival plaque increased numbers
of enteric rods and pseudomonads in older
• Mombelli suggests caution in the
interpretation of this finding because of
increased oral carriage of these species
among older adults.
• Increased role for ??
• Decreased role for ??.
• Differences between young and older
individuals can be demonstrated B cell,T
cell, cytokines, and natural killer cells
• Not different for polymorphonuclear cells
and macrophage activity.
• A comparison of developing gingivitis
between young and older individuals
demonstrated a greater inflammatory
response in older subjects, both in humans
• The conclusions from these studies are
strikingly consistent and show that the effect
of age either is non-existent or provides a
small and clinically insignificant increased
risk of loss of periodontal support.
• Age has been suggested as being not a true
risk factor for periodontitis.
• A recent study has identified greater
compliance with supportive maintenance
among older individuals than younger
• Current smokers were defined as those who
had smoked 100 or more cigarettes over their
lifetime and smoked at the time of the
• Former smokers had smoked 100 or more
cigarettes in their lifetime but were not
• Nonsmokers had not smoked 100 cigarettes
in their lifetime.
• The prevalence of smoking is higher in
individuals older than 34 years of age
, males, low-income adults .
• Increasing evidence points to smoking
as a major risk factor for periodontitis.
• Affecting the prevalence, extent, and
severity of disease.
EFFECTS OF SMOKING ON GINGIVITIS
• The development of inflammation in response
to plaque accumulation is reduced in smokers
compared with nonsmokers.
• The smokers present with less gingival
inflammation than nonsmokers.
• The smokers have a decreased expression of
clinical inflammation in the presence of plaque
accumulation compared with nonsmokers.
EFFECTS OF SMOKING ON PERIODONTITIS
• The smoking is a major risk factor for
increasing the prevalence and severity
of periodontal destruction.
• The pocket depth, attachment
loss, and alveolar bone loss are more
prevalent and severe in patients who
smoke compared with nonsmokers.
• The study demonstrated a dose-
response relationship between
cigarettes smoked per day and the
odds of having periodontitis.
• The number of years of tobacco use is a
significant factor in tooth loss, coronal root
caries, and periodontal disease.
• The smoking is associated with increased
severity of generalized aggressive
periodontitis in young adults.
• Prevalence of moderate
and severe periodontitis
• The percentage of teeth
with 5 mm or more of
attachment loss was most
• Severity of disease
intermediate between the
current cigarette smokers
• tooth loss is increased in
cigar and pipe smokers
compared with nonsmokers
• Smokeless tobacco use has been
associated with oral leukoplakia and
• No generalized effects on periodontal
disease progression seem to occur, other
than localized attachment loss and
recession at the site of tobacco product
Risk for periodontitis
current smokers>former smokers >nonsmokers
Gingivitis Gingival inflammation and
bleeding on probing
Prevalence and severity of
periodontal destruction, Pocket depth,
attachment loss, bone loss, Rate of
Prevalence of severe periodontitis,
Tooth loss, Prevalence with increased
number of cigarettes smoked per day .
Prevalence and severity with
Effects of smoking on the microbiology
• A difference in the rate of plaque
accumulation of smokers compared
• It results from a qualitative rather than
quantitative alteration in the plaque.
• it was found that members of the
orange and red complexes including
were significantly more prevalent in
current smokers than in nonsmokers
and former smokers.
• The increased prevalence of these
periodontal pathogens was caused by an
increased colonization of shallow
• The pocket depth 4 mm or greater with
no differences among smokers, former
smokers, and nonsmokers.
• These pathogenic bacteria were more
prevalent in the maxilla than the
• The smokers have a greater extent of
colonization by periodontal pathogens
than nonsmokers or former smokers and
increased prevalence of periodontal
Effects of smoking on the immunology
• Smoking exerts a major effect on the
protective elements of the immune response,
resulting in an increase in the extent and
severity of periodontal destruction.
• The deleterious effects of smoking appear to
result in part from a downregulation of the
immune response to bacterial challenge.
• The neutrophil is an important component of
the host response to bacterial infection.
• Neutrophils obtained from the
peripheral blood, oral cavity, or saliva
of smokers or exposed in vitro to whole
tobacco smoke or nicotine have been
shown to demonstrate functional
chemotaxis, phagocytosis, and the
• The production of antibody essential
for phagocytosis and killing of
bacteria, specifically, immunoglobulin
G2 (lgG2) levels to periodontal
pathogens, has been reported to be
reduced in smokers versus nonsmokers
• Elevated levels of tumor necrosis factor alpha (TNF-α) ,
PGE2, neutrophil elastase have been demonstrated in the
GCF of smokers
• In vitro studies also have shown that exposure to nicotine
increases the secretion of PGE2 by monocytes in response
to lipopolysaccharide .
• These data suggest that smoking may impair the response
of neutrophils to periodontal infection but may also increase
the release of tissue-destructive enzymes.
• Although no significant differences in the vascular density
of healthy gingiva have been observed between smokers
• The response of the microcirculation to plaque
accumulation appears to be altered in smokers compared
• Subgingival temperatures are lower in smokers than
• recovery from the vasoconstriction caused by local
anaesthetic administration takes longer in smokers.
EFFECTS OF SMOKING ON RESPONSE
TO PERIODONTAL THERAPY
• Nonsurgical Therapy
• Surgical Therapy and Implants
• Maintenance Therapy
• Periodontal therapy
• The pocket depth reduction
• It can be concluded that smokers respond less
well to nonsurgical therapy than nonsmokers.
• With excellent plaque control, however, these
differences may be minimized.
• The former and nonsmoking subjects appear to
respond equally well to nonsurgical care
Surgical Therapy and Implants
• The smokers consistently showed less pocket
reduction and less gain in clinical attachment levels
than nonsmokers or former smokers.
• Intrabony defects,
• The impact of smoking on implant success is unclear
• Several studies have shown that implant success
rates are reduced in smokers
• The detrimental effects of smoking on
treatment outcomes appears to be long-
lasting and independent of the frequency
of maintenance therapy.
• approximately 90% of the "refractory”
patients were smokers.
• It is clear from these studies that smokers
• (1) may present with periodontal disease at an early age,
(2) may be difficult to treat with conventional therapy,
• (3) may continue to have progressive or recurrent
periodontitis leading to tooth loss