Aging and smoking effect on Periodontium

Presented by:

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.

Gingival Epithelium• Thinning and decreased keratinization of the

gingival epithelium.• An increase in epithelial permeability to

bacterial antigens• 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 periodontium.

Gingival Connective Tissue• Coarser and denser gingival connective

tissues.• An increased rate of conversion of soluble to

insoluble collagen• 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

Periodontal Ligament• 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.

Cementum• An increase in cemental width is a common

Finding• This increase may be 5 to 10 times with

increasing age. • The increase in width is greater apically and

lingually.

Alveolar Bone• 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.

Bacterial Plaque• 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 composition.

• For subgingival plaque increased numbers of enteric rods and pseudomonads in older adults.

• 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 ??.

Immune Responses• Immunosenescence • 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.

• McArthur?

• A comparison of developing gingivitis between young and older individuals demonstrated a greater inflammatory response in older subjects, both in humans and dogs.

• 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 patients.

Smoking and Periodontal Disease

• Current smokers were defined as those who had smoked 100 or more cigarettes over their lifetime and smoked at the time of the interview.

• Former smokers had smoked 100 or more cigarettes in their lifetime but were not currently smoking.

• 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 severe

• Severity of disease intermediate between the current cigarette smokers and nonsmokers

• tooth loss is increased in cigar and pipe smokers compared with nonsmokers

• Smokeless tobacco use has been associated with oral leukoplakia and carcinoma.

• No generalized effects on periodontal disease progression seem to occur, other than localized attachment loss and recession at the site of tobacco product placement.

Risk for periodontitiscurrent smokers>former smokers >nonsmokers

Gingivitis Gingival inflammation andbleeding on probing

Periodontitis

Prevalence and severity ofperiodontal destruction, Pocket depth,

attachment loss, bone loss, Rate of periodontal destruction,

Prevalence of severe periodontitis,Tooth loss, Prevalence with increased number of cigarettes smoked per day .

Prevalence and severity withsmoking cessation

Effects of smoking on the microbiology

• A difference in the rate of plaque accumulation of smokers compared with nonsmokers

• 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 sites(≤4mm).

• 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 mandible.

• The smokers have a greater extent of colonization by periodontal pathogens than nonsmokers or former smokers and increased prevalence of periodontal breakdown.

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 alterations in chemotaxis, phagocytosis, and the oxidative burst.

• 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 with periodontitis

• 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.

Physiology• Although no significant differences in the vascular density

of healthy gingiva have been observed between smokers and nonsmokers.

• The response of the microcirculation to plaque accumulation appears to be altered in smokers compared with non-smokers.

• Subgingival temperatures are lower in smokers than nonsmokers.

• recovery from the vasoconstriction caused by local anaesthetic administration takes longer in smokers.

EFFECTS OF SMOKING ON RESPONSETO PERIODONTAL THERAPY

• Nonsurgical Therapy• Surgical Therapy and Implants• Maintenance Therapy

Nonsurgical 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

at present. • Several studies have shown that implant success

rates are reduced in smokers

Maintenance Therapy• 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