This presentation describes the Effect of smoking on response to periodontal therapy 1. Non surgical periodontal therapy 2. Antimicrobial therapy 3. Conventional surgical therapy 4. Regenerative procedures 5. Mucogingival surgeries

1. SMOKING AND
PERIoDONTIUM part 2
DR MANISHA SINHA
I STYEAR PG
RAJARAJESWARI DENTAL COLLEGE AND HOSPITAL

2. CONTENTS
 Effect on response to periodontal therapy
1. Non surgical periodontal therapy 2. Antimicrobial therapy
3. Conventional surgical therapy 4. Regenerative procedures
5. Mucogingival surgeries
 Refractory periodontitis
 Role of smokeless tobacco products in periodontal diseases
 Cessation of smoking
 Conclusion
 References

3. EFFECTS OF
SMOKING ON
RESPONSETO
PERIODONTAL
THERAPY
 Smoking has also been implicated as a factor that reduces the
effectiveness of treatment
 It appears that smokers may respond to nonsurgical periodontal
therapy less favourably than nonsmokers, especially in terms of
probing depth and bone level
 When the effect of the level of cigarette consumption is considered,
it seems that the response to periodontal therapy is related to the
amount of cigarettes smoked ; and that previous smokers (quit-
smokers) have a similar response to treatment compared to non-
smokers

4. NON SURGICAL
PERIODONTAL
THERAPY
↓CLINICAL RESPONSETO SCALING AND ROOT
PLANING
↓REDUCTION IN POCKET DEPTH
↓ GAIN IN CLINICAL ATTACHMENT LEVELS
↓NEGATIVE IMPACT OF SMOKING WITH ↑LEVEL OF PLAQUE CONTROL.

5.  Wan et al. found that at 12 months after nonsurgical therapy,
smokers presented with a significantly higher percentage of
residual pockets.
 In addition, smokers showed less probing pocket depth (PPD)
reduction in sites with initial PPD ≥5 mm.
 The inhibitory effect of smoking on treatment response is more
pronounced at initially deeper sites.
 Studies by Preber and Bergström, Grossi et al. (1997),Renvert et
al., Machtei et al., and Jin et al. have shown that probing depth
reduction and clinical attachment level improvement in smokers
are 50%–75% those of nonsmokers, following nonsurgical and
surgical therapy.

6.  Darby et al. found that nonsmokers with aggressive periodontitis
had significantly greater probing depth reduction (2.4 mm)
compared with patients with aggressive periodontitis who smoke
(1.3 mm).
 However, in the presence of excellent plaque control, these
differences may be minimized.

7. When scaling and root planing were combined with adjunctive
doxycycline gel or minocycline (LDD) , the response in smokers was
similar to that seen for non-smokers receiving scaling and root planing
alone
Novak et al. 2002 reported a positive response to sub-antimicrobial
doxycycline therapy in combination with scaling and root planing in a
group of patients with severe periodontitis almost half of which were
smokers.
When scaling and root planing are used in combination with topical
subgingivally placed tetracycline fibers, subgingival minocycline gel,
or subgingival metronidazole gel, smokers continue to show less
pocket reduction than nonsmokers.'"
ANTIMICROBIAL
THERAPY

8.  In a 9-month, placebo-controlled, randomized trial in which
smokers and nonsmokers were treated by scaling and root planing
with and without sub-antimicrobial doxycycline,
 Preshaw et al. concluded that adjunctive sub-antimicrobial dose
doxycycline enhanced therapeutic outcomes in all groups with
smokers taking doxycycline, showing approximately the same
magnitude of clinical improvement as nonsmokers on placebo.

9.  On the other hand, in studies where adjunctive systemic
amoxicillin and metronidazole or locally delivered minocycline
microspheres enhanced the results of mechanical therapy, there
was a greater difference between the control and experimental
treatments within smokers as compared to within nonsmokers.
 These enhanced results might be due to antimicrobial actions,
and, in the case of tetracycline derivatives, anticollagenase
activity.
 Unique regimens that sequence systemic antimicrobial therapy or
combine local antimicrobial delivery with host modulatory therapy
might offer clinicians and patients options that address microbial
and host response alterations in smokers.

10. CONVENTIONAL
SURGICAL
THERAPY
Healing after a conventional surgical therapy is more complex
With smoking affecting most of the steps including
Initial inflammatory response
Organization of clot
Angiogenesis and revascularization of flap
Fibroblasts laying down collagen
Epithelial attachment

11.  Following surgical treatment such as osseous surgery,
modified Widman flap surgery, or flap debridement surgery,
smokers had approximately 0.5 mm less improvement in
probing depth and attachment levels.At furcation sites both
horizontal and vertical attachment gain were impaired by
smoking. These differences remained over a 6-year
maintenance period . Smokers respond less favourably to flap
debridement surgery in terms of pocket depth reduction and
attachment levels gains, especially in sites with deep initial
pocket depth.

12. Smoking has a strong
negative impact on
regenerative therapy,
including
• osseous grafting,
• guided tissue regeneration,
• a combination of these
treatments.
REGENERATIVE
PROCEDURES

13.  Studies byTrombelli et al. and Mayfield et al. (1998) reported that
evaluated osseous changes by sound probing or re-entry, vertical
bone gain in smokers ranged from 0.1 to 0.5 mm, whereas
nonsmokers demonstrated 0.9–3.7 mm improvement.
 Stavropoulos et al. showed that smoking exerted a detrimental
effect on the outcome of GTR treatment of intrabony defects with
bioresorbable membranes.

14.  When expanded polytetrafluoroethylene membranes were
utilized in GTR procedures at recession sites, smokers had
significantly less root coverage (57%) as compared to nonsmokers
(78%).
 The superior blood supply afforded by the subepithelial
connective tissue graft might be more resistant to the effects of
smoking as compared to the nonresorbable barrier membrane.
 However, root coverage following thick free gingival graft
procedures is reportedly diminished by heavy cigarette smoking
and there are conflicting reports on smoking’s effect on the
success of subepithelial connective tissue grafts.

15.  The most impressive report of clinical attachment gain in
nonsmokers (5.2 mm) compared with smokers (2.1 mm) was
observed byTonetti et al., who carried out guided tissue
regeneration (GTR) of infrabony defects using Gore-Tex
membranes and with a follow-up period of 1 year.
 They also concluded that higher plaque levels that are seen
consistently in smokers compared with nonsmokers will also have
influenced the clinical outcomes.

16. Smoking majorly affects revascularization of tissue
grafts in recession coverage
The majority of studies show that gingival grafting
for root coverage is less successful in smokers than
non smokers (Muller HP et al 1998; ZuchelliG et al
1998)
The majority of more recent studies indicate that
smokers exhibit three-quarters of the amount of root
coverage shown by non smokers
Erley et al. (2006) and Martins et al. (2004) reported
that root coverage was 82.3 and 58.4% for smokers,
respectively, as compared to 98.3 and 74.73% for
nonsmokers
MUCOGINGIVAL
SURGERIES

17.  According to the 1996, Report of the Academy of
Osseointegration Sinus Graft Consensus Conference, the
implant failure rate in grafted maxillary sinuses in smokers
was 12.7% compared to 4.8% in non smokers.
 A Retrospective cohort study that included both maxillary
sinus and ridge augmentation procedures, Woo et al. 2004
reported that smokers had a 4.4 times increased risk for
implant failure.
IMPLANTS AND
SITE DEVELOPMENT

18. Looking at the survival of osseointegrated implants in patients who were IL-1
genotype positive, investigators found that implant survival was significantly
influenced by the smoking status of the patients..implant failure was 2.5 times greater
in smokers,where the genotype status was not a significant factor.(Wilson et al 1999).
Carrlson et al 2000.. Periimplant bone loss in smokers was great and significant in the
mandible but not in the maxilla when compared to non smokers.
Failure rate --- hydroxyapatite-coated implants was 4.8% in smokers compared
to 2.4% in non smokers
--- non coated implants was 16% in smokers and 11.7% in non-smokers.

19.  In the studies reviewed, 0%–17% of implants placed in smokers
were reported as failures as compared to 2%–7% in nonsmokers,
with the majority of studies showing at least twice as many failed
implants in smokers.
 The 3-year data demonstrated that 8.9% of implants placed in
smokers failed as compared to 6% in individuals who had never
smoked or had quit smoking.

20.  Emerging data indicate that the impact of smoking on implant
therapy is more dramatic in grafted maxillary sinuses compared to
nongrafted sites.
 The percentage of implant failures in grafted sinuses in smokers is
1.4–3.9 times greater than that of nonsmokers, with the majority
of studies showing at least 2.5 times the number of failed implants
in smokers.

21.  The detrimental effects of smoking on treatment outcomes
appears to be long-lasting and independent of the frequency of
maintenance therapy.
 Kaldahl et al 1996, evaluated patients who had undergone four
different modalities of treatment and were on maintenance
phase every 3 months for 7 years
 Smokers had deeper pocket and lesser gain in attachment
consistently throughout the study than non smokers.
 smokers had deeper and more residual pockets than
nonsmokers, even though no significant differences in plaque
or bleeding on probing scores were found.
MAINTENANCE
PHASE

22.  Because of the difficulty in controlling periodontal disease in
smokers, many smokers become refractory to traditional periodontal
treatment and tend to show more periodontal breakdown than
nonsmokers after therapy.
 In studies of patient who failed to respond to the conventional
therapy, including different combinations of OHI, SRP, Surgery and
Antibiotics, approximately, 90% were smokers
REFRACTORY
PERIODONTITIS

23. Role of smokeless tobacco products in
periodontal diseases
 Smokeless tobacco products have demonstrated a strong
relationship to white oral mucosal lesions.
 A clear relationship between smokeless tobacco use &
generalized periodontal conditions has not been definitely
demonstrated.
 In vitro studies have demonstrated that smokeless tobacco
products affect monocyte & oral keratinocyte production of
inflammatory mediators & this may play a role in the
development of localized tissue alterations.

24.  Studies conducted in Sweden also have shown that the consumption
of moist snuff, an oral SLT product, is associated with increased
prevalence of gingival recession.
 Studies conducted in India have reported that oral SLT users tend to
have higher scores and risk for periodontal disease .
 A study on the patterns of tooth loss among tobacco users in central
India showed that mandibular tooth loss was more among oral SLT
users suggesting that the deleterious effects of SLT use is
manifested more in mandibular teeth .
 Studies reporting the occurrence of gingival recession among oral
SLT users have reported that these occurred at sites adjacent to
mucosal lesions suggesting that the recession was a result of long-
term injury to the gingival tissues from the SLT product

25.  Oral SLT users in a central Indian population
were shown to have an increase in prevalence
and severity of recession and attachment loss at
mandibular teeth, buccal surfaces, anterior
teeth, and molars-the surfaces most likely to
have prolonged exposure to SLT product due to
retention of the SLT product at the mandibular
buccal or anterior labial vestibule

26. SMOKING CESSATION
PROGRAM

27. Less than 50 percent of the 44.5 million current smokers make an
attempt to quit annually. Seventy percent of smokers who attempt
to quit do so without the use of evidence-based programs, and, of
those, 90 percent will relapse.
 One way to increase the overall impact of cessation within the
population is to increase the reach of current interventions using
social marketing to enhance smokers’ motivation and interest in
cessation.The Internet is proving to be a cost-effective vehicle for
reaching smokers, but few programs have been thoroughly
evaluated.

30. TOBACCOCOUNSELING –ACOMPONENT
OF PERIODONTALTHERAPY
 Nicotine dependence is classified as a chemical addiction by the
American PsychiatricAssociation in the Diagnostic and Statistical
Manual of Mental Disorders, 1994 (IV).
 A useful model brief intervention that uses a five-step approach is
recommended by the Agency for Health Care Research and Quality
(Fiore 2008,walsh2005).

32.  If a patient has expressed a sincere interest in quitting, the chance
of success are far greater than if the patient is unwilling to quit or
wishes to postpone the start of a cessation program.
 For these patients, before deciding whether to proceed with a
smoking cessation program, a Five R’s approach has been
developed.
 Success is most likely to be achieved when counseling and
pharmacological approaches, such as nicotine-replacement
therapies are used in combination.

35. PHARMACOTHERAPY
Pharmacotherapy + behavioural counselling improves long-term quit
rates
Smokers of 10 or more cigarettes a day who are ready to stop should be
encouraged to use pharmacologial support as a cessation aid.
Nicotine replacement
• Begin NRT on the quit date, (apply patches the night before)
• Use a dose that controls the withdrawal symptoms
• NRT provides levels of nicotine well below smoking
• Prescribe in blocks of two weeks
• Arrange follow up to provide support
• Use a full dose for 6 to 8 weeks then stop

37.  Nicotine replacement therapies (NRTs) appear to work because
they relieve withdrawal symptoms of anxiety, depression,
difficulty concentrating, insomnia, irritability, restlessness, and
nicotine craving.
 Because NRTs provide much lower levels of nicotine than does
smoking and because the nicotine is absorbed more slowly than it
is from cigarettes, they do not appear to cause
cardiovascularharm and their dependence potential is very small
(<2%).

38.  Four types of NRTs use ad-libitum dosing: nicotine gum, inhaler,
lozenge, and nasal spray.
 Their major advantage is they can be used to cope with
situationally induced cravings or withdrawal.
 Their disadvantage is the need to use multiple doses per day, the
need to avoid acidic beverages when using the product, and
possible embarrassment with use.

39. Advantage-
it requires only a once per day
dosage and it is more socially
acceptable and confidential
than the gum
NICOTINE
PATCHES
The nicotine patch, or transdermal nicotine, is available
OTC and provide a slow, consistent release of nicotine throughout
the day.
Available in various shapes and sizes,
as a 24-hour patch in doses of 21, 14, and 7 mg, and
as a 16-hour patch at a 15-mg dose.
Disadvantage –
it cannot be used for sudden
cravings. Whether 24-hour
versus 16-hour patch use or
whether tapering doses improves
quit rates is unclear.
Side effects include insomnia and skin rash.

40. NICOTINE
GUM
• Nicotine gum is an OTC medication that is
available in 2 mg (<25 cigarettes/day smoker) and 4
mg (>25 cigarettes/day smoker) doses.
• mint and citrus flavors
• Instruct the patient to ‘chew and park’. Absorption
may be impaired by coffee and some acidic drinks .
• . Side effects include jaw ache, nausea, and stomach
ache.

41. NRT:
NICOTINE
NASAL
SPRAYS
The nicotine nasal spray is available as a single
dose.
Advantage - it provides
higher and more rapid nicotine doses compared to other
NRTs
however, this still is less than one-tenth the arterial
nicotine levels seen with cigarettes.
Disadvantage- nasal irritation, lacrimation, rhinitis,
coughing, sneezing, and facial flushing are experienced by
more than 75% of users.

42. NICOTINE
LOZENGE
Available as an OTC medication in a 2-mg dose
for those smoking their first cigarette after 30
minutes of arising and a 4-mg dose for those
smoking less than 30 minutes after arising.
 produces nicotine levels, efficacy, and side
effects similar to nicotine gum but may be more
acceptable.

43. CONCL
USION
CONCLUSION

45. REFERENCES
 Clinical periodontology Carranza, 10th edition
 Clinical periodontology and implant dentistry Lindhe ,5th edition
 Smoking and periodontal disease, periodontology 2000.vol.32
 The effect of smoking on periodontal treatment response . J Clin
Periodontol 2006
 Systematic review of the effect of smoking on nonsurgical periodontal
therapy Periodontology 2000, Vol. 37
 The influence of smoking on host responses in periodontal infections
Periodontology 2000, Vol. 43

46.  Smoking and its Effect on Periodontium – Revisited. Gurparkash Singh
Chahal, Kamalpreet Chhina, Vipin Chhabra, Amna Chahal. Indian Journal
of Dental Sciences,Volume 9,Is.sue 1,January-March 2017.
 Smoking and periodontal disease,d.f. kinane,i.g. chestnutt. 11(3):356-365
(2000)
 Tobacco Use and Its Effects on the Periodontium and Periodontal Therapy
 Health Effects of Light and Intermittent Smoking: A Review,Rebecca et
al.2010 april 6: 121(13):1518-1524.
 Pharmacology of Nicotine: Addiction, Smoking-Induced Disease, and
Therapeutics ANNU Rev Pharmacol toxicl 2009:49:57-71.

47. THANK
YOU