INTRODUCTION

Cigarette smoke contains a wide variety of chemicals. Carbon monoxide, hydrogen cyanide and nitrogen oxides, formaldehyde, acrolein, benzene and N-nitrosamines, nicotine, phenol, polyaromatic hydrocarbons, and tobacco-specific nitrosamines are among these chemicals that are hazardous to human health1.

During smoking, the harmful chemicals first encounter the tissues of the oral cavity. Melanosis, which mostly occurs in the form of benign pigment increase in the vestibular gingiva and interdental papilla in the anterior region of both upper and lower jaws, is perceived as an annoying aesthetic problem2. Smoking is among the major aetiological factors for melanosis together with genetic factors, various drugs or various systemic diseases3. Smoking affects gene expressions of the epithelium in the respiratory tract, decreases immune resistance of the oral mucosa and damages buccal mucosa4. Moreover, nicotine, with its pharmacokinetic effect, stimulates the sympathetic nervous system and facilitates plaque accumulation on the tooth and soft tissue surfaces by reducing saliva secretion5.

A relationship between periodontal diseases and smoking was first reported by Pindborg6 in terms of a higher prevalence of acute necrotizing ulcerative gingivitis in smokers. Smokers have a much higher risk for periodontitis7 and when individuals with similar plaque levels were compared, pocket depth and attachment loss are higher in the smokers8. Smoking negatively affects the immune system. While the number of leukocytes in the circulation increases in smokers, fewer defence cells can migrate into the gingival groove/pocket7,9. Circulation in periodontal tissues deteriorates, formation and functions of vascular structures are adversely affected10.

Clinical findings from a study comparing non-smokers, smokers, and passive smokers provided further support for the adverse and dose-dependent effect of tobacco products consumption on periodontal health11. The prevalence of Treponema denticola was higher in smokers possibly explaining at least partially the increased occurrence and severity of periodontal tissue destruction11. In a recent study, the outcomes of non-surgical periodontal treatment were investigated in smoker and non-smoker patients with Stage III and IV periodontitis in terms of clinical periodontal, microbiological, and biochemical parameters and follow-up at 6 months revealed that Gram-negative bacteria recolonise faster in smokers12.

DEVELOPMENTS

Gingival recession

Pink aesthetics and smile design are popular, particularly among young individuals13. Gingival recession (GR) that makes the teeth look longer disturbs the pink aesthetics and is a common finding in the adult population14,15. According to the Glossary of the American Academy of Periodontology, gingival recession is described as the exposure of the root surface by an apical shift of the gingiva with respect to the cemento-enamel junction (CEJ)16. By definition, gingival recession is always associated with clinical attachment loss17 and can be localized or generalized affecting one tooth or several teeth in the same patient and may involve one or more surfaces of the same tooth18,19. Gingival recession can be associated with gingivitis or periodontitis, or it may develop due to traumatic occlusion, tissue trauma, proliferation of the pocket epithelium into the gingival connective tissue and its subsequent anastomosis with the outer epithelium as an extension of periodontal inflammation, traumatic tooth brushing and/or iatrogenic factors. The primary pathogenic factors (i.e. periodontal inflammation) and the local anatomic factors, which are environmentally conductive, not only affect the formation but also the quality and morphology of gingival recession lesions20.

Root coverage procedures

Root coverage procedures which have been used for the treatment of gingival recession are successful and predictable interventions in periodontics. Aesthetics, dental hypersensitivity, and the prevention of caries and non-carious cervical lesions are considered the main indications for root coverage procedures21. A number of different surgical techniques have been described and used for root coverage: lateral sliding flap, double papilla positioned flap, free gingival graft, lateral positioned flap, coronally advanced flap with free gingival graft, coronally advanced flap with a subepithelial connective tissue graft, semilunar flap, and coronally positioned flap. Coronally advanced flap (CAF) with subepithelial connective tissue graft (SCTG) is considered as the gold standard since it offers a greater probability of achieving complete root coverage when compared with other techniques22. The major goal for successful root coverage is to move the gingival margin up to the CEJ with a probing sulcus depth of 2 mm and no bleeding on probing, no hypersensitivity23. Several factors affect the outcome of root coverage procedures and smoking is one of the most important factors21.

Effects of smoking on root coverage procedures

Numerous studies have evaluated the possible effects of smoking on mucogingival surgical interventions (Table 1). The first study investigating the relationship between root coverage and smoking was published by Tolmie et al.24. They observed no adverse effects with cigarette smoking and obtained 100% root coverage in 11 of 12 (92%) sites in smokers. However, the number of cigarettes smoked or the duration of smoking was not reported. In another study25, gingival recession in non-smokers, light-smokers (≤10 cigarettes/day), and heavy-smokers (≥10 cigarettes/day) were treated by double pedicle graft and subepithelial connective tissue graft. No difference in clinical outcomes was found between the three study groups. On the other hand, in a retrospective study by Trombelli et al.26 reported that the rate of root coverage was lower in smoker patients than that obtained in non-smokers. In another clinical study, connective tissue graft was applied with the envelope technique modification and attachment gain was negatively affected by smoking27. Zuchelli et al.28, treated 54 teeth with gingival recession, and stated that smoking decreased the expected root coverage amount by 0.52 mm. In contrast, Amarante et al.29 reported that 62% of heavy smokers (≥20 cigarettes/day) had complete root coverage in comparison to 42% of non-smokers in the non-membrane group, and 37.5% of heavy smokers (≥20 cigarettes per day) had complete root coverage in comparison to 16.7% of non-smokers in the membrane group. On the other hand, Hirsch et al.30 found similar root coverage rates in smokers and non-smokers.

Table 1

Studies evaluating the effects of smoking on mucogingival surgical interventions

StudyStudy design and durationSubjectsInterventions and patients treated per groupOutcomesResults
Tolmie et al.23 1991
  • Saw no adverse effects of cigarette smoking. They obtained 100% root coverage in 11 of 12 (92%) sites in smokers.

  • Their mean root coverage for smokers was 97.9%. However, no mention was made as to how much the patients smoked.

Harris24 1994Clinical study, 8 to 72 weeks follow-up (mean 23 weeks)74 Patients (69 male and 5 female)
Age 18–48 years 100 recession defects Miller’s Class I and II recessions
Double pedicle graft+ SCTG
  • Non-smokers

  • Light-smokers (≤10 cigarettes/day)

  • Heavy-smokers (≥10 cigarettes/day)

GRH
GRW
PD
KTW
RC
MRC
  • No difference between non-smokers, light-smokers (≤10 cigarettes/day), and heavy-smokers (≥10 cigarettes/day)

  • Complete root coverage obtained 89%

  • RC Non-smokers 97.6%

  • RC Light-smokers 96.6%

  • RC Heavy-smokers 98.5%

Trombelli et al.25 1997Retrospective study, 6 months duration22 Patients
Aged 23–40 years Miller’s class l and class ll recessions
Guided tissue regeneration with e-PTFE membrane
9 Smokers (>10 cigarettes/day at initial examination)
13 Non-smokers
PD
RD
CAL
GRH
KTW
MRC
CRC
ME (membrane exposure)
NFT (newly formed tissue)
  • Membrane exposure significantly greater in smokers

  • Newly formed tissue gain is not statistically different between groups

  • Smokers significantly less RD reduction (2.5 ± 1.2 mm vs 3.6 ± 1.1 mm) and root coverage (57% vs 78%)

  • Complete root coverage was observed in one smoker (11%) and five non-smokers (38%)

Müller et al.26 1998Clinical trial study, 12 months duration22 Patients
(4 patients dropped-out from smokers)
Aged 22–73 years 18 Patients 28 recession sites included Miller’s class l and class ll recessions
Connective tissue graft + envelope technique modification
3 Smokers
15 Non-smokers
PD
CAL
KTW
GRH
GRW
KTT
MRC
CRC
  • Attachment level alteration during the postoperative observation period was negatively influenced by the location of the recession in the maxilla and by cigarette smoking (R2=0.395, p<0.001)

Zuchelli et al.27 1998Randomized clinical trial, 12 months duration54 Subjects
(29 female and 25 male) Aged 23–33 years 54 recession defects Miller’s Class I and II recessions
Compare the clinical efficacy of 3 surgical approaches
GTR + bioabsorbable membrane
GTR + non-resorbable membrane CAF + SCTG
16 Patients were smokers (≥10 cigarettes/day)
PD
GRH
CAL
RC
  • Smoking decreases the expected coverage to 0.52 mm

Amarente et al.28 2000Controlled clinical trial, 6 months duration20 Patients, mean age 38.4 years
Bilateral Miller Class I and II recessions
Total 40 sites
Coronally positioned flap, alone or combined with bioabsorbable membrane
8 Smokers (≥20 cigarettes/day)
12 Non-smokers
PD
RCAL
GRH
GRW
KTW
RC
CRC
  • 62% of heavy smokers (≥20 cigarettes/day) had complete root coverage compared to 42% of non-smokers in the non-membrane group

  • 37.5% of heavy smokers (≥20 cigarettes/day) had complete root coverage compared to 16.7% of non-smokers in the membrane group

Hirsch et al.29 2001Clinical study, mean follow-up 32.68 months25 Patients
(17 male and 8 female)
Aged 23–48 years
Miller Class I and II recessions
44 recessions
Subepithelial connective tissue graft with coronally positioned flap
9 Non-smokers
16 Smokers
11 Patients less than 10 cigarettes/day
5 Patients 10–20 cigarettes/day
PD
CAL
GRH
GRW
RC
CRC
  • No significant differences in root coverage between smokers and non-smokers

Martins et al.30 2004Prospective clinical study, 6 months duration15 Patients
Aged 27–55 years
Miller’s Class l and ll recessions
18 recessions defects
Coronally positioned flap with subepithelial connective tissue graft
7 Smokers (20 cigarettes/day for >5 years)
8 Non-smokers
PD
CAL
GRH
KTT
RC
CRC
  • Lower RC in smokers 58.84 ± 13.68% vs non-smokers 74.73 ± 14.72%

  • Less CAL gain in smokers 2.00 ± 1.04 mm vs non-smokers 2.54 ± 0.79 mm

  • Deeper PD in smokers 2.35 ± 0.67 mm vs non-smokers 1.56 ± 0.53 mm

  • Post-op 4th month smokers presented more keratinized tissue 4.50 ± 1.16 mm vs 3.30 ± 0.86 mm p<0.05

  • Complete root coverage was observed in 35% of the non-smokers and apparently not in the smokers

Erley et al.31 2006A comparative clinical study, 6 months duration17 Patients
(16 male and 1 female)
Aged 27–45 years
Miller's class l and II recessions
22 recession defects
Connective tissue graft
Smokers (10–20 cigarettes/day and >10 ng/mL cotinine level)
Non-smokers (0–10 ng/mL cotinine level)
PD
RCAL
GRH
GRW
KTW
RC
CRC
Salivary cotinine
level
  • RD 6 months statistically significant larger for smokers than non-smokers (1.0 ± 0.85 mm and 0.20 ± 0.42 mm, respectively)

  • RC at 6 months was 82.33 ± 14.90% for smokers and 98.3 ± 4.42% for non-smokers. This was statistically significant (p=0.001)

  • Only 25% of smokers healed with complete root coverage compared to 80% of non-smokers

Silva et al.32 2006Prospective clinical trial, 6 months duration20 Patients
Aged 22–53 years
Miller’s class l recessions
Coronally positioned flap
10 Smokers (≥10 cigarettes/day at least for 5 years)
10 Non-smokers
PD
CAL
GRH
KTW
RC
CRC
  • Smokers presented greater residual RD at 6 months (0.84 ± 0.49 mm and 0.22 ± 0.29 mm, respectively) and lower percentage of root coverage (69.3% vs 91.3%, p<0.05)

  • No smokers obtained complete root coverage compared to 50% of non-smokers

Silva et al.33 2007Prospective controlled clinical trial, 24 months duration20 Patients
Aged 22–53 years
Miller's class l recessions
Coronally positioned flap
10 Smokers (>10 cigarettes/day at least for 5 years)
10 Non-smokers
PD
CAL
GRH
KTW
RC
CRC
  • RD significantly increased in smokers (from 0.84 ± 0.49 mm to 1.28 ± 0.58 mm) and in non-smokers (from 0.22 ± 0.29 mm to 0.50 ± 0.41 mm) between 6 and 24 months

  • 50% of smokers and 10% of non-smokers lost between 0.5 and 1.0 mm of root coverage in the same period

  • Smokers had significantly greater residual recession (p=0.001) at 24 months

  • Both smokers and non-smokers lost CAL and experienced decreases in KT

Souza et al.34 2008Controlled clinical trial, 6 months duration30 Patients
(20 male and 10 female)
Aged 24–47 years
Miller's class l and ll recessions
Subepithelial connective tissue graft with coronally positioned flap
15 Smokers (≥10 cigarettes/day)
15 Non-smokers
PD
RCAL
GRH
KTW
RC
CRC
  • Smokers had less root coverage than non-smokers (58.02 ± 19.75% versus 83.35 ± 18.53%, p<0.05)

  • Smokers had more GR (1.48 ± 0.79 mm vs 0.52 ± 0.60 mm) than the non-smokers (p<0.05)

  • Histomorphometry of the donor tissue revealed a blood vessel density of 49.01 ± 11.91 vessels/200x field for non-smokers and 36.53 ± 10.23 vessels/200x field for smokers (p<0.05)

  • CRC was 6.7% in smokers compared to 53.3% in non-smokers

Andia et al.35 2008A controlled clinical study, 24 months duration22 Patients
Aged 22–55 years
Miller's class l and ll recessions
Subepithelial connective tissue graft with coronally positioned flap
11 Smokers (>20 cigarettes/day for >5 years)
11 Non-smokers
PD
CAL
GRH
KTW
KTT
RC
CRC
  • At 24 months postoperatively, statistical analysis showed that smokers presented poorer outcomes regarding PD, GR, and CAL (p<0.05); in addition, a more satisfactory stabilization of the gingival tissue was found in the non-smoker group

  • RC after 2 years was 50% (1.8 mm, range of residual recession: to 2.6 mm) and 77.8% (2.8 mm; range of residual recession: to 1.8 mm) for smokers and non-smokers, respectively

  • CRC was found in 27% of the non-smokers, whereas none of the smokers presented CRC

Reino et al.36 2012A controlled clinical trial, 6 months duration20 Patients
(10 male and 10 female) Aged 35–50 years
Bilateral Miller’s class I recessions
40 gingival recessions
Subepithelial connective tissue graft with coronally positioned flap
One side Langer-Langer technique, One side Barros technique
All heavy smokers (≥20 cigarettes/day for >5 years)
PD
CAL
GRH
GRW
KTW
RC
CRC
Saliva cotinine
analysis
  • Both techniques promoted low root coverage (Control group: 43.18% and Test group: 44.52%)

  • No difference was found in root coverage between the techniques

  • CRC occurred in 2 cases at 6 months (5%)

Alves et al.37 2012Randomized, controlled, split mouth design, 6 months duration19 Patients (12 female and 7 male)
Aged 30–50 years
Bilateral Miller’s Class I and II recessions
38 gingival recessions
Acellular dermal matrix graft + Emdogain vs Acellular dermal matrix graft All smokers (consuming ≥10 cigarettes/day for >5 years)PD
RCAL
GRH
GRW
KTW
KTT
RC
CRC
  • The percentage of root coverage was 55.4% for the ADMG + EMD and 44.0% for the ADMG group

  • The ADMG + EMD group showed CRC in three gingival recessions, whereas the ADMG group showed in one gingival recession

  • Considering the number of sites with CRC, there was a statistical difference between the groups

Nanavati et al.38 2013Controlled clinical trial, 6 months duration20 Patients
(14 male and 6 female) Aged 22–53 years
Miller’s class l recessions
Coronally positioned flap
10 Smokers (≥10 cigarettes/day for >5years)
10 Non-smokers
PD
CAL
GRH
GRW
KTW
RC
CRC
  • No smokers obtained complete root coverage compared to 30% of non-smokers (p<0.05)

  • Smokers presented greater residual RD at 6 months and lower percentage of root coverage (60.09% vs 76.05%, p<0.05)

Jankovic et al.39 2013Controlled clinical trial, 3 years duration55 Patients
(29 male 26 female)
Aged 30–41 years
Miller’s Class I and II recessions
Subepithelial connective tissue graft with coronally positioned flap
30 Non-smokers
25 Smokers ( ≥20 cigarettes/day)
19 gen+ patients
36 gen- patients
GI
CAL
GRH
IL-1 genotype
RC
CRC
  • RC was similar in gen+ (92%) and gen- (93.2%) subjects within smoking and non-smoking groups after 1 year

  • For non-smokers, RC was obtained 75% in gen+ subjects and 88% for gen- subjects. Statistically significant difference detected

  • For non-smokers, CRC was for gen- 75%, gen+ 70% at 1 year After 3 years, these values decreased 55% and 30%, respectively

  • For smokers, RC was obtained 86% in gen+ subjects and 92% for gen- subjects. At 3 years, 57% root coverage for gen+ and 79% for gen- subjects obtained. Statistically significant difference detected

  • For smokers, CRC was for gen- 68.75%, gen+ 55.55% at 1 year. After 3 years, these values decreased 25% and 0%, respectively

  • In a 3-year period, non-smokers with IL-gen+ lost approx. 20% of the root coverage gained at 1 year and almost four times more inferior compared with gen- group

  • Patients who smoked and had a positive IL-1 gen+ lost approx. 35% of the gained root coverage. IL-1 polymorphism and smoking habit did not affect gingival recession at 1 year but had a great impact on long-term stability

  • Smokers who were presented with IL gen- and gen+ significantly increased risk for root coverage failure compared with non-smoking patients, 3 years after surgical treatment

Kaval et al.40 2014Controlled clinical trial, 6 months duration32 Patients
(11 male and 21 female)
Aged 18–52 years
Miller's class l and ll recessions
2 Patients dropped out from smoker group 36 defects 18 each
Coronally advanced flap (microsurgical)
15 Smokers (>10 cigarettes/day for
>5 years)
15 Non-smokers
PD
CAL
GRH
GRW
KTW
KTT
RA
RC
CRC
Cotinine level
GCF samples
  • CAL gain, percentage of root coverage and complete root coverage rates were similar in the study groups

  • RC at 6 months, 90.33 ± 17.84% smokers, 94.11 ± 12.00% non-smokers

  • CRC at 6 months, 66.70% smokers, 72.20% non-smokers not statistically different

Reino et al.41 2015A pilot comparative clinical study, 12 months duration20 Patients
Bilateral Miller’s class I and II gingival recessions
40 recession sites
CPF + SCTG vs EFT + SCTG
20 Smokers
PD
CAL
GRH
KTT
KTW
RC
CRC
Cotinine levels
  • Percentage of root coverage, CPF group 48.60% and EFT group 54.28%

Costa et al.42 2016The randomized clinical trial, 12 months duration19 Patients
Aged 30–50 years
Bilateral Miller’s class l and class ll recessions
38 recession sites
Extended flap technique with Acellular dermal matrix graft + Emdogain or Acellular dermal matrix graft alone
19 Smokers (≥10 cigarettes/day for >5 years)
PD
RCAL
GRH
GRW
KTT
KTW
RC
CRC
  • Percentage of root coverage, ADMG + EMD group 59.7% and ADMG group 52.8%

Dwarakanath et al.43 2016A pilot comparative clinical study, 6 months duration20 Patients
Aged 19–58 years
Miller’s class l and class ll recessions
Subepithelial connective tissue graft with coronally advanced flap
10 Non-smokers (≥5cigarettes/day for ≥5years)
10 Smokers
  • 7 Light smokers (5–10 cigarettes/day)

  • 3 Moderate smokers (10–20 cigarettes/day)

PD
CAL
GRH
GRW
KTW
RA
RC
CRC
  • 60% non-smokers and 30% smokers showed CRC

  • MRC was 71.2% in non-smokers and 38% in smokers

Romanos et al.44 2017Prospective case series, 12 months period18 Patients
Mean age 36.7 years
Multiple recessions with Miller’s Class I, II and III 133 recession sites
Modified coronally advanced tunnel flap+ Acellular dermal matrix graft
8 Smokers (>10 cigarettes/day for ≥5 years)
10 Non-smokers
RD
KTW
VAS pain
RC
CRC
  • RC, 82.0 ± 20.2% for smokers and 90.5% ± 16.2% for non-smokers

  • CRC, 48.1% for smokers and 70.9% for non-smokers

Saima et al.45 2019Controlled clinical trial, 6 months duration20 Patients
(14 male and 6 female)
Aged 22–53 years
Miller’s Class I recessions
Coronally positioned flap
10 Smokers (≥10 cigarettes/day ≥5 years)
10 Non-smokers
PD
CAL
GRH
RC
CRC
  • At 6 months, RD in the smoker group was significantly greater than the non-smoker group, when the average root coverage percentage was compared, smokers had a significantly lower percentage than non-smokers

  • The frequency of complete root coverage was significantly greater in the non-smoker group

  • In the smoker group average RC was 60%, while for nonsmokers was 76%

  • In the smoker group, CRC was 0%, while in the non-smoker group it was 30% at 6 months

Tawfik et al.46 2020Controlled clinical trial, 6 months duration22 Patients
Aged 20–35 years
Miller’s Class I and II gingival recessions
Free Gingival Graft
12-Non-smokers
10 Smokers (≥10 cigarettes/day)
PD
CAL
GRW
GRH
KTW
KTT
Graft shrinkage
  • The non-smokers group showed a significant decrease of recession width and graft shrinkage area compared to the smokers group. The clinical parameters showed improvement In the non-smoker group more than smoker group, but the difference was not statistically significant

[i] PD: probing depth. CAL: clinical attachment level. GRW: gingival recession width. GRH: gingival recession height. KTW: keratinized tissue width. KTT: keratinized tissue thickness. RC: root coverage. CRC: complete root coverage. RD: recession depth. RA: recession area. VAS: visual analog scale. ADMG: acellular dermal matrix graft. EMD: Emdogain®. EFT: extended flap technique. CPF: coronally positioned flap. SCTG: subepithelial connective tissue graft.

In time, complete coverage became the desired ultimate goal of root coverage interventions. Therefore, the effects of smoking on complete root coverage have been investigated in more recent studies. Martins et al.31 found less root coverage, less clinical attachment gain, and deeper probing depth values in the smokers in a 6-month follow-up clinical study. Furthermore, no complete root coverage was obtained in the smokers. Likewise, in another study32, the rate of root coverage was found to be lower in smoker patients. Moreover, the recession depths were statistically significantly larger in smokers than those in non-smokers. Silva et al.33,34 presented the 6- and 24-month results comparing root coverage in smokers and non-smokers using the coronally repositioned flap technique. In the 6 months results, the smoker patients presented greater residual recession depths and a lower rate of root coverage (69.3% versus 91.3%, p<0.05). Moreover, complete root coverage was obtained in none of the smoker patients compared to 50% of the non-smokers. According to the 24-month results of the study, recession depths significantly increased in both groups (in the smokers: from 0.84 ± 0.49 mm to 1.28 ± 0.58 mm; and in the non-smokers: from 0.22 ± 0.29 mm to 0.50 ± 0.41 mm) between follow-up at 6 and 24 months. Half of the smokers and 10% of the non-smokers exhibited between 0.5 and 1.0 mm of recurrence of gingival recession during this period35. Smokers had significantly greater residual recession (p=0.001) at 24 months. In another clinical study35, root coverage rates were less in the smokers than in the non-smokers (58.02 ± 19.75% versus 83.35 ± 18.53%, p=0.003) and complete root coverage was obtained in 6.7% of the recession defects in the smokers compared to 53.3% in the non-smokers. Accordingly, Andia et al.36 stated that smokers responded poorly to the root coverage intervention and complete root coverage was not obtained in the 24-month follow-up clinical study.

Instead of comparing smokers and non-smokers, Reino et al.37 compared subepithelial connective tissue grafts with a coronally positioned flap and used Langer-Langer technique on one side and Barros technique on the other side, in heavy smokers. Both techniques were found to be unsuccessful in this group of patients. Similarly, Alves et al.38 compared the possible benefits of enamel matrix derivative (Emdogain®) combined with acellular dermal matrix graft and only acellular dermal matrix graft application in smokers and reported that the clinical outcomes were slightly improved in the combination group. Complete root coverage was observed in three gingival recession defects in the combination group, whereas the acellular dermal matrix graft group showed complete root coverage only in one defect. Nanavati et al.39 compared the effects of smoking on coronally positioned flap outcomes and reported that no complete root coverage was obtained in the smokers, whereas 30% complete root coverage was detected in the non-smokers (p<0.05) and smokers revealed greater residual recession depth and lower percentage of root coverage (60.09% vs 76.05%, p<0.05) at 6 months follow-up.

Jankovic et al.40 investigated the effects of smoking and IL-1 genotype on root closure outcomes with a 1-year follow-up study. Root coverage rates were similar in genotype+ (92%) and genotype- (93.2%) individuals within the smoker and non-smoker groups. Patients who smoked and were positive for IL-1 genotype lost approximately 35% of the obtained root coverage. IL-1 polymorphism and smoking habit did not affect gingival recession at 1 year, but follow-up at 3 years revealed less stability in smokers. In another study41, the coronally repositioned flap was performed with microsurgical technique in smokers and non-smokers with Miller I - II gingival recessions. The smoking status of the patients was chemically validated by salivary cotinine levels. At 6 months evaluation, complete root coverage rate was 66.70% and 72.20% in smokers and non-smokers, respectively, without statistically significant difference.

On the other hand, Reino et al.42 included only smoker patients and compared the coronally positioned flap and extended flap technique with regard to clinical success and reported similar outcomes. Accordingly, possible benefits of enamel matrix derivative (Emdogain®) were investigated in a split-mouth study conducted only on smokers43. While the extended flap technique and acellular dermal matrix grafts were applied on one side, enamel matrix derivative was applied additionally on the other side. No significant difference was found between the two treatment approaches. The possible effects of smoking on root coverage surgery were investigated in another study and 60% of the non-smokers and 30% of the smokers showed complete root coverage44. Romanos et al.45 investigated the effects of smoking on the modified coronally advanced flap technique with a cellular dermal matrix graft procedure and reported rather low success rates in smokers compared to non-smokers with complete root coverage ratios of 48.1% and 70.9%, respectively.

Coronally advanced flap was used in another study comparing the clinical outcomes of root coverage between smoker and non-smoker patients46. At 6 months follow-up, gingival recession depth in the smoker group was significantly greater than in the non-smoker group with a significantly lower percentage of root coverage in smokers. The non-smoker group exhibited a significantly greater rate of complete root coverage. The mean root coverage rate was 60.09% in smokers and 76.05% in non-smokers. In another study47, using the free gingival graft procedure, significantly better outcomes were obtained in the non-smokers in terms of the decrease in recession width and graft shrinkage compared to the smokers.

CONCLUSION

Within the limits of the available studies and within the context of a non-systematic narrative literature review, it may be concluded that smoking adversely affects the clinical success of various surgical techniques used for root coverage. This fact may encourage smokers who are concerned about dental aesthetics to quit smoking along with non-surgical periodontal treatment.