Edit · Periodontal Disease and Smoking: Key Concepts and Effects

Calculus crystal forms — Brushite

Newly formed calculus deposit

Calculus crystal forms — Octacalcium phosphate

Primary form in deposits less than 6 months old

Calculus crystal forms — Hydroxyapatite

Primary form in deposits older than 6 months

Pellicle

Thin, bacteria-free membrane of glycoprotein that forms on the tooth surface during late stages of eruption

Pellicle attachment

Most common mode of calculus attachment on enamel

Calculus attached by pellicle

Deposits are more easily removed by toothbrushing because they are not embedded in the tooth

Smoking and periodontitis risk

Smoking is a very strong risk factor for periodontitis, associated with about 2-3× greater risk

Smoking affects periodontal health

Smoking changes the oral microbiome, immune response, blood flow, wound healing, and bone metabolism

Smoking and periodontal destruction

Smokers have greater periodontal destruction than former and never smokers

Smoking risk

Periodontal risk from smoking is dose-dependent and duration-dependent

Smoking and tooth loss

Smoking is strongly correlated with higher rates of tooth loss due to periodontal disease

Pack-year formula

Pack-years = packs smoked per day × years smoked

1.5 packs/day for 20 years

30 pack-years

Higher pack-years

Associated with increased periodontal destruction, greater attachment loss, more alveolar bone loss, higher risk of tooth loss, and poorer treatment outcomes

Smoking as a periodontal risk factor

Smoking is recognized as a major risk factor for periodontal and peri-implant diseases

Smoking and periodontitis progression

Smoking increases the rate of progression of periodontitis

Smoking and periodontal treatment

Smoking alters responsiveness to standard periodontal therapeutic practices

Smoking and periodontal pathogens

Smoking is associated with increased colonization by Porphyromonas gingivalis, Treponema, and other pathogens

Smoking and beneficial bacteria

Smoking can deplete beneficial bacteria and increase pathogenic bacteria, increasing virulence

Smoking and oxygen

Smoking lowers oxygen tension in periodontal pockets

Low oxygen in periodontal pockets

Creates an environment favorable to anaerobic bacteria

Innate immunity

First line of defense; does not require prior exposure; includes neutrophils and macrophages

Adaptive immunity

Second line of defense; learns from previous exposures; uses B lymphocytes, T lymphocytes, and antibodies

Cytokines

Chemical messengers that allow immune cells to communicate

Smoking and blood flow

Nicotine causes vasoconstriction, resulting in less oxygen, fewer nutrients, fewer immune cells, and slower healing

Smoking and neutrophils

Smoking impairs neutrophil function even though neutrophils may be present in higher amounts

Neutrophils

Most abundant white blood cell and essential for controlling bacteria

Smoking and IgG2

Smoking decreases IgG2 antibody production

Smoking and alveolar bone

Smoking is associated with greater alveolar bone destruction

Nicotine and osteoblasts

Nicotine suppresses osteoblasts

Smoking and IL-6/TNF-α

Nicotine can increase secretion of IL-6 and TNF-α in osteoblasts

Smoking and MMPs

Nicotine can increase release of matrix metalloproteinases involved in bone remodeling

Nicotinic stomatitis

Affects the palate and is caused by regular exposure to heat and smoke

Nicotinic stomatitis appearance

Dry, thickened, irritated palate with white/gray patches, tiny red dots, and a rough/cracked appearance

Environmental tobacco smoke (ETS)

Secondhand smoke

ETS and periodontitis

ETS increases the risk for periodontitis in nonsmokers

High ETS exposure

High exposure to environmental tobacco smoke can double the odds of periodontitis compared with negligible exposure

Waterpipe/hookah

Contains significant nicotine and carcinogens and has a periodontal impact similar to cigarette smoking

Smokeless tobacco

Associated with oral carcinoma and white oral mucosal lesions

E-cigarettes/ENDS

Highly addictive, contain known toxins, may increase periodontal disease risk, and long-term effects remain unclear

Smoking and periodontal therapy

Smokers show poorer responses to periodontal therapy than nonsmokers

Smoking and probing depth treatment outcome

Smokers show less reduction in probing depth after periodontal treatment

Smoking and attachment gain

Smokers show less clinical attachment gain after treatment

Smoking and wound healing

Cigarette smoke chemicals may delay wound healing by impairing normal repair functions

Smoking and fibroblasts

Acrolein and acetaldehyde may inhibit gingival fibroblast attachment and proliferation

Smoking and collagen

Smoking can result in less extracellular matrix and collagen and more collagenase

Smoking and bleeding on probing

Smokers often have less bleeding on probing because nicotine causes vasoconstriction

Less bleeding in smokers

Does NOT mean healthier periodontal tissues; reduced blood flow can mask inflammation

Smoking — 3 big periodontal effects

Creates a more pathogenic biofilm; weakens/disrupts immune defenses; accelerates bone destruction

Cannabis and nicotine

Cannabis does not contain nicotine

Cannabis and periodontal disease

Cannabis may be an independent risk factor for periodontal disease

Cannabis and periodontitis

Frequent recreational cannabis use is associated with deeper probing depths, more clinical attachment loss, and higher odds of severe periodontitis

Cannabis oral effects

Associated with gingival enlargement, erythroplakia, chronic inflammation, hyperkeratosis, and leukoplakia

Cannabis smoking

Associated with periodontal disease, xerostomia, leukoplakia, and oral cancer

Cannabis edibles

No direct heat/smoke exposure, but high sugar content can increase caries risk, plaque accumulation, and inflammation

Cannabis in any form

Causes xerostomia

Smoking and dental implants

Smoking increases risk of impaired healing and implant failure

Smoking and osseointegration

Smoking disrupts osseointegration through decreased blood flow and oxygen delivery

Peri-implant disease risk factors

Poor plaque control, history of periodontitis, diabetes, and smoking

Smoking cessation

Former smokers have better periodontal treatment outcomes than current smokers and outcomes similar to never smokers

Smoking cessation benefits

Can reduce pathogenic subgingival bacteria, improve gingival vascular circulation, and improve the host inflammatory response

Smoking cessation counseling

The AAP strongly recommends including tobacco cessation counseling as part of periodontal therapy