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HomeHealth articlesperiodontal gum diseaseWhat Is Periodontal Disease and Chronic Obstructive Pulmonary Disease Association?

Periodontal Disease and Chronic Obstructive Pulmonary Disease- The Inflammatory Association

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5 min read


Lung infections caused by oral bacteria are linked to poor periodontal health and flares of COPD.

Medically reviewed by

Dr. Kaushal Bhavsar

Published At February 8, 2024
Reviewed AtFebruary 28, 2024


Periodontitis is an inflammatory condition marked by the overreaction of the inflammatory process, which leads to the destruction of the tooth-supporting tissues. A restriction in airflow is a key feature of the primary lung disease, chronic obstructive pulmonary disease (COPD).

There has been a rise in the potential link between COPD and chronic periodontitis. Since oral pathogens can potentially cause pneumonia directly, aspiration of these pathogens to the lung is the main contributing factor. The early buildup of dental plaque makes it easier for pulmonary pathogens to colonize the upper airways, and there are links between chronic periodontitis, a history of COPD, and deteriorating lung function.

It is reasonable to use periodontal treatment and prevention as therapeutic options to correct lung malfunction or, at the very least, to promote dedicated therapies for pulmonary diseases if periodontitis is causally linked to a decline in lung function. The shared risk factor may also explain the link between periodontitis and COPD.

What Is COPD?

Chronic obstructive pulmonary disease (COPD) ranks among the most prevalent and financially burdensome respiratory disorders. Chronic obstructive pulmonary disease (COPD) is distinguished by a gradual and permanent restriction of airflow, accompanied by the deterioration of lung tissue, resulting in emphysema and tissue remodeling, including fibrosis. These pathological changes collectively contribute to a subsequent decline in lung function and an elevated risk of mortality. Patients with chronic obstructive pulmonary disease (COPD) frequently have symptoms like dyspnea, cough, and sputum production, which can be attributed to the presence of a persistent airflow limitation. The presence of a direct anatomical connection between the lungs and the mouth cavity establishes the latter as a plausible reservoir for respiratory pathogens. The reduction of chronic obstructive pulmonary disease (COPD) exacerbation was observed following periodontal therapy.

What Is Periodontitis?

Periodontitis is a pathological condition characterized by an inflammatory response triggered by bacterial infections, leading to the progressive degradation of the tissues supporting the tooth. The condition is distinguished by the interplay between various anaerobic microorganisms, including Gram-negative bacteria, and the inflammatory response of the host, leading to the degradation of tissues and eventual tooth loss. Untreated periodontitis has been found to be linked with other systemic health issues, including cardiovascular disease, diabetes, and low birth weight. These diseases exhibit a high prevalence and are linked to a significant impact on human health.

What Is the Impact of Prolonged Inflammation?

Chronic neutrophilic inflammation, primarily caused by the action of enzymes produced from neutrophil granules, is a defining feature of COPD and chronic periodontitis. It is widely recognized that the sensitivity of the individual, as well as varied exposure to risky variables like cigarette smoking, play a role in the development of COPD. Additionally, some people experience mild, moderate, and severe illness development. 80 to 90 percent of COPD patients are either current or former smokers. A lesser extent of COPD cases have also been linked to work exposure and air pollution.

However, in the case of periodontitis, there is a combination of environmental and genetic variables that eventually result in the illness. The pathophysiological processes of COPD and periodontitis both include neutrophil aggregation and activation. Neutrophil granules' released substances harm the connective tissue.

The severity of the disorder, which is correlated with the amount of muscle atrophy and dysfunction, is thought to be determined by the levels of the inflammatory proteins C-reactive protein (CRP), interleukin-8 (IL-8), and tumor necrosis factor (TNF). Additionally connected to the onset of diabetes and coronary artery disease are these cytokines. Social and economic issues also affect morbidity and death.

The existence of anaerobic bacteria frequently brings on periodontitis-related inflammatory reactions. As a result, pro-inflammatory cytokines like CRP and TNF are noticeably increased. Chronic inflammation is linked to an increased risk of heart stroke, osteoporosis, diabetes mellitus, and rheumatoid arthritis in both COPD and periodontitis.

What Are the Risk Factors?

  • Smoking: Previous or ongoing smoking is a major risk factor for COPD. It is a known periodontitis risk. Tobacco use worsens periodontitis. Smoking is a major independent risk factor for periodontitis that affects the host’s immune-inflammatory response. Various research on smoking and IL-1β levels in saliva or GCF have conflicting results, with some indicating increased levels, others decreasing levels, and others no difference. Cigarette smoke damages the host and can induce chronic respiratory disorders like COPD and lung cancer. COPD is an incurable airflow blockage caused by emphysema, fibrosis, mucus hypersecretion, and opportunistic lower airway colonization.

  • BMI: A substantial correlation existed between BMI and periodontitis severity. Patients with diabetes, asthma, and respiratory symptoms, excluding chronic productive cough, had higher BMIs. In COPD patients, the mean BMI was marginally but significantly lower.

  • Inflammation Chronic: Microbial plaque and the host interact to cause multi-factorial periodontitis, which increases the host’s immune-inflammatory response. The mean PD and CAL increased with WBC level. In periodontal tissues and gingival crevicular fluid, cytokines and prostaglandins are significantly elevated. These mediators enter the systemic circulation and may stimulate the acute phase response in the liver.

Atherosclerosis in the endothelium would follow this response. In addition, gingival crevice bacteria can penetrate the systemic circulation and directly influence it. Local pro-inflammatory cytokines cause most alterations. Thus, these mediators in GCF, saliva, and serum may be diagnostic or predictive markers for periodontitis progression. GCF levels fall significantly after periodontitis treatment, but IL-1β is present in both gingival and untreated periodontitis. Systemic inflammation is increasingly linked to periodontitis, with serum C-reactive protein (CRP) levels decreasing after therapy. IL-6 stimulates osteoclast production, bone resorption, and T-cell differentiation, contributing to periodontitis. IL-8 stimulates neutrophil recruitment and activation, but its levels fluctuate throughout periodontal disease.

  • Sex: These associations usually include sex, but earlier, they mirrored smoking and working behaviors. However, female incidence has grown due to smoking, resulting in an increasingly even sex prevalence of the disease. Male sex greatly affected periodontal pocket depth.

  • The Colonization of Bacteria: The human pulmonary microbiota is well adapted to the host, and some human-restricted opportunistic diseases have co-evolved. Poor dental hygiene is linked to periodontitis, a prevalent oral infectious disease. The mouth cavity's humidity and warmth promote bacterial development. Periodontal bacteria can penetrate epithelial cells and enter the bloodstream through gingival disturbance, activating the inflammatory and immunological response in numerous ways. Epithelial cells can let periodontal bacteria into the circulation, infiltrate endothelial cells, cause dysfunction, and stimulate inflammatory and immunological responses.

Aspirating dental plaque, which can contain respiratory infections such as Staphylococcus aureus, Acinetobacter spp., and Candida albicans, can cause lung irritation. The immune system's reaction can cause, mature, and worsen atheromas. Oral microorganisms can induce lung infections, and severe PD causes pneumonia.

Inflammation within the periodontium causes subgingival plaque bacteria like anaerobic Gram-negative rods, which can worsen COPD. Aspirating dental plaque can cause lung irritation by including respiratory infections such as Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter spp., and Candida albicans. Aspiration of oral germs into the lung is the most prevalent way the mouth affects pulmonary function. Oral bacteria harm tiny airways when aspirated. Periodontitis may be connected to COPD by microbial species enabling respiratory pathogen colonization in tooth plaque or periodontal.

What Are the Various Antibiotic Treatments for the Condition?

Short-term flares of COPD cause increased cough, breathing difficulties, and purulent sputum. They accelerate lung function degradation, lower quality of life, and increase death. Besides severity, frequency also affects exacerbation management. Therapeutic methods vary on exacerbation severity. Mild exacerbations require additional bronchodilators, moderate ones require systemic corticosteroids and antibiotics, and severe ones necessitate hospitalization. Bacterial or viral infections cause 60 to 80 percent of exacerbations. Noninfectious exacerbations are less severe than infectious ones.

COPD and chronic periodontitis are neutrophilic, inflammatory diseases that cause connective tissue degeneration. The two disorders may be linked causally. Oral epithelial cells from colonized patients may attach better to respiratory infections. The trypsin treatment of non-colonized epithelial cells improved respiratory pathogen adherence. This shows mucosal modification increased bacterial adherence. Removing fibronectin from the epithelial cell surface by proteases may reveal respiratory pathogen adhesion receptors on the mucosal surface.

Poor hygiene may increase salivary hydrolytic enzymes. Enzymes may break down mucins to prevent them from binding to and clearing infections like Haemophilus influenzae. In secretions, oral bacteria may attach to the mucosal membrane and induce respiratory epithelial cells to release cytokines. Stimulated cells may release cytokines that attract inflammatory cells. These inflammatory cells emit hydrolytic enzymes that destroy epithelium, making it more susceptible to respiratory infections. Smoking, environmental pollutants, viral infections, and genetics may worsen pulmonary disease and poor oral health.


The occurrence of periodontal disease is considerably more prevalent in individuals with chronic obstructive pulmonary disease (COPD) in comparison to individuals without COPD who are of the same age and sex while also accounting for any confounding factors. In the cohort of individuals with chronic obstructive pulmonary disease (COPD), several factors were found to be correlated with a reduced probability of developing periodontal disease. These factors include advanced age, higher level of education, few dental visits, and possession of private dental insurance. It is imperative for dentists, particularly periodontists and physicians, to enhance their knowledge regarding patients with chronic obstructive pulmonary disease (COPD), particularly those who are younger and have mental difficulties, as these variables have been identified as potential risk factors for the development of periodontal disease.

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Dr. Kaushal Bhavsar
Dr. Kaushal Bhavsar

Pulmonology (Asthma Doctors)


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