Periodontal diseases refer to conditions affecting the tooth-supporting structures (periodontal tissues), which are mainly categorized into two types: gingival diseases that only involve the gingival tissue, and periodontitis that affects the deeper periodontal tissues (periodontal ligament, alveolar bone, and cementum). As common oral diseases, periodontal diseases are one of the primary causes of tooth loss in adults and also pose a major threat to both dental health and overall human health.
The early symptoms of periodontal diseases are often overlooked, leading to long-term chronic infection of the periodontal tissues and recurrent inflammation. This not only impairs the function of the oral masticatory system but also seriously affects overall health.
Currently, there are multiple classification methods for periodontal diseases, with the main types including gingivitis, periodontitis, periodontal trauma, juvenile periodontitis, and periodontal atrophy.
It is an inflammatory lesion confined to the gingival tissue, typically not involving the deeper periodontal structures.
The most common type of periodontal disease, its main manifestations include redness and bleeding of the gums, formation of periodontal pockets, pus discharge from periodontal pockets, tooth mobility, gingival recession, and periodontal abscesses. The key pathological feature of periodontitis is the formation of pathological periodontal pockets.
A condition where the periodontal supporting tissues are damaged due to excessive occlusal force or abnormal direction of force that exceeds the load-bearing capacity of the periodontal tissues. It progresses slowly and usually has no obvious symptoms; sometimes, patients may experience weakness during chewing, or occasional dull or vague pain.
A chronic degenerative lesion involving the periodontal tissues of multiple teeth. It is characterized by onset in relatively young patients, rapid progression of the lesion—leading to tooth mobility, displacement, and periodontal pocket formation even in the early stage—followed by secondary infection. Genetic factors may be involved in its pathogenesis.
A degenerative lesion mainly involving the recession of the gingiva and alveolar bone tissue. Its manifestations include gingival recession and exposure of the tooth neck or root. The main causes of periodontal atrophy are: pressure on the gingiva from tartar at the tooth neck; long-term disuse of the affected tooth or systemic factors; mechanical irritation from incorrect toothbrushing methods; and pressure on the gingiva from dental restorations.
The main clinical manifestations include gingival inflammation, gingival bleeding, periodontal pocket formation, alveolar bone resorption, reduction in alveolar bone height, tooth mobility, tooth displacement, and chewing weakness. In severe cases, teeth may fall out spontaneously or require extraction.
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Concurrent symptoms such as pain, pus discharge, and halitosis (bad breath) may occur.
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Local complications: Periodontal abscesses, tooth mobility, etc. Systemic impacts are generally minor. Some scholars suggest a potential association with certain rheumatic diseases.
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Chronic inflammation progresses with recurrent episodes. Clinically, it is mainly characterized by alveolar bone resorption and tooth mobility, which gradually leads to occlusal trauma and tooth displacement, eventually resulting in tooth loss. The remaining teeth have poor supporting capacity, making restorative treatment difficult.
In addition to plaque microorganisms, several local factors promote the occurrence and progression of periodontal diseases, including tartar, traumatic occlusion, food impaction, bad habits, defective restorations, and malocclusion.
Tartar refers to calcified or calcifying plaque and deposits that accumulate on the tooth surface or the surface of dental restorations. It can be classified into supragingival tartar (above the gingival margin) and subgingival tartar (below the gingival margin) based on its location.
Tartar has a close relationship with periodontal diseases:
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It provides an ideal surface for plaque adhesion and reduces the effectiveness of daily oral hygiene practices, promoting further plaque formation.
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Plaque and hard, rough tartar irritate the gingiva; tartar also easily absorbs bacterial toxins, increasing irritation to the gingiva and causing gingivitis.
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Subgingival tartar can deepen periodontal pockets, which in turn provide a specific environment for plaque accumulation and supply minerals for tartar deposition, further promoting plaque mineralization.
Thus, tartar is a key promoting factor for periodontal diseases.
Food impaction occurs when food particles or fibers are wedged into the interdental space between two adjacent teeth by occlusal pressure during chewing. It can be divided into vertical food impaction and horizontal food impaction based on the direction of impaction.
Food impaction is one of the most common causes of localized periodontal tissue destruction. Due to the mechanical effect of impaction and bacterial colonization, it not only causes inflammation of the periodontal tissues but also leads to gingival recession, interproximal caries, alveolar bone resorption, and halitosis.
The health of periodontal tissues depends on the functional stimulation of normal occlusal force. When occlusal force exceeds the bearing capacity of the periodontal tissues, damage to the periodontal tissues (i.e., occlusal trauma or periodontal trauma) occurs. The occlusal state causing such trauma is called traumatic occlusion, which can result from premature tooth contact, excessively high restorations, bruxism (teeth grinding), or improper force application during orthodontic treatment.
Bad habits are important promoting factors in the occurrence and progression of periodontal diseases:
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Bruxism (teeth grinding) and clenching can exacerbate periodontal tissue destruction.
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Other oral bad habits, such as biting hard objects, mouth breathing, tongue thrusting, unilateral chewing, and incorrect toothbrushing, can affect the lips, cheeks, teeth, and periodontal ligament, leading to damage to the periodontal tissues.
Poorly designed or improperly placed restorations not only directly compress and irritate the gingival tissue but also are difficult to clean. This leads to the accumulation of food debris and plaque, causing inflammation of the periodontal tissues.
Abnormal tooth position or malocclusion can create areas that are difficult to clean, promoting plaque and tartar accumulation and increasing the risk of periodontal diseases.
Systemic factors act as risk factors for periodontal diseases by reducing or altering the resistance of periodontal tissues to external pathogenic factors, increasing the host’s susceptibility to bacteria and their products, and promoting the occurrence and progression of periodontal diseases.
Smoking is one of the most important risk factors for periodontal diseases. Numerous studies have confirmed a close association between smoking and the occurrence and progression of periodontal diseases. It is generally believed that smoking affects local blood circulation, impairs humoral immunity, cellular immunity, and inflammatory processes—particularly weakening the chemotaxis and phagocytic function of oral neutrophils.
The effects of smoking on periodontal tissues are multifaceted:
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Smoke and heat from burning cigarettes act as specific local irritants to the gingiva, causing chronic gingival inflammation.
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Tar deposits on the tooth surface of smokers promote tartar accumulation and accelerate plaque formation; smokers often have poorer oral hygiene, leading to higher prevalence of gingivitis and periodontitis compared to non-smokers.
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Smokers experience more alveolar bone resorption than non-smokers.
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Smoking-induced immunological changes reduce the periodontal tissues’ resistance to infection.
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Smoking inhibits the growth of fibroblasts and their adhesion to the root surface, impairing the healing of periodontal wounds.
Extensive research on the relationship between smoking and periodontal diseases has shown that smoking pattern and quantity affect gingival health, periodontal tissue loss, and the severity of periodontitis. Cross-sectional studies indicate that the prevalence, extent, and severity of periodontal diseases are significantly higher in smokers than in non-smokers. For example, a study found that young adults aged 20–33 who smoke have a significantly higher relative risk (OR = 14) of developing severe periodontal attachment loss and deep periodontal pockets compared to non-smokers. A similar relationship has been observed in the elderly population. A dose-response relationship exists between smoking and the severity of periodontal diseases: heavier daily smokers have more severe periodontal diseases than lighter smokers, and smoking duration is significantly associated with tooth loss and periodontal diseases—independent of other social and behavioral risk factors.
The destructive inflammatory process of periodontal diseases is interconnected with diabetes. Epidemiological surveys confirm that both type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes—especially long-term diabetes—are significant risk factors for periodontal diseases. A longitudinal study showed that patients with non-insulin-dependent diabetes have a 3.2-fold higher risk of developing periodontal diseases than non-diabetic patients, while patients with insulin-dependent diabetes have an increased risk of destructive periodontal diseases. A survey by the U.S. National Institute of Dental Research (NIDR) in the Pima Indian population found that patients with non-insulin-dependent diabetes are 15 times more likely to become edentulous (toothless) due to alveolar bone resorption than non-diabetic patients.
Existing evidence suggests that a history of chronic periodontal disease can affect diabetes control. Epidemiological and biological studies have concluded that enhanced glycosylation in diabetic patients leads to the deposition of macromolecules in tissues, causing thickening of the walls and basement membranes of small blood vessels, narrowing of lumens, dysfunction of polymorphonuclear leukocytes, and abnormalities in collagen synthesis, bone matrix production, and inflammatory mediator release—all of which exacerbate the progression of periodontitis. Thus, diabetes is not only a risk factor for periodontal diseases but also has a bidirectional interaction with them.
Oral hygiene behavior directly affects oral hygiene status, which is closely related to the health of periodontal tissues. A strong positive correlation exists between the amount of plaque/tartar and periodontal diseases.
In 1965, Löe et al. conducted a study on experimental gingivitis: 12 healthy subjects stopped brushing and other oral hygiene practices. A few developed gingivitis after 10 days, and most developed gingivitis after 15–21 days. After receiving detailed guidance and resuming toothbrushing and toothpick use, their gingival tissue became healthier than before the experiment. This classic study demonstrated that discontinuing toothbrushing can lead to gingivitis.
Socio-demographic risk factors refer to the impact of factors such as age, gender, education level, and socioeconomic status on the prevalence of periodontal diseases.
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Age: The strongest correlation with periodontal health. Epidemiologically, the severity of periodontal diseases is positively correlated with age: simple gingivitis mainly occurs in children and adolescents, while periodontitis is more common in middle-aged and elderly individuals.
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Gender: Males tend to have more severe periodontal diseases than females.
Risk factors for periodontal diseases are generally divided into two categories:
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Innate risk factors: Include ethnicity, gender, genetic factors, congenital immunodeficiency, defective phagocytic function, and Down syndrome.
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Acquired and environmental risk factors: Include poor oral hygiene, age, medication use (e.g., phenytoin and non-steroidal anti-inflammatory drugs), smoking, acquired immunodeficiency, acquired endocrine diseases (e.g., diabetes), stress, and nutritional deficiencies.
Both innate and acquired/environmental risk factors determine the occurrence, progression, and response to treatment of periodontal diseases. In recent years, the impact of oral health on overall health has received widespread attention, and it has been confirmed that untreated moderate to severe periodontal diseases are harmful to systemic health. Sufficient evidence shows that periodontitis increases the risk of coronary heart disease, adverse pregnancy outcomes (e.g., preterm birth and low birth weight infants), and diabetes.
The prevention of periodontal diseases is of great importance, with the main goal of eliminating the initiating pathogenic factors and risk factors that promote disease progression.
Prevention of periodontal diseases should focus on the following aspects:
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Based on health education, enhance public awareness of periodontal disease prevention and improve individuals’ ability to maintain oral self-care and periodontal health.
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Develop good oral hygiene habits to remove pathogenic microorganisms and protect periodontal supporting tissues from damage.
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Improve the host’s defense capacity and maintain a healthy physical and mental state.
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Maintain the efficacy of periodontal treatment.
Practice has shown that combining daily self-plaque control with regular professional oral health care is the most effective way to prevent the occurrence and control the progression of periodontal diseases.
According to the natural course of periodontal diseases, their prevention can be divided into three levels:
Also known as "primary prevention," it refers to eliminating pathogenic factors before they invade the periodontal tissues, or removing them immediately after invasion but before they cause damage to the periodontal tissues. The aim is to reduce the incidence of new cases of periodontal diseases in the population. It mainly involves oral health education and guidance for the general public, ultimately achieving the goal of removing plaque and other irritants. It also helps people develop good oral hygiene habits (e.g., mastering correct toothbrushing methods), improves the host’s disease resistance, and ensures regular oral health care to maintain oral health. Primary prevention includes all interventions targeting the causes of periodontal diseases.
Aims for early detection, early diagnosis, and early treatment to reduce the severity of existing periodontal diseases and control their progression. For lesions confined to the gingiva, scaling (removal of plaque and tartar) is performed promptly to prevent further development. Regular X-ray examinations are used to monitor alveolar bone conditions, and appropriate treatment is provided based on specific conditions to improve the health of periodontal tissues. The effectiveness of secondary prevention is built on the foundation of primary prevention, and its long-term efficacy depends on the patient’s long-term adherence to preventive measures.
Involves treatment measures for severe and advanced periodontal diseases, as well as tooth restoration to rebuild function. It also includes follow-up care and oral health maintenance to sustain treatment efficacy and prevent recurrence. Additionally, systemic diseases (e.g., diabetes) should be treated to enhance the resistance of periodontal tissues.
In summary, the prevention of periodontal diseases requires combining health education with specific preventive measures, and its effectiveness largely depends on the patient’s adherence to and correct implementation of home care measures.
Plaque is the main irritant of periodontal diseases and re-forms on the tooth surface within hours after removal. Therefore, consistent and effective daily plaque removal is essential to prevent the occurrence and recurrence of periodontal diseases. For patients with existing periodontal diseases, in addition to thorough removal of plaque and tartar from the tooth surface during treatment, mastering self-plaque control methods is crucial to ensure the smooth progress of periodontal treatment, maintain efficacy, and prevent recurrence.
To achieve effective plaque control, it is necessary to master clinical methods for plaque assessment. This helps identify areas of poor tooth surface cleanliness, evaluate the degree of plaque control, ensure thorough plaque removal, and accurately assess the effectiveness of plaque control.
Plaque is a colorless, soft substance adhering to the tooth surface, making it difficult to identify with the naked eye. Plaque disclosing agents (dyes) can be used to stain plaque, making it visible. These agents are available in two forms: solutions and tablets.
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Liquid disclosing agents: A small cotton ball dipped in the agent is applied to the tooth surface. After 1 minute, the patient rinses their mouth. The agent is washed away from areas without plaque but remains and stains areas with plaque.
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Tablet disclosing agents: The patient chews the tablet for 1 minute (moving it between the left and right sides of the mouth), then uses their tongue to spread the agent to the buccal and lingual surfaces of the teeth. After rinsing, plaque is stained and visible.
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2% Basic Fuchsin: Composition: 1.5g basic fuchsin, 25ml ethanol. For rinsing, a 1% aqueous solution is used.
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2%–5% Erythrosine Tablets: 15mg per tablet.
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Tartrazine: Mixed with patent blue at an 85:15 ratio, then prepared into a 4% aqueous solution for local application.
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1.0%–2.5% Malachite Green.
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Fluorescein Sodium: Under a special blue light, plaque appears yellow; no color is visible under natural light.
Note: Some individuals may be allergic to certain components in disclosing agents. Therefore, a detailed allergy history should be obtained before use.
