Comprehensive Notes on Periodontitis

Periodontitis

Definition

• Periodontitis is an inflammatory disease affecting the supporting tissues of the teeth.
• It is caused by specific microorganisms or groups of microorganisms.
• Results in progressive destruction of the periodontal ligament and alveolar bone.
• Leads to increased probing depth formation and/or gingival recession.
• A key clinical feature distinguishing periodontitis from gingivitis is clinically detectable attachment loss.

Assessment

• Probing depth measurement alone is insufficient for assessing periodontitis.
• Clinical attachment loss (CAL) is usually assessed by adding the extent of gingival recession to the probing depth measurement.
• This estimates the total extent of tissue loss from the cementoenamel junction (CEJ) of the tooth.
• Attachment loss may progress continuously or in episodic bursts.

1999 AAP Classification

• Chronic periodontitis
• Aggressive periodontitis
• Periodontitis as a manifestation of systemic diseases

Chronic Periodontitis

• Most prevalent form of periodontitis.
• Characterized as a slowly progressing inflammatory disease, but with potential periods of rapid destruction.
• Most prevalent in adults.
• Associated with chronic plaque and calculus formation.
• Can be modified by systemic factors.
• May be associated with severe systemic diseases like cardiovascular disease, stroke, and diabetes mellitus.
• Diagnosed by assessing clinical attachment level and detecting inflammatory changes in the marginal gingiva.
• Measurements of probing pocket depth, along with the location of the marginal gingiva, aid in determining clinical attachment loss.
• Dental radiographs reveal the extent of bone loss.
• Can be difficult to differentiate from aggressive periodontitis during initial evaluation.

Forms of Localized Periodontitis

• Localized: <30% of teeth involved.
• Generalized: >30% of teeth involved.
• Mild: 1 to 2 mm CAL.
• Moderate: 3 to 4 mm CAL.
• Severe: $≥5$ mm CAL.

Comparison with Gingivitis

• Gingivitis:
  • Inflammation of the gingiva without attachment/bone loss.
  • Reversible.
  • Not all sites with gingivitis progress to periodontitis.
  • Dental implant counterpart is peri-implant mucositis.
• Chronic Periodontitis:
  • Inflammation of periodontal apparatus with attachment/bone loss.
  • Irreversible.
  • All patients with chronic periodontitis must have experienced prior gingivitis.
  • Dental implant counterpart is peri-implantitis.

Consequences

• Untreated chronic periodontitis can lead to tooth loss and may negatively impact distant organs.

Symptoms

• Generally pain-free.
• Gingival bleeding.
• Purulence.
• Black triangles between teeth.
• Tooth sensitivity.
• Food impaction.
• Halitosis.
• Fanned out or elongated teeth.

Disease Progression

• May develop at any time in life.
• First clinical signs of inflammation may occur during adolescence.
• Progression rate is generally slow.
• Disease progression is more rapid at interproximal sites.

Models of Disease Progression

• Continuous Model:
  • Sites exhibit a constant progression rate of attachment loss throughout the duration of the disease.
• Random or Episodic-Burst Model:
  • Episodic occurrence of short progressive bursts of periodontal destruction followed by periods of stagnation.
  • Sites, teeth, and the chronology of bursts and stagnation are subject to random effects.
• Asynchronous, Multiple-Burst Model:
  • Occurrence of periodontal destruction (bursts) during defined periods, which are asynchronously interrupted by periods of stagnation or remission for individual sites and teeth.

Microbiologic Aspect

• Gram-negative organisms (red complex):
  • Porphyromonas gingivalis
  • Tannerella forsythia
  • Treponema denticola (red complex bacteria)

Aggressive Periodontitis

Features

1. Rapid loss of attachment and tooth-supporting bone.
   • Requires evaluation of clinical or radiographic data from earlier points in time to estimate the start of disease.
   • Patient age is not the primary criterion for diagnosis.
2. Subject is otherwise healthy.
   • Not suffering from any systemic disease or condition that could be responsible for the periodontitis.
   • Differentiated from “periodontitis as a manifestation of systemic disease”.
3. Familiar aggregation.
   • Determined through medical/dental history questionnaires and interviewing the patient.
   • Verification of similar cases in the family is advisable.

Localized Aggressive Periodontitis (LAP)

• Circumpubertal onset of disease.
• Localized to first molars or incisors with proximal attachment loss on at least two permanent teeth, one of which is a first molar.
• Robust serum antibody response to infecting agents.

Generalized Aggressive Periodontitis (GAP)

• Usually affects persons under 30 years of age but may occur in older individuals.
• Generalized proximal attachment loss affecting at least three teeth other than first molars and incisors.
• Pronounced episodic nature of periodontal destruction.
• Poor serum antibody response to infecting agents.

Common but Not Universal Features

• Amount of microbial deposits inconsistent with disease severity.
• Increased levels of Actinobacillus actinomycetemcomitans.
• Abnormalities in phagocyte function.
• Hyper-responsive macrophages, producing increased prostaglandin $E2$ ($PGE2$) and interleukin-$1β$ ($IL-1β$).
• In some cases, self-arresting disease progression.

Key Characteristics

• Inconsistency of the low amounts of present etiologic factors and the observed pronounced tissue destruction.
• Strong colonization by Aggregatibacter actinomycetemcomitans and, in some populations, Porphyromonas gingivalis.
• Immunologic differences that do not entail the diagnosis “periodontitis as a manifestation of systemic disease”:
  • Hyperresponsive macrophages
  • Abnormalities of neutrophil function
• Self-limiting disease

Gingival Responses in GAP

• Severe, acutely inflamed tissue, often proliferating, ulcerated, and fiery red. Bleeding may occur spontaneously or with slight stimulation. Suppuration may be an important feature (destructive stage).
• Pink, free of inflammation, and occasionally with some degree of stippling, although it may be absent. Deep pockets can be demonstrated by probing despite the mild clinical appearance.

Localized Aggressive Periodontitis (LAP) specifics

• Characterized by more pronounced systemic antibody titers against periodontal pathogens than found in GAP patients.
• Could indicate that in individuals susceptible to disease, but with the ability to enact a robust response against pathogens, the disease might be limited in extent.
• A.A. causally linked to LAP development in adolescents.

Periodontitis as a Manifestation of Systemic Disease

Major Effects

• Through alterations in immune response, such as in the case of interleukin-17 over expression in leukocyte adhesion deficiency, or due to tissue metabolic disorders (e.g., Ehlers-Danlos syndrome).

General Points

• Appears at an early age.
• Diagnosis used when the systemic condition is the major predisposing factor.
• Local factors (e.g., plaque and calculus) are not clearly evident or, if present, do not justify the severity/progression of disease.
• Reserved for a specific group of diseases and syndromes.

Treatment Considerations

• Removal of local factors as part of conventional periodontal therapy is often inadequate to arrest the periodontal destruction.
• When periodontal destruction clearly results from local factors but has been exacerbated by the onset of conditions such as diabetes mellitus or HIV infection, the diagnosis should be chronic periodontitis modified by the systemic condition.

Systemic Diseases Associated with Periodontitis

1. Hematologic disorders
   • Acquired neutropenia
   • Leukemias
   • Other
2. Genetic disorders
   • Familial and cyclic neutropenia
   • Down syndrome
   • Leukocyte adhesion deficiency syndromes
   • Papillon-Lefèvre syndrome
   • Chédiak-Higashi syndrome
   • Histiocytosis syndromes
   • Glycogen storage disease
   • Infantile genetic agranulocytosis
   • Cohen syndrome
   • Ehlers-Danlos syndrome (types IV and VIII autosomal dominant [AD])
   • Hypophosphatasia
   • Other
3. Not otherwise specified

Papillon-Lefèvre Syndrome

• Severe periodontitis.
• Diffuse keratoderma on the palms, soles, or knees.
• Impaired neutrophil function is considered the primary cause, leading to deregulation of the polymorphonuclear leukocyte response to microbial infection.
• By 4 to 5 years, the primary teeth have typically exfoliated or been extracted.
• Successful treatment requires eradication of AA.
• Treatment includes frequent prophylaxis appointments.

Necrotizing Ulcerative Periodontitis (NUP)

• May be an extension of necrotizing ulcerative gingivitis (NUG), or NUP and NUG may be different diseases.
• More cases described among immunocompromised patients, especially those who were human immunodeficiency virus (HIV) positive or who had acquired immunodeficiency syndrome (AIDS).
• Idiopathic etiology, but fusiform-spirochete bacterial flora appears to play a key role.

Clinical Features

• Necrosis and ulceration of the coronal portion of the interdental papillae and gingival margin.
• Painful, bright-red marginal gingiva that bleeds easily.
• Deep interdental osseous craters.
• Periodontal pockets with deep probing depth are not found.

Periodontitis and HIV/AIDS

• Linear gingival erythema, NUG, and NUP are the most common HIV-associated periodontal conditions.
• Periodontal attachment and bone loss associated with NUP in an HIV-positive patient may be extremely rapid.
• Clinicians should check all patients who present with NUP to ascertain their HIV status.
• Treatment: local debridement, local antiplaque agents, and systemic antibiotics.

Periodontitis and Diabetes Mellitus (DM)

• Periodontitis is considered the 6th complication of DM.
• Patients with diabetes mellitus exhibit a higher risk to develop periodontitis.
• Periodontal infection/inflammation may negatively interfere with the glycemic control of the diabetic patient.
• Average pocket depth, as well as clinical attachment loss, is increased in patients with diabetes mellitus.

Periodontitis and Smoking

• Smoking is a major risk factor; risk increases drastically with $≥10$ cigarettes per day.

Features Found in Smokers

• Increased periodontal pocket depth with more than 3 mm.
• Increased attachment loss.
• More recessions.
• Increased loss of alveolar bone.
• Increased tooth loss.
• Fewer signs of gingivitis (less bleeding upon probing).
• A greater incidence of furcation involvement.

Treatment

• Systematic periodontal therapy includes:
  • Optimal long-term plaque control.
  • Debridement of soft and hard deposits.
  • Surgical pocket reduction (resective osseous surgery or regenerative surgery, case-dependent).
• Patient should be remotivated, reinstructed, and retreated (if necessary) during a systematic supportive periodontal therapy regimen.

Chronic Periodontitis - Questions & Answers

• Q1: Which type of nonsurgical periodontal therapy is most effective in reducing periodontal probing depths and gaining clinical attachment level in patients with chronic periodontitis?
  • A: All of the above (Quadrant-wise scaling and root planing, Full-mouth scaling, Full-mouth disinfection)
• Q2: Does the adjunctive administration of systemic antibiotics provide added benefit for reducing periodontal probing depth in smokers with generalized chronic periodontitis, in addition to nonsurgical periodontal therapy?
  • A: Yes
• Q3: Does the risk for chronic periodontitis change in patients who quit smoking compared to patients who continue to smoke?
  • A: The risk lowers continuously, and 11 years after smoking cessation, the risk is comparable to a never-smoker.

Case Study

• Chief Complaint: "My gum is bleeding so much."

• Background: nonsmoker suffering from type 2 diabetes mellitus. Hemoglobin A1c parameter has ranged from 8.5% to 9.3% within the past 10 years. He takes 500 mg metformin three times a day. Furthermore, he reports a high normal blood pressure and is not taking antihypertensive medications. The patient reports brushing his teeth twice a day and not using interdental cleaning aids.

• Current Findings: Probing depths were in the range of 4 to 7 mm, bleeding on probing was 72%, poor oral hygiene.

• Q1: What percentage change of glycated hemoglobin (HbA1c as a percentage) can be expected 3 months after nonsurgical periodontal therapy in patients with diabetes mellitus and chronic periodontitis?

  • A: Approximately 0.5%

• Q2: Does locally administered antibiotics in combination with nonsurgical periodontal therapy lead to improvements of periodontal pocket depths in patients with chronic periodontitis and diabetes?

  • A: Yes, independent of the glycemic control, there will be an improvement in periodontal probing depths.

• Q3: Do diabetic patients with chronic periodontitis benefit from adjunctive systemic antibiotics?

  • A: Yes