Flossing Technique

Flossing is an essential part of oral hygiene that helps remove plaque and food particles from between the teeth and along the gumline, areas that toothbrushes may not effectively clean. Proper flossing technique is crucial for maintaining gum health and preventing cavities.

Flossing Technique

1. Preparation:

   • Length of Floss: Take 12 to 18 inches of dental floss. This length allows for adequate maneuverability and ensures that you can use a clean section of floss for each tooth.
   • Grasping the Floss: Hold the floss taut between your hands, leaving a couple of inches of floss between your fingers. This tension helps control the floss as you maneuver it between your teeth.

2. Inserting the Floss:

   • Slip Between Teeth: Gently slide the floss between your teeth. Be careful not to snap the floss, as this can cause trauma to the gums.
   • Positioning: Insert the floss into the area between your teeth and gums as far as it will comfortably go, ensuring that you reach the gumline.

3. Flossing Motion:

   • Vertical Strokes: Use 8 to 10 vertical strokes with the floss to dislodge food particles and plaque. Move the floss up and down against the sides of each tooth, making sure to clean both the front and back surfaces.
   • C-Shaped Motion: For optimal cleaning, wrap the floss around the tooth in a C-shape and gently slide it beneath the gumline.

4. Frequency:

   • Daily Flossing: Aim to floss at least once a day. Consistency is key to maintaining good oral hygiene.
   • Best Time to Floss: The most important time to floss is before going to bed, as this helps remove debris and plaque that can accumulate throughout the day.

5. Flossing and Brushing:

   • Order of Operations: Flossing can be done either before or after brushing your teeth. Both methods are effective, so choose the one that fits best into your routine.

Gingival crevicular fluid is an inflammatory exudate found in the gingival sulcus. It plays a significant role in periodontal health and disease.

A. Characteristics of GCF

• Glucose Concentration: The glucose concentration in GCF is 3-4 times greater than that in serum, indicating increased metabolic activity in inflamed tissues.
• Protein Content: The total protein content of GCF is much less than that of serum, reflecting its role as an inflammatory exudate.
• Inflammatory Nature: GCF is present in clinically normal sulci due to the constant low-grade inflammation of the gingiva.

B. Drugs Excreted Through GCF

• Tetracyclines and Metronidazole: These antibiotics are known to be excreted through GCF, making them effective for localized periodontal therapy.

C. Collection Methods for GCF

GCF can be collected using various techniques, including:

1. Absorbing Paper Strips/Blotter/Periopaper: These strips absorb fluid from the sulcus and are commonly used for GCF collection.
2. Twisted Threads: Placing twisted threads around and into the sulcus can help collect GCF.
3. Micropipettes: These can be used for precise collection of GCF in research settings.
4. Intra-Crevicular Washings: Flushing the sulcus with a saline solution can help collect GCF for analysis.

 Naber’s Probe and Furcation Involvement

Furcation involvement is a critical aspect of periodontal disease that affects the prognosis of teeth with multiple roots. Naber’s probe is a specialized instrument designed to assess furcation areas, allowing clinicians to determine the extent of periodontal attachment loss and the condition of the furcation. This lecture will cover the use of Naber’s probe, the classification of furcation involvement, and the clinical significance of these classifications.

Naber’s Probe

• Description: Naber’s probe is a curved, blunt-ended instrument specifically designed for probing furcation areas. Its unique shape allows for horizontal probing, which is essential for accurately assessing the anatomy of multi-rooted teeth.

• Usage: The probe is inserted horizontally into the furcation area to evaluate the extent of periodontal involvement. The clinician can feel the anatomical fluting between the roots, which aids in determining the classification of furcation involvement.

Classification of Furcation Involvement

Furcation involvement is classified into four main classes using Naber’s probe:

1. Class I:

   • Description: The furcation can be probed to a depth of 3 mm.
   • Clinical Findings: The probe can feel the anatomical fluting between the roots, but it cannot engage the roof of the furcation.
   • Significance: Indicates early furcation involvement with minimal attachment loss.

2. Class II:

   • Description: The furcation can be probed to a depth greater than 3 mm, but not through and through.
   • Clinical Findings: This class represents a range between Class I and Class III, where there is partial loss of attachment but not complete penetration through the furcation.
   • Significance: Indicates moderate furcation involvement that may require intervention.

3. Class III:

   • Description: The furcation can be completely probed through and through.
   • Clinical Findings: The probe passes from one furcation to the other, indicating significant loss of periodontal support.
   • Significance: Represents advanced furcation involvement, often associated with a poor prognosis for the affected tooth.

4. Class III+:

   • Description: The probe can go halfway across the tooth.
   • Clinical Findings: Similar to Class III, but with partial obstruction or remaining tissue.
   • Significance: Indicates severe furcation involvement with a significant loss of attachment.

5. Class IV:

   • Description: Clinically, the examiner can see through the furcation.
   • Clinical Findings: There is complete loss of tissue covering the furcation, making it visible upon examination.
   • Significance: Indicates the most severe form of furcation involvement, often leading to tooth mobility and extraction.

Measurement Technique

• Measurement Reference: Measurements are taken from an imaginary tangent connecting the prominences of the root surfaces of both roots. This provides a consistent reference point for assessing the depth of furcation involvement.

Clinical Significance

• Prognosis: The classification of furcation involvement is crucial for determining the prognosis of multi-rooted teeth. Higher classes of furcation involvement generally indicate a poorer prognosis and may necessitate more aggressive treatment strategies.

• Treatment Planning: Understanding the extent of furcation involvement helps clinicians develop appropriate treatment plans, which may include scaling and root planing, surgical intervention, or extraction.

• Monitoring: Regular assessment of furcation involvement using Naber’s probe can help monitor disease progression and the effectiveness of periodontal therapy.

Aggressive periodontitis (AP) is a multifactorial, severe, and rapidly progressive form of periodontitis that primarily affects younger patients. It is characterized by a unique set of clinical and microbiological features that distinguish it from other forms of periodontal disease.

Key Characteristics

• Rapid Progression: AP is marked by a swift deterioration of periodontal tissues.
• Age Group: Primarily affects adolescents and young adults, but can occur at any age.
• Multifactorial Etiology: Involves a combination of microbiological, immunological, genetic, and environmental factors.

Other Findings

• Presence of Aggregatibacter actinomycetemcomitans (A.a.) in diseased sites.
• Abnormal host responses, including impaired phagocytosis and chemotaxis.
• Hyperresponsive macrophages leading to exaggerated inflammatory responses.
• The disease may exhibit self-arresting tendencies in some cases.

Classification

Aggressive periodontitis can be classified into two main types:

1. Localized Aggressive Periodontitis (LAP): Typically affects the permanent molars and incisors, often with localized attachment loss.
2. Generalized Aggressive Periodontitis (GAP): Involves more widespread periodontal tissue destruction.

Risk Factors

Microbiological Factors

• Aggregatibacter actinomycetemcomitans: A primary pathogen associated with LAP, producing a potent leukotoxin that kills neutrophils.
• Different strains of A.a. produce varying levels of leukotoxin, with highly toxic strains more prevalent in affected individuals.

Immunological Factors

• Human Leukocyte Antigens (HLAs): HLA-A9 and B-15 are candidate markers for aggressive periodontitis.
• Defective neutrophil function leads to impaired chemotaxis and phagocytosis.
• Hyper-responsive macrophage phenotype, characterized by elevated levels of PGE2 and IL-1β, may contribute to connective tissue breakdown and bone loss.

Genetic Factors

• Familial clustering of neutrophil abnormalities suggests a genetic predisposition.
• Genetic control of antibody responses to A.a., with variations in the ability to produce protective IgG2 antibodies.

Environmental Factors

• Smoking is a significant risk factor, with smokers experiencing more severe periodontal destruction compared to non-smokers.

Treatment Approaches

General Considerations

• Treatment strategies depend on the type and extent of periodontal destruction.
• GAP typically has a poorer prognosis compared to LAP, as it is less likely to enter spontaneous remission.

Conventional Periodontal Therapy

• Patient Education: Informing patients about the disease and its implications.
• Oral Hygiene Instructions: Reinforcing proper oral hygiene practices.
• Scaling and Root Planing: Removal of plaque and calculus to control local factors.

Surgical Resection Therapy

• Aimed at reducing or eliminating pocket depth.
• Contraindicated in cases of severe horizontal bone loss due to the risk of increased tooth mobility.

Regenerative Therapy

• Potential for regeneration is promising in AP cases.
• Techniques include open flap surgical debridement, root surface conditioning with tetracycline, and the use of allogenic bone grafts.
• Recent advances involve the use of enamel matrix proteins to promote cementum regeneration and new attachment.

Antimicrobial Therapy

• Often required as adjunctive treatment to eliminate A.a. from periodontal tissues.
• Tetracycline: Administered in various regimens to concentrate in periodontal tissues and inhibit A.a. growth.
• Combination Therapy: Metronidazole combined with amoxicillin has shown efficacy alongside periodontal therapy.
• Doxycycline: Used at a dose of 100 mg/day.
• Chlorhexidine (CHX): Irrigation and home rinsing to control bacterial load.

Host Modulation

• Involves the use of sub-antimicrobial dose doxycycline (SDD) to prevent periodontal attachment loss by modulating the activity of matrix metalloproteinases (MMPs), particularly collagenase and gelatinase.

Erythema Multiforme

• Characteristics: Erythema multiforme presents with "target" or "bull's eye" lesions, often associated with:
  • Etiologic Factors:
    • Herpes simplex infection.
    • Mycoplasma infection.
    • Drug reactions (e.g., sulfonamides, penicillins, phenylbutazone, phenytoin).

Changes in Plaque pH After Sucrose Rinse

The pH of dental plaque is a critical factor in the development of dental caries and periodontal disease. Key findings from various studies that investigated the changes in plaque pH following carbohydrate rinses, particularly focusing on sucrose and glucose.

Key Findings from Studies

1. Monitoring Plaque pH Changes:

   • A study reported that changes in plaque pH after a sucrose rinse were monitored using plaque sampling, antimony and glass electrodes, and telemetry.
   • Results:
     • The minimum pH at approximal sites (areas between teeth) was approximately 0.7 pH units lower than that on buccal surfaces (outer surfaces of the teeth).
     • The pH at the approximal site remained below resting levels for over 120 minutes.
     • The area under the pH response curves from approximal sites was five times greater than that from buccal surfaces, indicating a more significant and prolonged acidogenic response in interproximal areas.

2. Stephan's Early Studies (1935):

   • Method: Colorimetric measurement of plaque pH suspended in water.
   • Findings:
     • The pH of 211 plaque samples ranged from 4.6 to 7.0.
     • The mean pH value was found to be 5.9, indicating a generally acidic environment in dental plaque.

3. Stephan's Follow-Up Studies (1940):

   • Method: Use of an antimony electrode to measure in situ plaque pH after rinsing with sugar solutions.
   • Findings:
     • A 10% solution of glucose or sucrose caused a rapid drop in plaque pH by about 2 units within 2 to 5 minutes, reaching values between 4.5 and 5.0.
     • A 1% lactose solution lowered the pH by 0.3 units, while a 1% glucose solution caused a drop of 1.5 units.
     • A 1% boiled starch solution resulted in a reduction of 1.5 pH units over 51 minutes.
     • In all cases, the pH tended to return to initial values within approximately 2 hours.

4. Investigation of Proximal Cavities:

   • Studies of actual proximal cavities opened mechanically showed that the lowest pH values ranged from 4.6 to 4.1.
   • After rinsing with a 10% glucose or sucrose solution, the pH in the plaque dropped to between 4.5 and 5.0 within 2 to 5 minutes and gradually returned to baseline levels within 1 to 2 hours.

Implications

• The studies highlight the significant impact of carbohydrate exposure, particularly sucrose and glucose, on the pH of dental plaque.
• The rapid drop in pH following carbohydrate rinses indicates an acidogenic response from plaque microorganisms, which can contribute to enamel demineralization and caries development.
• The prolonged acidic environment in approximal sites suggests that these areas may be more susceptible to caries due to the slower recovery of pH levels.