Acquired Pellicle in the Oral Cavity

The acquired pellicle is a crucial component of oral health, serving as the first line of defense in the oral cavity and playing a significant role in the initial stages of biofilm formation on tooth surfaces. Understanding the composition, formation, and function of the acquired pellicle is essential for dental professionals in managing oral health.

Composition of the Acquired Pellicle

1. Definition:

   • The acquired pellicle is a thin, organic layer that coats all surfaces in the oral cavity, including both hard (tooth enamel) and soft tissues (gingiva, mucosa).

2. Components:

   • The pellicle consists of more than 180 peptides, proteins, and glycoproteins, which include:
     • Keratins: Structural proteins that provide strength.
     • Mucins: Glycoproteins that contribute to the viscosity and protective properties of saliva.
     • Proline-rich proteins: Involved in the binding of calcium and phosphate.
     • Phosphoproteins: Such as statherin, which helps in maintaining calcium levels and preventing mineral loss.
     • Histidine-rich proteins: May play a role in buffering and mineralization.
   • These components function as adhesion sites (receptors) for bacteria, facilitating the initial colonization of tooth surfaces.

Formation and Maturation of the Acquired Pellicle

1. Rapid Formation:

   • The salivary pellicle can be detected on clean enamel surfaces within 1 minute after exposure to saliva. This rapid formation is crucial for protecting the enamel and providing a substrate for bacterial adhesion.

2. Equilibrium State:

   • By 2 hours, the pellicle reaches a state of equilibrium between adsorption (the process of molecules adhering to the surface) and detachment. This dynamic balance allows for the continuous exchange of molecules within the pellicle.

3. Maturation:

   • Although the initial pellicle formation occurs quickly, further maturation can be observed over several hours. This maturation process involves the incorporation of additional salivary components and the establishment of a more complex structure.

Interaction with Bacteria

1. Bacterial Adhesion:

   • Bacteria that adhere to tooth surfaces do not contact the enamel directly; instead, they interact with the acquired enamel pellicle. This interaction is critical for the formation of dental biofilms (plaque).

2. Active Role of the Pellicle:

   • The acquired pellicle is not merely a passive adhesion matrix. Many proteins within the pellicle retain enzymatic activity when incorporated. Some of these enzymes include:
     • Peroxidases: Enzymes that can break down hydrogen peroxide and may have antimicrobial properties.
     • Lysozyme: An enzyme that can lyse bacterial cell walls, contributing to the antibacterial defense.
     • α-Amylase: An enzyme that breaks down starches and may influence the metabolism of adhering bacteria.

Clinical Significance

1. Role in Oral Health:

   • The acquired pellicle plays a protective role by providing a barrier against acids and bacteria, helping to maintain the integrity of tooth enamel and soft tissues.

2. Biofilm Formation:

   • Understanding the role of the pellicle in bacterial adhesion is essential for managing plaque-related diseases, such as dental caries and periodontal disease.

3. Preventive Strategies:

   • Dental professionals can use knowledge of the acquired pellicle to develop preventive strategies, such as promoting saliva flow and maintaining good oral hygiene practices to minimize plaque accumulation.

4. Therapeutic Applications:

   • The enzymatic activities of pellicle proteins can be targeted in the development of therapeutic agents aimed at enhancing oral health and preventing bacterial colonization.

Zones of Periodontal Disease

Listgarten described four distinct zones that can be observed in periodontal lesions. These zones may blend with each other and may not be present in every case.

Zones of Periodontal Disease

1. Zone 1: Bacterial Zone

   • Description: This is the most superficial zone, consisting of a diverse array of bacteria.
   • Characteristics:
     • The bacterial zone is primarily composed of various microbial species, including both pathogenic and non-pathogenic bacteria.
     • This zone is critical in the initiation and progression of periodontal disease, as the presence of specific bacteria can trigger inflammatory responses in the host.

2. Zone 2: Neutrophil Rich Zone

   • Description: This zone contains numerous leukocytes, predominantly neutrophils.
   • Characteristics:
     • The neutrophil-rich zone is indicative of the body’s immune response to the bacterial invasion.
     • Neutrophils are the first line of defense and play a crucial role in phagocytosing bacteria and releasing inflammatory mediators.
     • The presence of a high number of neutrophils suggests an acute inflammatory response, which is common in active periodontal disease.

3. Zone 3: Necrotic Zone

   • Description: This zone consists of disintegrated tissue cells, fibrillar material, remnants of collagen fibers, and spirochetes.
   • Characteristics:
     • The necrotic zone reflects tissue destruction and is characterized by the presence of dead or dying cells.
     • Fibrillar material and remnants of collagen fibers indicate the breakdown of the extracellular matrix, which is essential for maintaining periodontal tissue integrity.
     • Spirochetes, which are associated with more aggressive forms of periodontal disease, can also be found in this zone, contributing to the necrotic process.

4. Zone 4: Zone of Spirochetal Infiltration

   • Description: This zone consists of well-preserved tissue that is infiltrated with large and medium spirochetes.
   • Characteristics:
     • The zone of spirochetal infiltration indicates a more chronic phase of periodontal disease, where spirochetes invade the connective tissue.
     • The presence of well-preserved tissue suggests that while spirochetes are present, the tissue has not yet undergone extensive necrosis.
     • This zone is significant as it highlights the role of spirochetes in the pathogenesis of periodontal disease, particularly in cases of necrotizing periodontal diseases.

Influence of Host Response on Periodontal Disease

The host response plays a critical role in the progression and management of periodontal disease. Various host factors influence bacterial colonization, invasion, tissue destruction, and healing processes. Understanding these interactions is essential for developing effective treatment strategies.

Aspects of Periodontal Disease and Host Factors

1. Bacterial Colonization:

   • Host Factor: Antibody C in crevicular fluid.
   • Mechanism:
     • Antibody C inhibits the adherence and coaggregation of bacteria in the subgingival environment.
     • This action potentially reduces bacterial numbers by promoting lysis (destruction of bacterial cells).
   • Implication: A robust antibody response can help control the initial colonization of pathogenic bacteria, thereby influencing the onset of periodontal disease.

2. Bacterial Invasion:

   • Host Factor: Antibody C-mediated lysis and neutrophil activity.
   • Mechanism:
     • Antibody C-mediated lysis reduces bacterial counts in the periodontal tissues.
     • Neutrophils, through processes such as chemotaxis (movement towards chemical signals), phagocytosis (engulfing and digesting bacteria), and lysis, further reduce bacterial counts.
   • Implication: An effective neutrophil response is crucial for controlling bacterial invasion and preventing the progression of periodontal disease.

3. Tissue Destruction:

   • Host Factors: Antibody-mediated hypersensitivity and cell-mediated immune responses.
   • Mechanism:
     • Activation of tissue factors, such as collagenase, leads to the breakdown of connective tissue and periodontal structures.
     • The immune response can inadvertently contribute to tissue destruction, as inflammatory mediators can damage host tissues.
   • Implication: While the immune response is essential for fighting infection, it can also lead to collateral damage in periodontal tissues, exacerbating disease progression.

4. Healing and Fibrosis:

   • Host Factors: Lymphocytes and macrophage-produced chemotactic factors.
   • Mechanism:
     • Lymphocytes and macrophages release chemotactic factors that attract fibroblasts to the site of injury.
     • Fibroblasts are activated by specific factors, promoting tissue repair and fibrosis (the formation of excess connective tissue).
   • Implication: A balanced immune response is necessary for effective healing and regeneration of periodontal tissues following inflammation.

Sutures for Periodontal Flaps

Suturing is a critical aspect of periodontal surgery, particularly when managing periodontal flaps. The choice of suture material can significantly influence healing, tissue adaptation, and overall surgical outcomes.

1. Nonabsorbable Sutures

Nonabsorbable sutures are designed to remain in the tissue until they are manually removed. They are often used in situations where long-term support is needed.

A. Types of Nonabsorbable Sutures

1. Silk (Braided)

   • Characteristics:
     • Excellent handling properties and knot security.
     • Provides good tissue approximation.
   • Applications: Commonly used in periodontal surgeries due to its ease of use and reliability.

2. Nylon (Monofilament) (Ethilon)

   • Characteristics:
     • Strong and resistant to stretching.
     • Less tissue reactivity compared to silk.
   • Applications: Ideal for delicate tissues and areas requiring minimal tissue trauma.

3. ePTFE (Monofilament) (Gore-Tex)

   • Characteristics:
     • Biocompatible and non-reactive.
     • Excellent tensile strength and flexibility.
   • Applications: Often used in guided tissue regeneration procedures and in areas where long-term support is needed.

4. Polyester (Braided) (Ethibond)

   • Characteristics:
     • High tensile strength and good knot security.
     • Less pliable than silk.
   • Applications: Used in situations requiring strong sutures, such as in flap stabilization.

2. Absorbable Sutures

Absorbable sutures are designed to be broken down by the body over time, eliminating the need for removal. They are often used in periodontal surgeries where temporary support is sufficient.

A. Types of Absorbable Sutures

1. Surgical Gut

   • Plain Gut (Monofilament)

     • Absorption Time: Approximately 30 days.
     • Characteristics: Made from sheep or cow intestines; provides good tensile strength initially but loses strength quickly.
     • Applications: Suitable for soft tissue approximation where rapid absorption is desired.

   • Chromic Gut (Monofilament)

     • Absorption Time: Approximately 45 to 60 days.
     • Characteristics: Treated with chromium salts to delay absorption; retains strength longer than plain gut.
     • Applications: Used in areas where a longer healing time is expected.

2. Synthetic Absorbable Sutures

   • Polyglycolic Acid (Braided) (Vicryl, Ethicon)

     • Absorption Time: Approximately 16 to 20 days.
     • Characteristics: Provides good tensile strength and is absorbed predictably.
     • Applications: Commonly used in periodontal and oral surgeries due to its handling properties.

   • Dexon (Davis & Geck)

     • Characteristics: Similar to Vicryl; made from polyglycolic acid.
     • Applications: Used in soft tissue approximation and ligation.

   • Polyglycaprone (Monofilament) (Maxon)

     • Absorption Time: Similar to Vicryl.
     • Characteristics: Offers excellent tensile strength and is absorbed more slowly than other synthetic options.
     • Applications: Ideal for areas requiring longer support during healing.

Periodontal Fibers

Periodontal fibers play a crucial role in maintaining the integrity of the periodontal ligament and supporting the teeth within the alveolar bone. Understanding the different groups of periodontal fibers is essential for comprehending their functions in periodontal health and disease.

1. Gingivodental Group

• Location:
  • Present on the facial, lingual, and interproximal surfaces of the teeth.
• Attachment:
  • These fibers are embedded in the cementum just beneath the epithelium at the base of the gingival sulcus.
• Function:
  • They help support the gingiva and maintain the position of the gingival margin.

2. Circular Group

• Location:
  • These fibers course through the connective tissue of the marginal and interdental gingiva.
• Attachment:
  • They encircle the tooth in a ring-like fashion.
• Function:
  • The circular fibers help maintain the contour of the gingiva and provide support to the marginal gingiva.

3. Transseptal Group

• Location:
  • Located interproximally, these fibers extend between the cementum of adjacent teeth.
• Attachment:
  • They lie in the area between the epithelium at the base of the gingival sulcus and the crest of the interdental bone.
• Function:
  • The transseptal fibers are primarily responsible for the post-retention relapse of orthodontically positioned teeth.
  • They are sometimes classified as principal fibers of the periodontal ligament.
  • Collectively, they form the interdental ligament of the arch, providing stability to the interproximal areas.

4. Semicircular Fibers

• Location:
  • These fibers attach to the proximal surface of a tooth immediately below the cementoenamel junction (CEJ).
• Attachment:
  • They go around the facial or lingual marginal gingiva of the tooth and attach to the other proximal surface of the same tooth.
• Function:
  • Semicircular fibers help maintain the position of the tooth and support the gingival tissue around it.

5. Transgingival Fibers

• Location:
  • These fibers attach to the proximal surface of one tooth and traverse the interdental space diagonally to attach to the proximal surface of the adjacent tooth.
• Function:
  • Transgingival fibers provide support across the interdental space, helping to maintain the position of adjacent teeth and the integrity of the gingival tissue.

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).