Aggressive Periodontitis (formerly Juvenile Periodontitis)

• Historical Names: Previously referred to as periodontosis, deep cementopathia, diseases of eruption, Gottleib’s diseases, and periodontitis marginalis progressive.
• Risk Factors:
  • High frequency of Actinobacillus actinomycetemcomitans.
  • Immune defects (functional defects of PMNs and monocytes).
  • Autoimmunity and genetic factors.
  • Environmental factors, including smoking.
• Clinical Features:
  • Vertical loss of alveolar bone around the first molars and incisors, typically beginning around puberty.
  • Bone loss patterns often described as "target" or "bull" shaped lesions.

Dark Field Microscopy in Periodontal Microbiology

Dark field microscopy and phase contrast microscopy are valuable techniques in microbiological studies, particularly in the field of periodontal research. These methods allow for the direct observation of bacteria in plaque samples, providing insights into their morphology and motility. This lecture will discuss the principles of dark field microscopy, its applications in periodontal disease assessment, and its limitations.

Dark Field Microscopy

• Definition: Dark field microscopy is a technique that enhances the contrast of unstained, transparent specimens, allowing for the visualization of live microorganisms in their natural state.
• Principle: The method uses a special condenser that directs light at an angle, creating a dark background against which the specimen appears bright. This allows for the observation of motility and morphology without the need for staining.

Applications in Periodontal Microbiology

1. Alternative to Culture Methods:

   • Dark field microscopy has been suggested as a rapid alternative to traditional culture methods for assessing bacterial populations in periodontal plaque samples. It allows for immediate observation of bacteria without the time-consuming process of culturing.

2. Assessment of Morphology and Motility:

   • The technique enables direct and rapid assessment of the morphology (shape and structure) and motility (movement) of bacteria present in plaque samples. This information can be crucial for understanding the dynamics of periodontal disease.

3. Indication of Periodontal Disease Status:

   • Dark field microscopy has been used to indicate the status of periodontal disease and the effectiveness of maintenance programs. By observing the presence and activity of specific bacteria, clinicians can gain insights into the health of periodontal tissues.

Limitations of Dark Field Microscopy

1. Analysis of Major Periodontal Pathogens:

   • While dark field microscopy can visualize motile bacteria, it is important to note that many major periodontal pathogens, such as Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Eikenella corrodens, and Eubacterium species, are motile. However, the technique may not provide detailed information about their specific characteristics or pathogenic potential.

2. Differentiation of Treponema Species:

   • Dark field microscopy cannot differentiate between species of Treponema, which is a limitation when identifying specific pathogens associated with periodontal disease. This lack of specificity can hinder the ability to tailor treatment based on the exact microbial profile.

3. Limited Quantitative Analysis:

   • While dark field microscopy allows for qualitative observations, it may not provide quantitative data on bacterial populations, which can be important for assessing disease severity and treatment outcomes.

Theories Regarding the Mineralization of Dental Calculus

Dental calculus, or tartar, is a hard deposit that forms on teeth due to the mineralization of dental plaque. Understanding the mechanisms by which plaque becomes mineralized is essential for dental professionals in managing periodontal health. The theories regarding the mineralization of calculus can be categorized into two main mechanisms: mineral precipitation and the role of seeding agents.

1. Mineral Precipitation

Mineral precipitation involves the local rise in the saturation of calcium and phosphate ions, leading to the formation of calcium phosphate salts. This process can occur through several mechanisms:

A. Rise in pH

• Mechanism: An increase in the pH of saliva can lead to the precipitation of calcium phosphate salts by lowering the precipitation constant.
• Causes:
  • Loss of Carbon Dioxide: Bacterial activity in dental plaque can lead to the loss of CO2, resulting in an increase in pH.
  • Formation of Ammonia: The degradation of proteins by plaque bacteria can produce ammonia, further elevating the pH.

B. Colloidal Proteins

• Mechanism: Colloidal proteins in saliva bind calcium and phosphate ions, maintaining a supersaturated solution with respect to calcium phosphate salts.
• Process:
  • When saliva stagnates, these colloids can settle out, disrupting the supersaturated state and leading to the precipitation of calcium phosphate salts.

C. Enzymatic Activity

• Phosphatase:
  • This enzyme, released from dental plaque, desquamated epithelial cells, or bacteria, hydrolyzes organic phosphates in saliva, increasing the concentration of free phosphate ions and promoting mineralization.
• Esterase:
  • Present in cocci, filamentous organisms, leukocytes, macrophages, and desquamated epithelial cells, esterase can hydrolyze fatty esters into free fatty acids.
  • These fatty acids can form soaps with calcium and magnesium, which are subsequently converted into less-soluble calcium phosphate salts, facilitating calcification.

2. Seeding Agents and Heterogeneous Nucleation

The second theory posits that seeding agents induce small foci of calcification that enlarge and coalesce to form a calcified mass. This concept is often referred to as the epitactic concept or heterogeneous nucleation.

A. Role of Seeding Agents

• Unknown Agents: The specific seeding agents involved in calculus formation are not fully understood, but it is believed that the intercellular matrix of plaque plays a significant role.
• Carbohydrate-Protein Complexes:
  • These complexes may initiate calcification by chelating calcium from saliva and binding it to form nuclei that promote the deposition of minerals.

Clinical Implications

1. Understanding Calculus Formation:

   • Knowledge of the mechanisms behind calculus mineralization can help dental professionals develop effective strategies for preventing and managing calculus formation.

2. Preventive Measures:

   • Maintaining good oral hygiene practices can help reduce plaque accumulation and the conditions that favor mineralization, such as stagnation of saliva and elevated pH.

3. Treatment Approaches:

   • Understanding the role of enzymes and proteins in calculus formation may lead to the development of therapeutic agents that inhibit mineralization or promote the dissolution of existing calculus.

4. Research Directions:

   • Further research into the specific seeding agents and the biochemical processes involved in calculus formation may provide new insights into preventing and treating periodontal disease.

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.

Trauma from Occlusion

Trauma from occlusion refers to the injury sustained by periodontal tissues when occlusal forces exceed their adaptive capacity.

1. Trauma from Occlusion

• This term describes the injury that occurs to periodontal tissues when the forces exerted during occlusion (the contact between opposing teeth) exceed the ability of those tissues to adapt.
• Traumatic Occlusion: An occlusion that produces such injury is referred to as a traumatic occlusion. This can result from various factors, including malocclusion, excessive occlusal forces, or parafunctional habits (e.g., bruxism).

2. Clinical Signs of Trauma to the Periodontium

The most common clinical sign of trauma to the periodontium is:

• Increased Tooth Mobility: As the periodontal tissues are subjected to excessive forces, they may become compromised, leading to increased mobility of the affected teeth. This is often one of the first observable signs of trauma from occlusion.

3. Radiographic Signs of Trauma from Occlusion

Radiographic examination can reveal several signs indicative of trauma from occlusion:

1. Increased Width of Periodontal Space:

   • The periodontal ligament space may appear wider on radiographs due to the increased forces acting on the tooth, leading to a loss of attachment and bone support.

2. Vertical Destruction of Inter-Dental Septum:

   • Trauma from occlusion can lead to vertical bone loss in the inter-dental septa, which may be visible on radiographs as a reduction in bone height between adjacent teeth.

3. Radiolucency and Condensation of the Alveolar Bone:

   • Areas of radiolucency may indicate bone loss, while areas of increased radiopacity (condensation) can suggest reactive changes in the bone due to the stress of occlusal forces.

4. Root Resorption:

   • In severe cases, trauma from occlusion can lead to root resorption, which may be observed as a loss of root structure on radiographs.

Anatomy and Histology of the Periodontium

Gingiva (normal clinical appearance): no muscles, no glands; keratinized

• Color: coral pink but does vary with individuals and races due to cutaneous pigmentation
• Papillary contour: pyramidal shape with one F and one L papilla and the col filling interproximal space to the contact area (col the starting place gingivitis)
• Marginal contour: knife-edged and scalloped
• Texture: stippled (orange-peel texture); blow air to dry out and see where stippling ends to see end of gingiva
• Consistency: firm and resilient (push against it and won’t move); bound to underlying bone
• Sulcus depth: 0-3mm
• Exudate: no exudates (blood, pus, water)

  Anatomic and histological structures

Gingival unit: includes periodontium above alveolar crest of bone

a. Alveolar mucosa: histology- non-keratinized, stratified, squamous epithelium, submucosa with glands, loose connective tissue with collagen and elastin, muscles.  No epithelial ridges, no stratum granulosum (flattened cells below keratin layer)

b. Mucogingival junction: clinical demarcation between alveolar mucosa and attached gingiva

c. Attached gingiva: histology- keratinized, stratified, squamous epithelium with epithelial ridges (basal cell layer, prickle cell layer, granular cell layer (stratum granulosum), keratin layer); no submucosa

• Dense connective tissue: predominantly collagen, bound to periosteum of bone by Sharpey fibers
• Reticular fibers between collagen fibers and are continuous with reticulin in blood vessels

d. Free gingival groove: demarcation between attached and free gingiva; denotes base of gingival sulcus in normal gingiva; not always seen

e. Free gingival margin: area from free gingival groove to epithelial attachment (up and over ® inside)

• Oral surface: stratified, squamous epithelium with epithelial ridges
• Tooth side surface (sulcular epithelium): non-keratinized, stratified, squamous epithelium with no epithelial ridges (basal cell and prickle cell layers)

f. Gingival sulcus: space bounded by tooth surface, sulcular epithelium, and junctional epithelium; 0-3mm depth; space between epithelium and tooth

g. Dento-gingival junction: combination of epithelial and fibrous attachment

• Junctional epithelium (epithelial attachment): attachment of epithelial cells by hemi-desmosomes and sticky substances (basal lamina- 800-1200 A, DAS-acid mucopolysaccharides, hyaluronic acid, chondroitin sulfate A, C, and B), to enamel, enamel and cementum, or cementum depending on stage of passive eruption.  Length ranges from 0.25-1.35mm.
• Fibrous attachment: attachment of collagen fibers (Sharpey’s fibers) into cementum just beneath epithelial attachment; ~ 1mm thick

h. Nerve fibers: myelinated and non-myelinated (for pain) in connective tissue.  Both free and specialized endings for pain, touch pressure, and temperature -> proprioception.  If dentures, rely on TMJ.

i.Mesh of terminal argyophilic fibers (stain silver), some extending into epithelium

ii  Meissner-type corpuscles: pressure sensitive sensory nerve encased in CT

iii.Krause-type corpuscles: temperature receptors

iv. Encapsulated spindles

i. Gingival fibers:

i.  Gingivodental group:

• Group I (A): from cementum to free gingival margin
• Group II (B): from cementum to attached gingiva
• Group III (C): from cementum over alveolar crest to periosteum on buccal and lingual plates

ii.  Circular (ligamentum circularis): encircles tooth in free gingiva

iii. Transeptal fibers: connects cementum of adjacent teeth, runs over interdental septum of alveolar bone.  Separates gingival unit from attachment apparatus.

Transeptal and Group III fibers the major defense against stuff getting into bone and ligament.

2.  Attachment apparatus: periodontium below alveolar crest of bone

Periodontal ligament: Sharpey’s fibers (collagen) connecting cementum to bone (bundle bone).  Few elastic and oxytalan fibers associated with blood vessels and embedded in cementum in cervical third of tooth.  Components divided as follows:

i. Alveolar crest fibers: from cementum just below CEJ apical to alveolar crest of bone

ii.Horizontal fibers: just apical to alveolar crest group, run at right angles to long axis of tooth from cementum horizontally to alveolar bone proper

iii.Oblique fibers: most numerous, from cementum run coronally to alveolar bone proper

iv. Apical fibers: radiate from cementum around apex of root apically to alveolar bone proper, form socket base

v. Interradicular fibers: found only between roots of multi-rooted teeth from cementum to alveolar bone proper

vi. Intermediate plexus: fibers which splice Sharpey’s fibers from bone and cementum

vii. Epithelial Rests of Malassez: cluster and individual epithelial cells close to cementum which are remnants of Hertwig’s epithelial root sheath; potential source of periodontal cysts.

viii. Nerve fibers: myelinated and non-myelinated; abundant supply of sensory free nerve endings capable of transmitting tactile pressure and pain sensation by trigeminal pathway and elongated spindle-like nerve fiber for proprioceptive impulses

Cementum: 45-50% inorganic; 50-55% organic (enamel is 97% inorganic; dentin 70% inorganic)

i.  Acellular cementum: no cementocytes; covers dentin (older) in coronal ½ to 2/3 of root, 16-60 mm thick

ii. Cellular cementum: cementocytes; covers dentin in apical ½ to 1/3 of root; also may cover acellular cementum areas in repair areas, 15-200 mm thick

iii. Precementum (cementoid): meshwork of irregularly arranged collagen in surface of cementum where formation starts

iv. Cemento-enamel junction (CEJ): 60-65% of time cementum overlaps enamel; 30% meet end-to-end; 5-10% space between

v. Cementum slower healing than bone or PDL.  If expose dentinotubules ® root sensitivity.

Alveolar bone: 65% inorganic, 35% organic

i. Alveolar bone proper (cribriform plate): lamina dura on x-ray; bundle bone receive Sharpey fibers from PDL

ii. Supporting bone: cancellous, trabecular (vascularized) and F and L plates of compact bone

Blood supply to periodontium

i. Alveolar blood vessels (inferior and superior)

A) Interalveolar: actually runs through bone then exits, main supply to alveolar bone and PDL

B) Supraperiosteal: just outside bone, to gingiva and alveolar bone

C) Dental (pulpal): to pulp and periapical area

D) Terminal vessels (supracrestal): anastomose of A and B above beneath the sulcular epithelium

E) PDL gets blood from: most from branches of interalveolar blood vessels from alveolar bone marrow spaces, supraperiosteal vessels when interalveolar vessels not present, pulpal (apical) vessels, supracrestal gingival vessels

ii. Lymphatic drainage: accompany blood vessels to regional lymph nodes (esp. submaxillary group)