NEET MDS Lessons
Periodontology
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)
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
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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).
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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.
- The pellicle consists of more than 180 peptides, proteins,
and glycoproteins, which include:
Formation and Maturation of the Acquired Pellicle
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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.
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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.
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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
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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).
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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.
- 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:
Clinical Significance
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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.
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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.
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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.
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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.
- GTR Membrane Placement:
- Apical border: 3 – 4 mm below defect margin.
- Lateral extension: 2 – 3 mm beyond defect.
- Root Surface Biomodification: Citric acid (pH 1.0) for 2 – 5 min.
- Enamel Matrix Derivative: Emdogain (from porcine teeth).
- Cervical Enamel Projections: Seen in 8.6 – 28.6% of molars.
- Smoking: Preventable risk factor; damages cilia via hydrogen cyanide.
- Angulation vs Adaptation:
- Angulation: Angle between blade face and tooth surface.
- Adaptation: Relationship of blade’s working end to tooth surface.
- Curettes:
- Gracey: Blade offset at 60°.
- Universal: Blade angle at 90°.
- After Five: Extended shank by 3 mm; available in all Gracey numbers except 9 – 10.
- Mini Five: Blade half the length of conventional curette.
- Langer Curette: Gracey curette modified with universal blade angle.
- Scaling & Sharpening:
- Blade angulation for scaling: 45 – 90°; for curettage: >90°.
- Sharpening angle: 100 – 110°.
- Chisel scaler: Push motion; Hoe scaler: Blade bent at 99°.
- Sickle scaler blade-to-shank angle: 70°.
- Microsurgery:
- Instrument weight: 15 – 20 g.
- Principles: Butt joint approximation, enhanced motor skills, minimal trauma.
- Suturing:
- Needle entry: Right angle, 2 – 3 mm from incision.
Immunological Profile
- T4:T8 Ratio: 1:1 in healthy periodontitis patients
- HIV Association: Altered ratio of 0.6:1 indicates immunocompromise
Radiographic Changes
- First Sign: Fuzziness or break in lamina dura at alveolar crest
- Progression: Loss of cortical outline, trabecular pattern changes
- Most Severe Changes: Occur along the lateral wall of the periodontal pocket
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).
- Etiologic Factors:
Plaque Formation
Dental plaque is a biofilm that forms on the surfaces of teeth and is a key factor in the development of dental caries and periodontal disease. The process of plaque formation can be divided into three major phases:
1. Formation of Pellicle on the Tooth Surface
- Definition: The pellicle is a thin, acellular film that forms on the tooth surface shortly after cleaning.
- Composition: It is primarily composed of salivary glycoproteins and other proteins that are adsorbed onto the enamel surface.
- Function:
- The pellicle serves as a protective barrier for the tooth surface.
- It provides a substrate for bacterial adhesion, facilitating the subsequent stages of plaque formation.
2. Initial Adhesion & Attachment of Bacteria
- Mechanism:
- Bacteria in the oral cavity begin to adhere to the pellicle-coated tooth surface.
- This initial adhesion is mediated by specific interactions between bacterial adhesins (surface proteins) and the components of the pellicle.
- Key Bacterial Species:
- Primary colonizers, such as Streptococcus sanguis and Actinomyces viscosus, are among the first to attach.
- Importance:
- Successful adhesion is crucial for the establishment of plaque, as it allows for the accumulation of additional bacteria.
3. Colonization & Plaque Maturation
- Colonization:
- Once initial bacteria have adhered, they proliferate and create a more complex community.
- Secondary colonizers, including gram-negative anaerobic bacteria, begin to join the biofilm.
- Plaque Maturation:
- As the plaque matures, it develops a three-dimensional structure, with different bacterial species occupying specific niches within the biofilm.
- The matrix of extracellular polysaccharides and salivary glycoproteins becomes more pronounced, providing structural integrity to the plaque.
- Coaggregation:
- Different bacterial species can adhere to one another through coaggregation, enhancing the complexity of the plaque community.
Composition of Plaque
- Matrix Composition:
- Plaque is primarily composed of bacteria embedded in a matrix of salivary glycoproteins and extracellular polysaccharides.
- Implications for Removal:
- The dense and cohesive nature of this matrix makes it difficult to remove plaque through simple rinsing or the use of sprays.
- Effective plaque removal typically requires mechanical means, such as brushing and flossing, to disrupt the biofilm structure.