NEET MDS Lessons
Periodontology
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
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Understanding Calculus Formation:
- Knowledge of the mechanisms behind calculus mineralization can help dental professionals develop effective strategies for preventing and managing calculus formation.
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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.
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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.
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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.
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)
Bacterial Properties Involved in Evasion of Host Defense Mechanisms
Bacteria have evolved various strategies to evade the host's immune defenses, allowing them to persist and cause disease. Understanding these mechanisms is crucial for developing effective treatments and preventive measures against bacterial infections, particularly in the context of periodontal disease. This lecture will explore the bacterial species involved, their properties, and the biological effects of these properties on host defense mechanisms.
Host Defense Mechanisms and Bacterial Evasion Strategies
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Specific Antibody Evasion
- Bacterial Species:
- Porphyromonas gingivalis
- Prevotella intermedia
- Prevotella melaninogenica
- Capnocytophaga spp.
- Bacterial Property:
- IgA- and IgG-degrading proteases
- Biologic Effect:
- Degradation of specific antibodies, which impairs the host's ability to mount an effective immune response against these bacteria.
- Bacterial Species:
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Evasion of Polymorphonuclear Leukocytes (PMNs)
- Bacterial Species:
- Aggregatibacter actinomycetemcomitans
- Fusobacterium nucleatum
- Porphyromonas gingivalis
- Treponema denticola
- Bacterial Properties:
- Leukotoxin: A toxin that can induce apoptosis in PMNs.
- Heat-sensitive surface protein: May interfere with immune recognition.
- Capsule: A protective layer that inhibits phagocytosis.
- Inhibition of superoxide production: Reduces the oxidative burst necessary for bacterial killing.
- Biologic Effects:
- Inhibition of PMN function, leading to decreased bacterial killing.
- Induction of apoptosis (programmed cell death) in PMNs, reducing the number of immune cells available to fight infection.
- Inhibition of phagocytosis, allowing bacteria to evade clearance.
- Bacterial Species:
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Evasion of Lymphocytes
- Bacterial Species:
- Aggregatibacter actinomycetemcomitans
- Fusobacterium nucleatum
- Tannerella forsythia
- Prevotella intermedia
- Bacterial Properties:
- Leukotoxin: Induces apoptosis in lymphocytes.
- Cytolethal distending toxin: Affects cell cycle progression and induces cell death.
- Heat-sensitive surface protein: May interfere with immune recognition.
- Cytotoxin: Directly damages immune cells.
- Biologic Effects:
- Killing of mature B and T cells, leading to a weakened adaptive immune response.
- Nonlethal suppression of lymphocyte activity, impairing the immune response.
- Impairment of lymphocyte function by arresting the cell cycle, leading to decreased responses to antigens and mitogens.
- Induction of apoptosis in mononuclear cells and lymphocytes, further reducing immune capacity.
- Bacterial Species:
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Inhibition of Interleukin-8 (IL-8) Production
- Bacterial Species:
- Porphyromonas gingivalis
- Bacterial Property:
- Inhibition of IL-8 production by epithelial cells.
- Biologic Effect:
- Impairment of PMN response to bacteria, leading to reduced recruitment and activation of neutrophils at the site of infection.
- Bacterial Species:
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
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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.
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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.
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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.
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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.
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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.
Classification of Cementum According to Schroeder
Cementum is a specialized calcified tissue that covers the roots of teeth and plays a crucial role in periodontal health. According to Schroeder, cementum can be classified into several distinct types based on its cellular composition and structural characteristics. Understanding these classifications is essential for dental professionals in diagnosing and treating periodontal conditions.
Classification of Cementum
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Acellular Afibrillar Cementum:
- Characteristics:
- Contains neither cells nor collagen fibers.
- Present in the coronal region of the tooth.
- Thickness ranges from 1 µm to 15 µm.
- Function:
- This type of cementum is thought to play a role in the attachment of the gingiva to the tooth surface.
- Characteristics:
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Acellular Extrinsic Fiber Cementum:
- Characteristics:
- Lacks cells but contains closely packed bundles of Sharpey’s fibers, which are collagen fibers that anchor the cementum to the periodontal ligament.
- Typically found in the cervical third of the roots.
- Thickness ranges from 30 µm to 230 µm.
- Function:
- Provides strong attachment of the periodontal ligament to the tooth, contributing to the stability of the tooth in its socket.
- Characteristics:
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Cellular Mixed Stratified Cementum:
- Characteristics:
- Contains both extrinsic and intrinsic fibers and may contain cells.
- Found in the apical third of the roots, at the apices, and in furcation areas.
- Thickness ranges from 100 µm to 1000 µm.
- Function:
- This type of cementum is involved in the repair and adaptation of the tooth root, especially in response to functional demands and periodontal disease.
- Characteristics:
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Cellular Intrinsic Fiber Cementum:
- Characteristics:
- Contains cells but no extrinsic collagen fibers.
- Primarily fills resorption lacunae, which are areas where cementum has been resorbed.
- Function:
- Plays a role in the repair of cementum and may be involved in the response to periodontal disease.
- Characteristics:
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Intermediate Cementum:
- Characteristics:
- A poorly defined zone located near the cementoenamel junction (CEJ) of certain teeth.
- Appears to contain cellular remnants of the Hertwig's epithelial root sheath (HERS) embedded in a calcified ground substance.
- Function:
- Its exact role is not fully understood, but it may be involved in the transition between enamel and cementum.
- Characteristics:
Clinical Significance
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Importance of Cementum:
- Understanding the different types of cementum is crucial for diagnosing periodontal diseases and planning treatment strategies.
- The presence of various types of cementum can influence the response of periodontal tissues to disease and trauma.
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Cementum in Periodontal Disease:
- Changes in the thickness and composition of cementum can occur in response to periodontal disease, affecting tooth stability and attachment.
Gingivitis
Gingivitis is an inflammatory condition of the gingiva that can progress through several distinct stages. Understanding these stages is crucial for dental professionals in diagnosing and managing periodontal disease effectively. This lecture will outline the four stages of gingivitis, highlighting the key pathological changes that occur at each stage.
I. Initial Lesion
- Characteristics:
- Increased Permeability: The microvascular bed in the gingival tissues becomes more permeable, allowing for the passage of fluids and immune cells.
- Increased GCF Flow: There is an increase in the flow of gingival crevicular fluid (GCF), which is indicative of inflammation and immune response.
- PMN Cell Migration: The migration of
polymorphonuclear leukocytes (PMNs) is facilitated by various adhesion
molecules, including:
- Intercellular Cell Adhesion Molecule 1 (ICAM-1)
- E-selectin (ELAM-1) in the dentogingival vasculature.
- Clinical Implications: This stage marks the beginning of the inflammatory response, where the body attempts to combat the initial bacterial insult.
II. Early Lesion
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Characteristics:
- Leukocyte Infiltration: There is significant infiltration of leukocytes, particularly lymphocytes, into the connective tissue of the junctional epithelium.
- Fibroblast Degeneration: Several fibroblasts within the lesion exhibit signs of degeneration, indicating tissue damage.
- Proliferation of Basal Cells: The basal cells of the junctional and sulcular epithelium begin to proliferate, which may be a response to the inflammatory process.
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Clinical Implications: This stage represents a transition from initial inflammation to more pronounced tissue changes, with the potential for further progression if not managed.
III. Established Lesion
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Characteristics:
- Predominance of Plasma Cells and B Lymphocytes: There is a marked increase in plasma cells and B lymphocytes, indicating a more advanced immune response.
- Increased Collagenolytic Activity: The activity of collagen-degrading enzymes increases, leading to the breakdown of collagen fibers in the connective tissue.
- B Cell Subclasses: The B cells present in the established lesion are predominantly of the IgG1 and IgG3 subclasses, which are important for the immune response.
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Clinical Implications: This stage is characterized by chronic inflammation, and if left untreated, it can lead to further tissue destruction and the transition to advanced lesions.
IV. Advanced Lesion
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Characteristics:
- Loss of Connective Tissue Attachment: There is significant loss of connective tissue attachment to the teeth, which can lead to periodontal pocket formation.
- Alveolar Bone Loss: Extensive damage occurs to the alveolar bone, contributing to the overall loss of periodontal support.
- Extensive Damage to Collagen Fibers: The collagen fibers in the gingival tissues are extensively damaged, further compromising the structural integrity of the gingiva.
- Predominance of Plasma Cells: Plasma cells remain predominant, indicating ongoing immune activity and inflammation.
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Clinical Implications: This stage represents the transition from gingivitis to periodontitis, where irreversible damage can occur. Early intervention is critical to prevent further progression and loss of periodontal support.
Classification of Embrasures
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Type I Embrasures:
- Description: These are characterized by the presence of interdental papillae that completely fill the embrasure space, with no gingival recession.
- Recommended Cleaning Device:
- Dental Floss: Dental floss is most effective in cleaning Type I embrasures. It can effectively remove plaque and debris from the tight spaces between teeth.
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Type II Embrasures:
- Description: These embrasures have larger spaces due to some loss of attachment, but the interdental papillae are still present.
- Recommended Cleaning Device:
- Interproximal Brush: For Type II embrasures, interproximal brushes are recommended. These brushes have bristles that can effectively clean around the exposed root surfaces and between teeth, providing better plaque removal than dental floss in these larger spaces.
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Type III Embrasures:
- Description: These spaces occur when there is significant loss of attachment, resulting in the absence of interdental papillae.
- Recommended Cleaning Device:
- Single Tufted Brushes: Single tufted brushes (also known as end-tuft brushes) are ideal for cleaning Type III embrasures. They can reach areas that are difficult to access with traditional floss or brushes, effectively cleaning the exposed root surfaces and the surrounding areas.