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Periodontology

Necrotizing Ulcerative Gingivitis (NUG)

Necrotizing Ulcerative Gingivitis (NUG), also known as Vincent's disease or trench mouth, is a severe form of periodontal disease characterized by the sudden onset of symptoms and specific clinical features.

Etiology and Predisposing Factors

  • Sudden Onset: NUG is characterized by a rapid onset of symptoms, often following debilitating diseases or acute respiratory infections.
  • Lifestyle Factors: Changes in living habits, such as prolonged work without adequate rest, poor nutrition, tobacco use, and psychological stress, are frequently noted in patient histories .
  • Smoking: Smoking has been identified as a significant predisposing factor for NUG/NDP .
  • Immune Compromise: Conditions that compromise the immune system, such as poor oral hygiene, smoking, and emotional stress, are major contributors to the development of NUG .

Clinical Presentation

  • Symptoms: NUG presents with:
    • Punched-out, crater-like depressions at the crest of interdental papillae.
    • Marginal gingival involvement, with rare extension to attached gingiva and oral mucosa.
    • Grey, pseudomembranous slough covering the lesions.
    • Spontaneous bleeding upon slight stimulation of the gingiva.
    • Fetid odor and increased salivation.

Microbiology

  • Mixed Bacterial Infection: NUG is caused by a complex of anaerobic bacteria, often referred to as the fusospirochetal complex, which includes:
    • Treponema vincentii
    • Treponema denticola
    • Treponema macrodentium
    • Fusobacterium nucleatum
    • Prevotella intermedia
    • Porphyromonas gingivalis

Treatment

  1. Control of Acute Phase:

    • Clean the wound with an antibacterial agent.
    • Irrigate the lesion with warm water and 5% vol/vol hydrogen peroxide.
    • Prescribe oxygen-releasing mouthwash (e.g., hydrogen peroxide DPF, sodium perborate DPF) to be used thrice daily.
    • Administer oral metronidazole for 3 to 5 days. If sensitive to metronidazole, prescribe penicillin; if sensitive to both, consider erythromycin or clindamycin.
    • Use 2% chlorhexidine in select cases for a short duration.
  2. Management of Residual Condition:

    • Remove predisposing local factors (e.g., overhangs).
    • Perform supra- and subgingival scaling.
    • Consider gingivoplasty to correct any residual gingival deformities.

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)

Alveolar Process

The alveolar process is a critical component of the dental anatomy, providing support for the teeth and playing a vital role in periodontal health. Understanding its structure and composition is essential for dental professionals in diagnosing and treating various dental conditions.

Components of the Alveolar Process

  1. External Plate of Cortical Bone:

    • Description: The outer layer of the alveolar process is composed of cortical bone, which is dense and forms a protective outer shell.
    • Composition:
      • Formed by Haversian bone, which consists of organized structures called osteons.
      • Compacted bone lamellae contribute to the strength and stability of the alveolar process.
  2. Alveolar Bone Proper:

    • Description: The inner socket wall of the alveolar process is known as the alveolar bone proper.
    • Radiographic Appearance:
      • It is seen as the lamina dura on radiographs, appearing as a radiopaque line surrounding the tooth roots.
    • Histological Features:
      • Contains a series of openings known as the cribriform plate.
      • These openings allow neurovascular bundles to connect the periodontal ligament with the central component of the alveolar bone, which is the cancellous bone.
  3. Cancellous Bone:

    • Description: Located between the external cortical bone and the alveolar bone proper, cancellous bone consists of trabecular structures.
    • Function:
      • Acts as supporting alveolar bone, providing strength and flexibility to the alveolar process.
    • Interdental Septum:
      • The interdental septum consists of cancellous supporting bone enclosed within a compact border, providing stability between adjacent teeth.

Structural Characteristics

  • Facial and Lingual Portions:
    • Most of the facial and lingual portions of the tooth socket are formed by compact bone alone, providing robust support for the teeth.
  • Cancellous Bone Distribution:
    • Cancellous bone surrounds the lamina dura in specific areas:
      • Apical Areas: The region at the tip of the tooth root.
      • Apicolingual Areas: The area where the root meets the lingual surface.
      • Interradicular Areas: The space between the roots of multi-rooted teeth.

Periodontics: Dental specialty deals with the supporting and surrounding tissues of the teeth. 

1. Periodontium: tissues that invest and support teeth Includes Gingiva, Alveolar mucosa  Cementum, Periodontal ligament, Alveolar bone, Support bone

2. Periodontal disease: changes to periodontium beyond normal range of variation

a. Specific plaque hypothesis: specific microorganisms cause periodontal disease; mostly anaerobes. Three implicated: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteriodes forsythus

b. Contributing factors: often a combination of factors

i. Local: calculus (tarter, home for bacteria, ­ with age), traumatic occlusal forces, caries (root caries), overhangs and over-contoured restorations, open contacts with food impaction, missing/malaligned teeth

Invasion of biological width: from free gingival margin -> attached gingiva need ~ 3 mm.  If enter this area -> problems (e.g., resorption)

ii. Host factors: exacerbate periodontal problems; e.g., smoking/tobacco use, pregnancy and puberty (hormonal changes, ­ blood vessel permeability), stress, poor diet

iii.Medications: often -> tissue overgrowth; e.g., oral contraceptives, antidepressants, heart medicines, transplant anti-rejection drugs

iv.Systemic diseases: e.g., diabetes, immunosuppression

B. Gingivitis: inflammation of gingiva; ­ with age; generally reversible

C. Periodontitis: inflammation of supporting tissues of teeth, characterized by loss of attachment (PDL) and bone; generally irreversible

D.       Periodontal disease as risk factor for systemic diseases:

1.        Causes difficulty for diabetics to control blood sugar

2.        Pregnant women with periodontal disease ~ 7 times more likely to have premature and/or underweight baby

3.        Periodontal diseased patients may be at risk for heart disease

Gingival Crevicular Fluid (GCF)

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.

Dental Calculus

Dental calculus, also known as tartar, is a hard deposit that forms on teeth due to the mineralization of dental plaque. Understanding the composition and crystal forms of calculus is essential for dental professionals in diagnosing and managing periodontal disease.

Crystal Forms in Dental Calculus

  1. Common Crystal Forms:

    • Dental calculus typically contains two or more crystal forms. The most frequently detected forms include:
      • Hydroxyapatite:
        • This is the primary mineral component of both enamel and calculus, constituting a significant portion of the calculus sample.
        • Hydroxyapatite is a crystalline structure that provides strength and stability to the calculus.
      • Octacalcium Phosphate:
        • Detected in a high percentage of supragingival calculus samples (97% to 100%).
        • This form is also a significant contributor to the bulk of calculus.
  2. Other Crystal Forms:

    • Brushite:
      • More commonly found in the mandibular anterior region of the mouth.
      • Brushite is a less stable form of calcium phosphate and may indicate a younger calculus deposit.
    • Magnesium Whitlockite:
      • Typically found in the posterior areas of the mouth.
      • This form may be associated with older calculus deposits and can indicate changes in the mineral composition over time.
  3. Variation with Age:

    • The incidence and types of crystal forms present in calculus can vary with the age of the deposit.
    • Younger calculus deposits may have a higher proportion of brushite, while older deposits may show a predominance of hydroxyapatite and magnesium whitlockite.

Clinical Significance

  1. Understanding Calculus Formation:

    • Knowledge of the crystal forms in calculus can help dental professionals understand the mineralization process and the conditions under which calculus forms.
  2. Implications for Treatment:

    • The composition of calculus can influence treatment strategies. For example, older calculus deposits may be more difficult to remove due to their hardness and mineral content.
  3. Assessment of Periodontal Health:

    • The presence and type of calculus can provide insights into a patient’s oral hygiene practices and periodontal health. Regular monitoring and removal of calculus are essential for preventing periodontal disease.
  4. Research and Development:

    • Understanding the mineral composition of calculus can aid in the development of new dental materials and treatments aimed at preventing calculus formation and promoting oral health.

Microbes in Periodontics

Bacteria Associated with Periodontal Health

  • Primary Species:

    • Gram-Positive Facultative Bacteria:
      • Streptococcus:
        • S. sanguis
        • S. mitis
        • A. viscosus
        • A. naeslundii
      • Actinomyces:
        • Beneficial for maintaining periodontal health.
  • Protective or Beneficial Bacteria:

    • Key Species:
      • S. sanguis
      • Veillonella parvula
      • Corynebacterium ochracea
    • Characteristics:
      • Found in higher numbers at inactive periodontal sites (no attachment loss).
      • Low numbers at sites with active periodontal destruction.
      • Prevent colonization of pathogenic microorganisms (e.g., S. sanguis produces peroxide).
  • Clinical Relevance:

    • High levels of C. ochracea and S. sanguis are associated with greater attachment gain post-therapy.

Microbiology of Chronic Plaque-Induced Gingivitis

  • Composition:

    • Roughly equal proportions of:
      • Gram-Positive: 56%
      • Gram-Negative: 44%
      • Facultative: 59%
      • Anaerobic: 41%
  • Predominant Gram-Positive Species:

    • S. sanguis
    • S. mitis
    • S. intermedius
    • S. oralis
    • A. viscosus
    • A. naeslundii
    • Peptostreptococcus micros
  • Predominant Gram-Negative Species:

    • Fusobacterium nucleatum
    • Porphyromonas intermedia
    • Veillonella parvula
    • Haemophilus spp.
    • Capnocytophaga spp.
    • Campylobacter spp.
  • Pregnancy-Associated Gingivitis:

    • Increased levels of steroid hormones and P. intermedia.

Chronic Periodontitis

  • Key Microbial Species:

    • High levels of:
      • Porphyromonas gingivalis
      • Bacteroides forsythus
      • Porphyromonas intermedia
      • Campylobacter rectus
      • Eikenella corrodens
      • Fusobacterium nucleatum
      • Actinobacillus actinomycetemcomitans
      • Peptostreptococcus micros
      • Treponema spp.
      • Eubacterium spp.
  • Pathogenic Mechanisms:

    • P. gingivalis and A. actinomycetemcomitans can invade host tissue cells.
    • Viruses such as Epstein-Barr Virus-1 (EBV-1) and human cytomegalovirus (HCMV) may contribute to bone loss.

Localized Aggressive Periodontitis

  • Microbiota Characteristics:
    • Predominantly gram-negative, capnophilic, and anaerobic rods.
    • Almost all localized juvenile periodontitis (LJP) sites harbor A. actinomycetemcomitans, which can comprise up to 90% of the total cultivable microbiota.

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