Finger Rests in Dental Instrumentation

Use of finger rests is essential for providing stability and control during procedures. A proper finger rest allows for more precise movements and reduces the risk of hand fatigue.

Importance of Finger Rests

• Stabilization: Finger rests serve to stabilize the hand and the instrument, providing a firm fulcrum that enhances control during procedures.
• Precision: A stable finger rest allows for more accurate instrumentation, which is crucial for effective treatment and patient safety.
• Reduced Fatigue: By providing support, finger rests help reduce hand and wrist fatigue, allowing the clinician to work more comfortably for extended periods.

Types of Finger Rests

1. Conventional Finger Rest:

   • Description: The finger rest is established on the tooth surfaces immediately adjacent to the working area.
   • Application: This is the most common type of finger rest, providing direct support for the hand while working on a specific tooth. It allows for precise movements and control during instrumentation.

2. Cross Arch Finger Rest:

   • Description: The finger rest is established on the tooth surfaces on the other side of the same arch.
   • Application: This technique is useful when working on teeth that are not directly adjacent to the finger rest. It provides stability while allowing access to the working area from a different angle.

3. Opposite Arch Finger Rest:

   • Description: The finger rest is established on the tooth surfaces of the opposite arch (e.g., using a mandibular arch finger rest for instrumentation on the maxillary arch).
   • Application: This type of finger rest is particularly beneficial when accessing the maxillary teeth from the mandibular arch, providing a stable fulcrum while maintaining visibility and access.

4. Finger on Finger Rest:

   • Description: The finger rest is established on the index finger or thumb of the non-operating hand.
   • Application: This technique is often used in areas where traditional finger rests are difficult to establish, such as in the posterior regions of the mouth. It allows for flexibility and adaptability in positioning.

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.

Components of Gingival Crevicular Fluid (GCF) and Matrix Metalloproteinases (MMPs)

Gingival crevicular fluid (GCF) is a serum-like fluid found in the gingival sulcus that plays a significant role in periodontal health and disease. Understanding its composition, particularly glucose and protein content, as well as the role of matrix metalloproteinases (MMPs) in tissue remodeling, is essential for dental professionals.

Composition of Gingival Crevicular Fluid (GCF)

1. Glucose and Hexosamines:

   • GCF contains compounds such as glucose, hexosamines, and hexuronic acid.
   • Glucose Levels:
     • Blood glucose levels do not correlate with GCF glucose levels; in fact, glucose concentration in GCF is three to four times greater than that in serum.
     • This elevated glucose level is interpreted as a result of the metabolic activity of adjacent tissues and the influence of local microbial flora.

2. Protein Content:

   • The total protein content of GCF is significantly less than that of serum.
   • This difference in protein concentration reflects the unique environment of the gingival sulcus and the specific functions of GCF in periodontal health.

Matrix Metalloproteinases (MMPs)

1. Definition and Function:

   • MMPs are a family of proteolytic enzymes that degrade extracellular matrix molecules, including collagen, gelatin, and elastin.
   • They are produced by various cell types, including:
     • Neutrophils
     • Macrophages
     • Fibroblasts
     • Epithelial cells
     • Osteoblasts and osteoclasts

2. Classification:

   • MMPs are classified based on their substrate specificity, although it is now recognized that many MMPs can degrade multiple substrates. The classification includes:
     • Collagenases: e.g., MMP-1 and MMP-8 (break down collagen)
     • Gelatinases: Type IV collagenases
     • Stromelysins
     • Matrilysins
     • Membrane-type metalloproteinases
     • Others

3. Activation and Inhibition:

   • MMPs are secreted in an inactive form (latent) and require proteolytic cleavage for activation. This activation is facilitated by proteases such as cathepsin G produced by neutrophils.
   • Inhibitors: MMPs are regulated by proteinase inhibitors, which possess anti-inflammatory properties. Key inhibitors include:
     • Serum Inhibitors:
       • α1-antitrypsin
       • α2-macroglobulin (produced by the liver, inactivates various proteinases)
     • Tissue Inhibitors:
       • Tissue inhibitors of metalloproteinases (TIMPs), with TIMP-1 being particularly important in periodontal disease.
   • Antibiotic Inhibition: MMPs can also be inhibited by tetracycline antibiotics, leading to the development of sub-antimicrobial formulations of doxycycline as a systemic adjunctive treatment for periodontitis, exploiting its anti-MMP properties.

Merkel Cells

1. Location and Function:
   • Merkel cells are located in the deeper layers of the epithelium and are associated with nerve endings.
   • They are connected to adjacent cells by desmosomes and are identified as tactile receptors.
   • These cells play a role in the sensation of touch and pressure, contributing to the sensory functions of the oral mucosa.

Clinical Implications

1. GCF Analysis:

   • The composition of GCF, including glucose and protein levels, can provide insights into the inflammatory status of the periodontal tissues and the presence of periodontal disease.

2. Role of MMPs in Periodontal Disease:

   • MMPs are involved in the remodeling of periodontal tissues during inflammation and disease progression. Understanding their regulation and activity is crucial for developing therapeutic strategies.

3. Therapeutic Applications:

   • The use of sub-antimicrobial doxycycline as an adjunctive treatment for periodontitis highlights the importance of MMP inhibition in managing periodontal disease.

4. Sensory Function:

   • The presence of Merkel cells in the gingival epithelium underscores the importance of sensory feedback in maintaining oral health and function.

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.

Pathogens Implicated in Periodontal Diseases

Periodontal diseases are associated with a variety of pathogenic microorganisms. Below is a list of key pathogens implicated in different forms of periodontal disease, along with their associations:

General Pathogens Associated with Periodontal Diseases

• Actinobacillus actinomycetemcomitans:

  • Strongly associated with destructive periodontal disease.

• Porphyromonas gingivalis:

  • A member of the "black pigmented Bacteroides group" and a significant contributor to periodontal disease.

• Bacteroides forsythus:

  • Associated with chronic periodontitis.

• Spirochetes (Treponema denticola):

  • Implicated in various periodontal conditions.

• Prevotella intermedia/nigrescens:

  • Also belongs to the "black pigmented Bacteroides group" and is associated with several forms of periodontal disease.

• Fusobacterium nucleatum:

  • Plays a role in the progression of periodontal disease.

• Campylobacter rectus:

  • These organisms include members of the new genus Wolinella and are associated with periodontal disease.

Principal Bacteria Associated with Specific Periodontal Diseases

1. Adult Periodontitis:

   • Porphyromonas gingivalis
   • Prevotella intermedia
   • Bacteroides forsythus
   • Campylobacter rectus

2. Refractory Periodontitis:

   • Bacteroides forsythus
   • Porphyromonas gingivalis
   • Campylobacter rectus
   • Prevotella intermedia

3. Localized Juvenile Periodontitis (LJP):

   • Actinobacillus actinomycetemcomitans
   • Capnocytophaga

4. Periodontitis in Juvenile Diabetes:

   • Capnocytophaga
   • Actinobacillus actinomycetemcomitans

5. Pregnancy Gingivitis:

   • Prevotella intermedia

6. Acute Necrotizing Ulcerative Gingivitis (ANUG):

   • Prevotella intermedia
   • Intermediate-sized spirochetes

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)