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ETIOLOGY OF PERIODONTAL DISEASE, Study notes of Dentistry

Periodontal disease is an inflammation of the tooth-supporting structures, primarily caused by bacterial plaque accumulation. Gingivitis is the initial inflammation confined to the gums, while periodontitis results in damage to the periodontal ligament and bone. The disease begins with bacterial colonization of the mouth shortly after birth, forming biofilms on teeth. Key pathogens, such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, contribute to tissue destruction. Plaque and calculus (mineralized plaque) play major roles in disease progression. Contributing factors include systemic diseases, smoking, hormonal changes, and immune response. The accumulation of plaque, if not removed, leads to gingival inflammation and can progress to periodontitis, making oral hygiene critical for prevention.

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ETIOLOGY OF PERIODONTAL DISEASE
PERIODONTAL DISEASE
- Disease of the supporting structures of the teeth
- Usually caused by PLAQUE
- Gingivitis– inflammation confined to the gingiva
- Periodontitis- inflammatory disease resulting to the destruction of periodontal ligament and
alveolar bone
ARE FETUSES STERILE
- Yes
- Microorganisms are first acquired during birth
- After around 2 years, there are 1.3-10x more bacteria than human cells
COLONIZERS OF INFANT MOUTH
- Colonization of the oral cavity also starts close to the time of birth
- Within hours after birth -> facultative and aerobic bacteria
- Vaginal microbiota or skin microbiota
- Second day -> anaerobic bacteria
1. Streptococcus salivarius and Streptococcus mitis
Streptococcus mitis
- First and most dominant
2. Veillonella spp., Neisseria spp., Actinomyces spp., and Staphylococcus spp.
- Also among the first colonizers of the oral cavity
3. Streptococcus sanguinis, Lactobacillus spp., and Streptococcus oralis
Streptococcus mitis (right)
- After tooth eruption
4. Oral Streptococci - after first year of life
a. S. oralis
b. Streptococcus anginosus
c. Streptococcus mutans
d. Streptococcus sobrinus
e. Streptococcus gordonii
5. Fusobacterium spp., Prevotella spp.
- For young children
Are all oral bacteria bad?
- No
- Most oral bacteria are harmless commensals
- Disease can still occur
- Increased mass and/or pathogenicity
- Suppression of commensal or beneficial bacteria
- Reduced host response
- e.g. candida infections; s. sanguinis
- Periodontal microbiota both affects and is affected by the host
MICROBES AND ORAL CAVITY
- Bacteria adhere to surfaces
- Soft tissue surfaces are actively involved in the process of bacterial adhesion
- In periodontal pockets, studies have shown high numbers of bacteria attached to pocket
epithelial cells in vivo
- Areas of gingival inflammation are characterized by an increased number of adhering bacteria
- Bacteria adhere to hard surfaces as well
- Teeth and implants- unique
- Hard and non-shedding
- Ectodermal interruption- protected by junctional epithelium
- Crevicular fluid aids in protection of periodontal pocket
- Accumulation and metabolism of bacteria on these hard surfaces are primary causes of caries,
gingivitis, periodontitis, peri-implantitis, and, sometimes, bad breath
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ETIOLOGY OF PERIODONTAL DISEASE

PERIODONTAL DISEASE

  • Disease of the supporting structures of the teeth
  • Usually caused by PLAQUE
  • Gingivitis– inflammation confined to the gingiva
  • Periodontitis- inflammatory disease resulting to the destruction of periodontal ligament and alveolar bone ARE FETUSES STERILE
  • Yes
  • Microorganisms are first acquired during birth
  • After around 2 years, there are 1.3-10x more bacteria than human cells COLONIZERS OF INFANT MOUTH
  • Colonization of the oral cavity also starts close to the time of birth
  • Within hours after birth -> facultative and aerobic bacteria
  • Vaginal microbiota or skin microbiota
  • Second day -> anaerobic bacteria
  1. Streptococcus salivarius and Streptococcus mitis Streptococcus mitis
  • First and most dominant
  1. Veillonella spp., Neisseria spp., Actinomyces spp., and Staphylococcus spp.
    • Also among the first colonizers of the oral cavity
  2. Streptococcus sanguinis, Lactobacillus spp., and Streptococcus oralis Streptococcus mitis (right)
    • After tooth eruption
  3. Oral Streptococci - after first year of life a. S. oralis b. Streptococcus anginosus c. Streptococcus mutans d. Streptococcus sobrinus e. Streptococcus gordonii
  4. Fusobacterium spp., Prevotella spp.
    • For young children Are all oral bacteria bad?
  • No
  • Most oral bacteria are harmless commensals
  • Disease can still occur
  • Increased mass and/or pathogenicity
  • Suppression of commensal or beneficial bacteria
  • Reduced host response
  • e.g. candida infections; s. sanguinis
  • Periodontal microbiota both affects and is affected by the host MICROBES AND ORAL CAVITY
  • Bacteria adhere to surfaces
  • Soft tissue surfaces are actively involved in the process of bacterial adhesion
  • In periodontal pockets, studies have shown high numbers of bacteria attached to pocket epithelial cells in vivo
  • Areas of gingival inflammation are characterized by an increased number of adhering bacteria
  • Bacteria adhere to hard surfaces as well
  • Teeth and implants- unique
  • Hard and non-shedding
  • Ectodermal interruption- protected by junctional epithelium
  • Crevicular fluid aids in protection of periodontal pocket
  • Accumulation and metabolism of bacteria on these hard surfaces are primary causes of caries, gingivitis, periodontitis, peri-implantitis, and, sometimes, bad breath

MICROBES AND TEETH

  • There is a theory that teeth are the primary habitat for periodontopathogens.
    • A. actinomycetemcomitans and P. gingivalis disappeared from the oral cavity after tooth extraction
    • P. intermedia and other black-pigmented Prevotella spp. remained
  • According to another study, numbers just decrease
  • Caufield and Gibbons concluded that most of the S. mutans cells in the saliva or on the tongue are derived from the biofilm present on the teeth
  • Clinical evidence now shows that S. mutans can be detected in the mouths of predentate children, before the eruption of the first tooth BACTERIA AND BIOFILM Bacteria
  • Major struggle faced by bacteria lies in obtaining sufficient nutrients to support growth
  • In the 1920s, it was observed that bacteria growing on glass slides submerged in soil were different from bacteria that could be cultured in broth. Biofilm
  • Composed of microbial cells encased within a matrix of extracellular polymeric substances, such as polysaccharides, proteins, and nucleic acids
  • Up to 1000 times more resistant to antimicrobial agents
  • Beneficial and competitive
  • Heterogenous
  • Common features:
  • Biofilms contain bacterial microcolonies
  • Water channels
  • Most natural biofilms contain multiple species that engage in a wide range of physical, metabolic, and molecular interactions—MICROBIAL COMMUNITIES MICROBIAL COMMUNITIES
  • Potential Benefits:
  • Broader habitat range for growth
  • Increased metabolic diversity and efficiency
  • Enhanced tolerance of environmental stress, antimicrobial agents, and
  • the host defenses
  • Enhanced ability to cause disease
  • Biofilms have reduced susceptibility to antimicrobial agents PLAQUE Components of intercellular matrix
  • Derived from saliva, GCF, and bacterial products
  • Organic components
  • Polysaccharides
  • proteins (albumin)
  • glycoproteins- important component of pellicle
  • lipid material
  • DNA
  • Inorganic components
  • Calcium
  • Phosphorus
  • Trace amounts of other minerals such as
  • Sodium, potassium, and fluoride Plaque
  • An example of a biofilm
  • Heterogenous
  • Fluid-filled channels
  • Sessile microcolonies get nutrients by diffusion from the water channels
  • Biofilm matrix functions as a barrier
  • structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations
  • tough extracellular matrix Material alba
  • Soft accumulations of bacteria, food matter, and tissue cells that lack the organized structure of dental plaque Calculus
  • Hard deposit that forms via the mineralization of dental plaque and that is generally covered by a layer of unmineralized plaque
  • Facing soft tissue
    • Lack definite intermicrobial matrix
    • Gram-negative rods and cocci
    • Host cells
  • Within host tissue
    • In soft tissue
    • Within epithelial cells
    • In dentinal tubules SITE SPECIFICITY OF PLAQUE Site specificity of plaque is significantly associated with diseases of the periodontium Is it necessary to brush the gums?
  • Sometimes ACCUMULATION OF DENTAL PLAQUE BIOFILM
  1. Pellicle Formation
  • Layer of organic material covering ALL surfaces of the oral cavity
  • Made up of peptides, proteins, , glycoproteins, and other molecules that can function as adhesion sites (receptors) for bacteria
  • From saliva, GCF, or bacteria
  • 2 layers of pellicle
  • Thin basal layer
  • Thicker globular layer
  • Microorganisms interact directly with this conditioning film
  • Protein enzymatic activity
  • Biologic and chemical properties of the surface are altered
  1. Initial Adhesion/Attachment
  • Initial steps of transport and interaction with the surface are essentially nonspecific
  • Three phases: a. Bacterial transport b. Initial adhesion c. Strong attachment
  • Primary colonizers
  • Provide binding sites for other bacteria
  • First 4-8 hrs
  • Streptococcus spp.
  • Obligate aerobes
  • Haemophilus spp.
  • Neiserria spp.
  • Facultative anaerobes
  • Actinomyces spp.
  • Veilonella spp. a. Bacterial transport
  • To the surface of the pellicle
  • Through:
  • Brownian motion
  • Sedimentation of microorganisms
  • Liquid flow
  • Active bacterial movement (chemotactic activity)
  • More of salivary flow or mechanical contact b. Initial adhesion
  • initial reversible adhesion
  • Long- and short-range forces, including van der Waals attractive forces and electrostatic repulsive forces c. Strong attachment
  • Interaction between microbial adhesins and pellicle receptors
  1. Co-adhesion and Plaque Maturation
    • Metabolism of these bacteria that attach early modifies the local environment
    • Adhesins on the cell surface of more fastidious secondary colonizers, such as obligate anaerobes, bind to receptors on bacteria that are already attached
    • The composition of the biofilm becomes more diverse
    • Fusobacterium nucleatum
      • Can co-adhere to most oral bacteria
      • Acts as an important bridging organism between early and late colonizing species
    • Synthesis of extracellular polymers
    • Matrix can bind and retain molecules, including enzymes, and also retard the penetration of charged molecules into the biofilm (Allison 2003; Vu et al. 2009; Marsh et al. 2011). Detachment
  • On occasions, cells can detach to colonize elsewhere PLAQUE FORMATION
  • First 24 hours- plaque growth is negligible from a clinical viewpoint
  • After 4 days, an average of 30% of the total coronal tooth area will be covered with plaque
  • Starts at gingival margin and interdental spaces (areas protected from shear forces)
  • Extension in coronal direction
  • May also originate from grooves, cracks, perikymata, or pits
  • Rough intraoral surfaces accumulate and retain more plaque and calculus
  • Smoothing an intraoral surface decreases the rate of plaque formation Do older people form more plaque?
  • No. MICROBIAL COMPOSITION Microbes
  • Clinically healthy gingiva
  • Predominant gram(+) bacteria or facultative anaerobes

Bacteria must be able to:

  1. Colonize
  2. Exert VIRULENCE FACTORS
    • Produce factors that either damage the host tissue or lead to the host tissue damaging itself TISSUE DESTRUCTION Direct Tissue Destruction
  • Virulence factors themselves damage the host cell/tissue and the extracellular matrix
  • Virulence factors, such as toxins and proteases, released/produced by the bacteria degrade/destroy ECM or cause cell death or inhibit a host cell Indirect Tissue Destruction
  • Virulence factors induce host tissues to damage themselves
  • Virulence factor would induce a host cell (fibroblast, macrophage, etc.) to produce a chemical mediator that will degrade the ECM or cause death of host cell HOW DOES PLAQUE CAUSE PERIODONTITIS
  1. Non-specific plaque hypothesis
  • Direct relationship between the total number of accumulated bacteria and the amplitude of pathogenic effect
  1. Specific plaque hypothesis
  • A single pathogenic species is the cause of inflamed periodontal disease
  1. Virulent clonal theory
  • There can be different genotypes/strains or clones of the bacteria which are of varying pathogenicity.
  • by Socransky and Haffajee, 1992
  • 3 factors that favor the progression of Gingivitis to Periodontitis: a. Virulent Pathogen b. Local Environment c. Susceptible Host CALCULUS Dental Calculus (aka TARTAR)
  • Mineralized plaque
  • Formation depends on amount of plaque and secretion of salivary glands
  • SUPRAGINGIVAL CALCULUS
  • above the gingival margin
  • SUBGINGIVAL CALCULUS
  • below the gingival margin CLINICAL APPEARANCE AND DISTRIBUTION Supragingival Calculus
  • Can be creamy-whitish to dark yellow or even brownish mass of moderate hardness
  • Can usually be found on lingual surface of mandibular anteriors and buccal aspect of maxillary first molars Subgingival Calculus
  • Not visible unless gingiva has receded; can be found by tactile sensation
  • May be seen on radiographs if there is sufficient mass
  • Brownish-to-black calcified hard mass with a rough surface
  • Around 0.5mm calculus free zone coronal to the apical extension of the periodontal pocket (Lindhe, 2006) FORMATION AND STRUCTURE
  • ALWAYS preceded by formation of dental biofilm
  • Supragingival calculus-mineral salts in saliva
  • Subgingival calculus-mineral salts in inflammatory exudate

Liesegang Rings

  • Concentric rings
  • Reflect successive phases of mineralization
  • Numerous mineralization foci that coalesce
  • Crystalline in structure (calcium phosphate) ATTACHMENT
  • Pellicle also calcifies
  • Surface irregularities are penetrated (esp. in cementum)
  • Implants, restoration overhangs, cements, prosthesis
  • Calculus DO NOT cause periodontitis.
  • It provides a surface for plaque to accumulate.
  • It is the most prominent plaque-retentive factor (predisposing factor). -end-