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Flashcards in 1 Oral Cavity and Periodontal Disease Deck (25)
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a chronic inflammatory disease of the tissues supporting a tooth


Tooth (p.2-6)

  • Enamel
  • Dentin
  • Cementum
  • Pulp

  • Enamel
    • The whitish crown that is visible above the gumline is covered with enamel.
    • 96% consists of the calcium phosphate crystal, hydroxyapatite.
    • Unlike bone, which is also mineralized with hydroxyapatite, enamel does not have any collagen.
  • Dentin
    • a mineralized collagen connective tissue underlying the enamel.
    • The dentin is less mineralized and therefore more flexible than enamel
    • necessary as a support for the crown of the tooth.
  • Cementum
    • a specialized bone-like substance that covers and protects the dentin where it projects into the root of the tooth.
    • junctions with the enamel at the border of the gumline.
    • softer than enamel or dentin.
    • Periodontal ligaments attach to cementum to anchor the tooth into the alveolar socket of the mandible or maxillary bones.
  • Pulp
    • the central part of the tooth.
    • a soft connective tissue with blood vessels and nerves.


Supporting structures = peridontium (p.7-8)

  • Gingiva
  • Peridontal ligament
  • Alveolar bone

  • Gingiva
    • faces the oral cavity
    • overlays the jaw bones.
    • a muscosa composed of a stratified squamous epithelium and lamina propria connective tissue.
    • Hemidesmosomes and a basal lamina attach to the tooth at the gum line.
  • Peridontal ligament
    • attaches cemuntum to bone.
    • Cells of the periodontal ligament include fibroblasts, cementoblasts, macrophages, osteoblasts and nerves.
    • anchors the tooth in the jaw
    • the source of new bone cells when the tooth moves within the bone (ex: eruption, braces)
  • Alveolar bone
    • forms the alveolar sockets around the tooth.


Periodontitis (p.9-10)

  • Gingivitis and periodontitis
  • Gingivitis
  • Periodontitis

  • Gingivitis and periodontitis
    • disease of the tissues of the periodontium
  • Gingivitis
    • a bacterial plaque induced inflammation of the gums without any loss of epithelial attachment.
    • As soon as the epithelial barrier is broken the severity of the disease changes.
  • Periodontitis
    • inflammation of gingiva
    • loss of epithelial attachment
    • irreversible damage to cementum, alveolar bone and/or the periodontal ligament


Pathogenesis of periodontitis (p.11-13)

  • Pathogenesis of periodontitis (in order of increasing severity):
  • Dental plaque

  • Pathogenesis of periodontitis (in order of increasing severity):
    • gingival redness and swelling
    • plaque to tartar
    • bleeding gums (spontaneous or at brushing)
    • deepening of the crevice between the tooth and the gingiva, resulting in the formation of a pathological periodontal pocket (measuring >3mm)
    • halitosis (sulfur-containing gases produced anaerobically)
  • Dental plaque
    • a biofilm of bacteria that adheres to the tooth surfaces adjacent to the gingival crevices.
    • can be any of 600 various gram-positive, aerobic, cocci.
    • removed by regular brushing.
    • buildup eventually produces a hard mineralized calculus or tartar that attaches to the enamel as well as the cementum.
      • can only be removed by professional dental cleaning.
    • When the gingiva becomes inflamed the gum pockets deepen and the bacterial flora shift to gram-negative, anaerobic rods, of which Porphyromonas gingivalis is the most common.


Pathogenesis of periodontitis (p.14-19)

  • Pathogenesis (starting from "long-in-the-tooth")
  • Cells of the humoral and cellular immune systems/
  • Osteoclasts are activated as/
  • Supporting structures of the teeth/

  • Pathogenesis
    • "long-in-the-tooth" -root exposure as the gingiva recedes
    • increased tooth mobility (due to bone loss)
    • tooth migration with impaired mastication
    • bone abscesses
    • tooth loss
  • Cells of the humoral and cellular immune systems react locally to produce pro-inflammatory cytokines (IL-1 & TNFalpha) and matrix metalloproteinases that further damage the attachment of the gingival epithelium to the cementum line.
  • Osteoclasts are activated as RANKL is increased and its inhibitor, osteoprotegrin, is decreased.
  • Supporting structures of the teeth, periodontal ligaments and alveolar bone, are compromised.


Pathogenesis of periodontitis (p.20-21)

  • Pathogenesis (starting from "systemic disease exacerbation")
  • Subsequent systemic responses/
  • transient bacteremia often occurs/
  • An autoimmune type of response may occur due to/
    • Antibodies to/
    • Antibodies to/

  • Pathogenesis
    • Systemic disease exacerbation
    • Molecular mimicry - autoimmunity
  • Eventual disruption of epithelial barrier allows entry of the bacteria and or bacterial products into the systemic circulation.
  • Subsequent systemic responses include the production of C-reactive protein and activation of vascular endothelium (E-selectin).
    • these particular strains of oral bacteria access the blood 
  • transient bacteremia often occurs during dental cleaning, tooth brushing, even vigorous chewing.
    • Thus the need for prophylactic antibiotics during dental procedures for any patient with an artificial heart valve, organ transplant or joint replacement.
  • An autoimmune type of response may occur due to homology between bacterial antigens and normal human proteins.
    • Antibodies to the bacterial heat shock protein, GroEL, of the hsp60 family, cross-react with the human hsp60.
    • Antibodies to hsp60 have been implicated in the pathogenesis of lupus erythematosus and coronary heart disease.


Periodontal disease risk factors (p.22-23)

  • poor tooth hygiene and plaque
  • specific oral bacteria, Porphyromonas gingivalis
  • environmental exposures ( esp cigarette smoke)
  • decreased access to fluorinated water
  • systemic illness - diabetes mellitus, cancer, HIV
  • genetics (reports of gene variation in the interleukin-1 gene cluster)
  • mental anxiety or depression
  • obesity
  • medications that decrease saliva (xerostomia)-
    • anticholinergics, antidepressants, antipsychotics, diuretics, antihypertensives, antihistamines and narcotics
  • hormonal changes - pregnancy, puberty, menopause and menstruation
  • elderly (cumulative exposure to risk factors)


Treatments for periodontal disease (p.24)

  • Brush & floss
  • Dental cleaning
    • Scaling will resolve the gingival inflammation by removing plaque, mineralized calcus and bacterial biofilm from the crown of the tooth.
      • This is performed at your 6 month cleaning.
    • Once the gingival attachment has been compromised, root planning is a more extensive procedure to remove buildup from the cementum surrounding the root of the tooth.
      • The more porous cementum is susceptible to bacterial invasion and mineralization.
  • Systemic antibiotics
    • questionable effectiveness on tooth biofilm
  • Doxycycline
    • given in low doses this tetracycline antibiotic acts as a matrix metalloproteinase inhibitor
    • the only FDA-approved host-modulating drug for the treatment of periodontitis.
  • Vaccine
    • against P. gingivalis 
  • Surgery
    • for severe bone loss


Periodontitis and systemic diseases:
All of these have in common an element of chronic inflammation.

  • Atherosclerosis, CVD
  • Diabetes mellitus
  • Pregnancy complications: preterm birth, low birth weight
  • Respiratory disease -COPD, pneumonia
  • Osteoporosis
  • Impaired mastication & nutrition
  • Hypertension
  • Arthritis
  • Inflammatory bowel disease
  • Psoriasis


Periodontitis and systemic diseases:
Cardiovascular disease (CVD) (p.27-32)

  • presence of/
  • P. gingivalis/
  • Simply brushing twice a day versus once/

  • presence of oral bacteria, Porphyromonas gingivalis, in atherosclerotic plaques.
  • P. gingivalis upregulates the expression of toll-like receptors (TLR2 and TLR4) on macrophages and endothelial cells, which , in turn, activate the innate immune responses to secrete pro-inflammatory cytokines.
    • This contributes to the loss of arterial smooth muscle in the media and the thickening of the connective tissue component of the intima.
  • Simply brushing twice a day versus once can decrease the amount of circulating C-reactive protein, a marker for systemic inflammation that is increased in cardiovascular disease.


Periodontitis and systemic diseases:
Diabetes (p.33-34)

  • As the Pima’s diet changed to high % fat, so also did the rates of diabetes and periodontal disease.
  • Simply treating the periodontal disease improved glycemic control in Pima diabetics.


Periodontitis and systemic diseases:
Pregnancy complications (p.35-41)

  • P. gingivalis can also be found in/
  • toll-like receptor activation/
  • PGE2 is the signal for/
  • COX enzymes/
  • pregnant women with periodontal disease had better outcomes simply by/

  • P. gingivalis can also be found in the amniotic fluid in pregnant women with periodontal disease.
  • toll-like receptor activation increases in IL-1 (general inflammation) and prostaglandin E2 (PGE2)
  • PGE2 is the signal for gap junctions to begin to form in the uterine myometrium.
  • COX enzymes, and therefore prostaglandin production, are suppressed throughout pregnancy, until just before partuition.
  • pregnant women with periodontal disease had better outcomes simply by using an antibacterial mouth rinse.


Periodontitis and systemic diseases:
Insurance companies (Aetna Dental)

  • Treat Periodontal disease in patients with CVD
  • Treat periodontal disease in pregnancy


Surfaces (1.6, p.45)

  • Dorsal
  • Ventral

  • Dorsal
    • rough surface of tongue with papillae and taste buds
    • stratified squamous epithelium with thin keratin
  • Ventral
    • undersurface of tongue
    • stratified squamous nonkeratinized epithelium


Musculature (1.6, p.46)

  • ?
  • intrinsic
  • extrinsic

  • ?
    • fine skeletal muscle bundles
    • multidirectional
    • small motor units
  • intrinsic
    • origin & insertion within tongue
  • extrinsic
    • origin outside of tongue
    • insertion into tongue


Dorsal papillae (1.6, p.47-50)

  • Filiform papillae
  • Fungiform papillae
  • Circumvallate papillae

  • Filiform papillae
    • keratinized peaks,
    • aid in mastication
  • Fungiform papillae
    • “mushroom” shaped
    • do not protrude above tongue surface
    • smooth keratinized surface
    • scattered over surface of dorsum
    • taste buds in the lateral sides
  • Circumvallate papillae
    • 8-12 in a V-shaped line at the rear of the tongue
    • large, easily visible
    • smooth keratinized surface
    • deep lateral sulcus with taste buds
    • dermal Von Ebner’s glands (serous glands) release watery
    • enzyme enriched secretions


Taste buds (p.51)

  • Neuroepithelial cells
  • Sustentacular cells
  • Basal cells

  • Neuroepithelial cells
    • with taste hairs (receptors) projecting through pore of taste bud
    • darker nuclei
  • Sustentacular cells
    • euchromatic nuclei
    • glycosaminoglycan secretions to flush out pore
  • Basal cell
    • precursors


Taste molecules (p.53)

  • Molecules
  • Where they function through / work with

  • Molecules
    • Sweet (CHO; gustducin)
    • Sour (H+)
    • Bitter (various, ~2 dozen bitter ligands)
    • Salty (Na+)
    • Umami (glutamic acid)
  • Where they function through / work with
    • Sweet, bitter and umami function through G-protein coupled receptors (Galphaq).
    • Salty and sour work with ion channels.


Taste buds innervation

  • anterior tongue
  • posterior tongue & pharynx
  • larynx
  • palate

  • anterior tongue
    • chorda tympany of facial nerve
  • posterior tongue & pharynx
    • glossopharyngeal nerve
  • larynx
    • vagus – superior laryngeal branch
  • palate
    • trigeminal, facial & glossopharyngeal nerves


Salivary glands:
Functions (1.7, p.55)

  • lubrication
  • antibacterial
    • lysozyme, lactoferrin, secretory IgA
    • all from intercalated duct
  • remineralize teeth enamel
  • buffer oral cavity
  • aqueous solvent for taste molecules
  • salivary amylase & lipase


Salivary glands:
General structure (1.7, p.57)

  • Compound tubuloacinar merocrine exocrine glands
  • How they secrete
  • Excrete via ducts:
    • Intercalated ducts
    • Striated or Secretory Intralobular ducts
    • Excretory ducts

  • Compound tubuloacinar merocrine exocrine glands, with myoepithelial cells
    • Serous acini
    • Mucous acini
  • Secrete in a stimulus-dependent fashion
    • in contrast, minor salivary glands are constitutive secretors
  • Excrete via ducts:
    • Intercalated ducts
      • smaller diameter than the secretory acinus;
      • secrete antibacterials
    • Striated or Secretory Intralobular ducts
      • diameter approximately equal to a secretory acinus,
      • basolateral striations due to mitochondria,
      • basal ion pumping,
      • this duct actually alters the secretions that pass through it via ion pumps
    • Excretory ducts
      • large, often stratified cuboidal or stratified columnar epithelium,
      • in connective tissue septa


Salivary glands:

  • Parasympathetic
  • Sympathetic

  • Parasympathetic
    • watery, protein-rich
    • Ach --> muscarinic receptors --> increase IP3/DAG --> increase Ca2+ --> secretion
  • Sympathetic
    • Norepinephrine = viscous, mucus-rich


Salivary glands:
Specific glands (p.59-62)

  • Parotid Gland
    • % of oral cavity secretions
    • Location
    • Secretions
  • Submandibular Gland
    • % of oral cavity secretions
    • Location
    • Secretions
  • Sublingual Gland
    • % of oral cavity secretions
    • Location
    • Secretions

  • Parotid Gland
    • 25% of oral cavity secretions
    • Location – between ear & the ramus of the mandible
    • Secretions – serous
  • Submandibular Gland
    • 60-65% of secretions
    • Location – floor of the mouth, just inside mandible
    • Secretions – 80% serous, 20% mucous, with serous demilunes
  • Sublingual Gland 
    • 10% of secretions
    • Location – base of the tongue
    • Secretions – 20% serous, 80% mucous, with serous demilunes


Sjogren's syndrome (p.63)

  • Autoimmune attack of exocrine glands producint tears & saliva
  • 90% are rheumatoid factor positive (RF+)
  • ANA+ (type SSB/La) also high
  • Autoantigen = alpha-Fodrin
    • A non-erythrocyte spectrin