1 Oral Cavity and Periodontal Disease Flashcards
1
Q
Peridontitis
A
a chronic inflammatory disease of the tissues supporting a tooth
2
Q
Tooth (p.2-6)
- Enamel
- Dentin
- Cementum
- Pulp
A
-
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.
3
Q
Supporting structures = peridontium (p.7-8)
- Gingiva
- Peridontal ligament
- Alveolar bone
A
-
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.
4
Q
Periodontitis (p.9-10)
- Gingivitis and periodontitis
- Gingivitis
- Periodontitis
A
- 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
5
Q
Pathogenesis of periodontitis (p.11-13)
- Pathogenesis of periodontitis (in order of increasing severity):
- Dental plaque
A
- 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.
6
Q
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/
A
- 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.
7
Q
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/
A
- 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.
8
Q
Periodontal disease risk factors (p.22-23)
A
- 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)
9
Q
Treatments for periodontal disease (p.24)
A
- 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.
-
Scaling will resolve the gingival inflammation by removing plaque, mineralized calcus and bacterial biofilm from the crown of the tooth.
- 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
10
Q
Periodontitis and systemic diseases:
All of these have in common an element of chronic inflammation.
A
- 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
11
Q
Periodontitis and systemic diseases: Cardiovascular disease (CVD) (p.27-32)
- presence of/
- P. gingivalis/
- Simply brushing twice a day versus once/
A
- 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.
12
Q
Periodontitis and systemic diseases:
Diabetes (p.33-34)
A
- 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.
13
Q
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/
A
- 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.
14
Q
Periodontitis and systemic diseases: Insurance companies (Aetna Dental)
A
- Treat Periodontal disease in patients with CVD
- Treat periodontal disease in pregnancy
15
Q
Tongue:
Surfaces (1.6, p.45)
- Dorsal
- Ventral
A
- Dorsal
- rough surface of tongue with papillae and taste buds
- stratified squamous epithelium with thin keratin
- Ventral
- undersurface of tongue
- stratified squamous nonkeratinized epithelium
