Perio II, Exam II

systemic risk factors

conditions/diseases that increase individuals susceptibilities to periodontal infection by modifying/amplifying host response to bacterial infection

diabetes

chronic disease which body doesn't produce insulin or properly use insulin
undiagnosed is the only time its a perio risk factor

insulin

hormone used to convert sugars, starches, food into energy

diabetic pts and perio disease

3x more likely to develop
glucose increases=perio health decreases
poor response to NSPT/surgery
increased risk acute perio abscess, attachment loss, bone loss

hypergylcemia and perio

increased glucose in crevicular fluid
bacteria thrive & alter biofilm colonies

diabetes and immune response

reduced PMN function & defective chemotaxis allow bacteria to grow
significantly higher IL-1B and PGE2
Hyperglycemia affects collagen synthesis, maturation, maintanence
excessive formation of accumulated gycaltion end-products

AGE and diabetes

derived from reaction of glucose/proteins
involved in biological process relating to collagen turnover
collagen cross linked w/ AGE formation
less likely to have repair normally

non perio oral complications of diabetes

reduced salivary flow
candidiasis
burning mouth/tongue
perio abscess

leukemia

cancer beginning in blood cells
abnormal WBC that don't function properly
crowd out normal WBC, RBC and platelets
types: chronic or acute and myeloid/lymphoid

myeloid leukemia

myelogenous
affects myeloid cells

lymphoid leukemia

affects lymphoid cells
lymphocytic

medical treatment

complex/varies on type, age, extent, symptoms
chemo
radiation
bone marrow transplant
biological therapy

chemotherapy effects

suppresses growth of bad and good cells
effects cell with higher turnover rate (mucosa)
can cause sensitive mouth that is easily infected and likely to bleed

oral complications of leukemia

associated gingivitis
swollen, glazed, spongey tissue
red/deep purple
spontaneous bleeding of lips, gingiva, tongue
gingival enlargement: papilla to margin to attached
oral mucositis
xerostomia

oral mucositis

inflammation caused by chemo killing rapidly dividing cells
mucosa lifespan is only 10-14 days so cells are dividing faster than they can regrow
causes sloughing & ulcerations

xerostomia caused by radiation

causes damage to salivary glands

implications of leukemia for DH

early diagnosis because first sign is in mucosa
look for: gingival swelling with no reason combined with facial swelling, tiredness, poor appetite, lethargy, skeletal pain

RDH involvement in leukemia

immunosuppression may cause serious oral infections
necessary care before, during, after chemo to prevent poor oral condition & further systemic disease
use soft toothbrush or dental sponge
chlorohexidine for mucositis

oral capsaicin

temporary relief for mucositis pain
active ingredient: chilli pepper
anti inflammatory
monitor use bc has sugar

what to eat with mouth sores

soften food with liquid- broth, milk
add olive oil to food to make slippery
use blender to mash fruit and veggies
use saliva substitute
smoothies, soup, mashed potatoes

what to avoid with mouth sores

caffeine
alcohol
tobacco
alcohol rinse
acidic food- orange, grapefruit, lemon
spicy food
salty
raw veggies
rice, chips, bread, cakes

HIV

causes weak immune system

perio and HIV

Linear gingival erythema
Necrotizing perio disease

linear gingival erythema

LGE
2-3mm gingival marginal band of intense erythema in free gingiva
may extend to attached
may be localized but commonly generalized
lack of response important in diagnosis

LGE RDH implications

monitored to prevent permanent damage
frequent recare
initial tx: cholorhexidine, DHT, antibiotics

drugs interactions with antiretroviral therapies

flucanozole, ketoconazole, intraconozole, metronidazole, ciprofloxicin, midazolam, trialzam

hormone flucations

puberty, pregnancy, menopause

puberty

increased levels of estradiol for females, testostorone for male
sex hormones cause blood circulation to gingiva and response to irritants

clinical features of puberty

end when puberty does
accumulation of plaque
red, inflammed, BOP
reversible with meticulous care

DH implications of puberty

daily self-care
professional care
recommend: antimicrobial rinse, antibiotic, perio therapy

pregnancy

inflammation increases with ANY plaque
increases in 2/3 trimester
enhanced estrogen=sensitive to biofilm
produce: estradoil, estriol, progesterone

elevated progesterone during pregnancy

enhance capillary permeability
dilation=increased exudate and edema

change in immune system for pregnant women

high levels of estrogen/progesterone suppress response to biofilm
PMN chemotaxis & phagocytosis reported to be depressed **less helpers!!

pregnancy gingivitis

gingival inflammation initiated by plaque biofilm and exacerbated by hormonal changes in the second and third trimesters of pregnancy

Pregnancy-associated pyogenic granuloma

localized overgrowth in interdental gingiva
benign, not painful
surgically removed if continues after pregnancy ends
probe depths, BOP and crevicular fluids increased

implications for DH of pregnancy

education on homecare, LA, xray safety
prenatal vitamins, folic acid to eliminate cleft
erosion from sickness: suggest small meals, avoid brushing after vomitting

menopause/post menopause

periodontium effected by hormones
dry mouth, burning mouth
decline of estrogen: cause bone loss
gingivostomatitis: gingiva bleed rapidly, abnormally pale, dry, shiny, erythemous

osteoporosis

reduction of bone mass resulting in susceptibility to fracture
does NOT initiate periodontitis but an adjunct

osteopenia

lower than average bone density no increase in susceptibility to fracture

bisphosphonates

commonly prescribed to inhibit bone resorption of systemic osteoporosis

osteonecrosis of the jaw

painful exposed bone in mouth that fail to heal after procedure
increased risk of bone and tooth loss

implication of DH menopause

calcium supplement
weight bearing excercise
meticulous oral care
estrogen+biofilm=host response=increased bone resorbing cytokines, monocytes, macrophages, osteoblasts

genetic risk factors

Chediak-Higashi syndrome
leukyocyte adhesion defiency syndrome
job syndrome
Papillon-Lefevre syndrome
Chron disease
acute monocyte leukemia
cyclic & chronic neutropenia-PMN malfunction more susceptible to perio

down syndrome & perio

orofacial features- under developed midfacial region (lip, tongue, palate)
maxilla, nose are smaller
proganathic occlusion
mouth breathing, tongue protrusion
strong gag reflex
palate highly vaulted
drooping lip
drooling

malocclusion and down syndrome

delayed eruption of permenant teeth
underdevelopment of maxilla
open bite=disease/caries

medical problems of pt w down syndrome

congenital heart defect
GI abnormalities
infection
respiratory problem
child leukemia
abnormal PMN

perio implications of down syndrome

often develop severe, aggressive perio
plaque, deep perio pocket, inflammation
lose teeth in teens
missing one salivary gland

down syndrome and immune response

impaired PMN chemotaxis/phagocytosis
impaired cellular motility of gingival fibroblasts that promote healing/regeneration

sugar containing meds

cough drops, liquid meds, syrups, tonics, chewables, antacids tablets
cause: enamel demineralization

salivary flow and meds

400+ meds cause dry mouth

drug induced gingival enlargement

anticonvulsants, immunosuppresants, Ca channel blockers
fibroblasts overproduce collagen matrix stimulated by inflammation

anticonvulsants

tx of epilespy
gingival overgrowth
interpapillae become firm
good biofilm control: pink, firm, rubbery
poor biofilm control: red, edematous, spongey

acute periodontal conditions

conditions commonly characterized by having sudden onset & rapid course of progression
Pain/discomfort
may be unrelated to pre-existing perio

periodontium abscess

acute infection involving circumscribed collection of pus in periodontium
gram negative, anaerobic
similar bacteria to periodontitis
pain is constant & localized
possible tooth mobility
radiographic bone loss
vital pulp
mastication difficulty, bad taste
s

causes of periodontium abscess

blockage of oriface of pocket
pre-existing perio pocket
forcing object into pocket: toothpick
incomplete calculus removal: site w/ deep pocket, coronal tissue heals & tightens preventing drainage

pulpal abscess

infection of tooth pulp that can extend to periodontium
cause: death of pulp: trauma or decay

gingival abscess

primarily limited to gingival margin & interdental papilla w/o deeper involvement
foreign object forced through sulcus
can be healthy

periodontal abscess

affects deeper perio tissue and gingiva
pre-existing perio disease

pericoronal abscess

perio abscess involving tissue around crown of partial erupted tooth
tissue cover occlusal of 3 molar
tissue flap (operculum) get infected

symptoms of pericoronal abscess

pain w/ occlusion
limited opening
swelling, redness
fever
lymphadenopathy

steps managing pt with abscess

1. establish drain path for pus
2. anthetized tissue
3. drain through pocket or surgery
4. perio instrumentation
5. adjustment of occlusion
6. possible antibiotics
7. salt water rinse
8. possible pain med

tx of pericoronal abscess

1. anesthetize
2. drain same as other abscess
3. through perio instrumentation
4. irrigate area of operculum w/ saline
5. possible antibiotics
6. possible extraction

Necrotizing Ulcerative Gingivitis

acute infection of periodontium limited to gingival tissue
aka: vincent, trench, ANUG

cause of NUG

poor nutrition
fatigue
psychosocial factors
systemic disease
drug/alcohol use
HIV

signs of NUG

punched out papilla
papilla destroyed interdentally
pseudomembrane gray/white
lots of blood
raw CT
dead cells, bacteria, debris

characteristic of NUG

oral pain
necrotic, punched out papilla
bleeding
pseudomembrane
swollen lymph nodes
discomfort
extreme halitosis
fever

treatment of NUG

3 appointments

appointment 1 of NUG treatment

remove pseudomembrane w/ irrigation
supragingival debridement
gentle homecare
cholorhexidine rinse

appointment 2 of NUG treatment

2 days after initial treatment
subgingival debridement
further self care instruction

appointment 3 of NUG tx

5 days after initial
further debridement
possible antibiotics
surgical reshaping of gingiva

Necrotizing ulcerative periodontitis

similar to NUG but effects deeper tissue including alveolar bone
can result from untreated NUG
formation of bone squestrum (dead bone)
tx: med consult and referral to periodontitis

Primary Herpetic Gingivostomatitis

viral infection of HSV1
painful
contagious during vesicular stage
virus is contained in clear liquid

PHG clinical signs

oral pain w/ eating
swelling
gingival bleeding
vesicles, ulcerations w red halo
fever
discomfort
swollen lymph nodes

beginning of wound healing

replace inflammed cells with collagen
healing surfaces consists of moderate inflammed CT tissue covered w granulation tissue
layered neutrophils
clot

regeneration

replace lost structure through new cells
this is our goal

hemostatis/clot formation

15 sec-1 min
epinephrine released from platelets
release cytokines
call PGE for vasodilation

sequence of wound healing

1. fibrin overlying CT (mesh)
2. CT produces granulation tissue

how is granulation tissue produced

proliferating CT w/ increased mitotic activity
-Fibroblast (3-5 days)
-endothelial cells fill in from edges of wound (0.5mm daily)
-undifferentiated mesochymal cells

extrinsic pathway

platelets cover by gylcoproteins so they don't stick and cause stroke
platelets go to injured epithelium with holes
platelets swell, become irregular shapes and sticky to stick into holes
forms prothrombic activator via injury
calcium is needed to turn pr

nutrition and clot formation

vitamin k help liver to make clotting factors
warfarin inactivates vitamin k

intrinsic pathway

comes in contact with blood
bleeding on probing
vitamin k/calcium activates bleeding factors
thrombin activates factor x and phospholipids help prothrombin activation=mesh

inflammatory phase

phase 2
5 signs: pain, swelling, heat, redness, loss of function
PMN first responders
macrophages replace after 4 days

Proliferation

stage 3
angiogenisis/granulation formation
granulation tissue penetrates thin clot
fibers extend from cementum to unite with new collagen formed by gingival fibroblasts
epithelium attach at original height
stimulation of collagen to get tensile strength

angiogenisis

blood vessel creation

maturation

last stage
scare
nutrition from blood
not as strong as original tissue

layers of wound

clot, neutrophils, granulation tissue, CT

host modulation therapy

altering pts defense response to help body defenses limit damage caused by disease

importance of host modulation

can help in periodontits
cost effective

biochemical mediators

stimulated by bacteria, causes inflammatory response

anti inflammatory mediators

biochemical mediators that are protective
help keep infection from doing serious harm
cytokines, IL4, IL10
bacterial challenge is great=damage

proinflammatory mediators

can damage periodontium
MMP, cytokine, prostnoids, prostaglandin E, interleukins

tetracycline as a host mod

doxycycline
non antibiotic dose (subantimicrobial)
decreases effects of enzyme collaganase/MMP
can inhibit progression of perio
20mg 2x daily
low side effects

NSAIDS as a host mod

treat pain and inflammation
reduce tissue inflammation by inhibiting PGE2
inhibit osteoclasts
takes up to 3 years to slow bone loss
if they stop taking there is risk of accelerated loss

Bisphosphonates as a host mod

inhibit bone resorption by altering osteoclast activity
not approved bc ONJ risk

statin meds as a host mod

simvastatin, atoravastatin
some protection against inflammation

primary intention

union of 2 granulation surfaces
clot fills space
PMNs show up at edge of wound at 24 hrs
48 hrs epithelial cells fuse edges
fills in with fibrin ends w/ scar
ex: sutures, paper cut

secondary intention

one surface does not have granulation tissue
epithelium cover part of wound
larger clot
depression at end of healing
ex: extraction site

Healing rate of epithelium

5mm daily

healing rate JE

5 days

healing rate SE

7-10 days

healing rate surface epithelium

10-14 days

healing rate CT

21-28 days

healing rate bone

4-6 weeks

new attachment prevention

to attach coronally cementum and collagen must have access to tooth surface
cementum is acellular and does not allow fibers to attach
alveolar crest fibers and transeptal fibers prevent fibroblasts and cementoblasts in PDL to access tooth surface coronal

healing by epithelial adaption

closing adapted but not attached
when probing you won't enter
how we heal after NSPT and why they need again

clinical signs of healing

no bleeding, no inflammation
decreased probe depth
more gram + anaerobes

JE healing

epithelium grows apically
JE grows until it gets to healthy collagen CT

reattachment healing

ideal b/c less susceptible to NSPT again
reestablish soft tissue infterface on surface
union of CT to root surface
JE shorter
tooth avulsed and put back in

new attachment healing

ideal w/ surgery
form new cementum, JE, CT
root conditioning to stimulate cementum
small amount of JE
remove JE, crest and transseptal fibers bc block attachement
gain access to PDL- fibroblast, cementoblasts

keyes technique

hydrogen peroxide to kill perio pathogens

acupuncture and dentistry

used as anesthetic
no rxns
no numbness
less post op pain

dental phobia natural help

hypnosis
biofeedback
relaxation
mind/body

cranberries

antiinflammatory
can help fight cares
polyphenols

Echinecea

stimulates t-cells and interferons

vitamin c and e

decreases gingival inflammation

gingko balboa

decreases gingival inflammation

magnesium citrate

increases muscle function

perio natural meds

aloe vera
blood root
calendula
echinecea
golden seal
grapefruit seed extract

decay reducation with natural meds

alfalfa
dandelion
horsetail
plankton

tooth pain and natural med

clove oil-dry socket
garlic
lemon balm
licorce
propolis

increase salivation and natural med

yohimbe

oil pulling

homecare supplement not replacement
1 Tbsp for 20 min
picks up microbes in gum and tubules lipid pathogen attracted to oil
swish until milky white

5 categories of alternative medicine

alternative medical systems
mind-body interventions
biologically based therapies
energy therapy
manipulative & body based therapy

holistic

support health before there is a problem
heal physical, mental, spiritual

natural interaction w/ anticlotting meds

Dong quai
Omega 3
gingko
vitamin e
danshen
aloene in garlic
ginger
anise
fucus
st. johns wort
american gingseng

natural meds that are anticoagulants

ginger
garlic
gingko biloba
gingseng
st johns wort

feverfew side effects

oral ulcers
lip irritant
bleeding
swollen gingiva

garlic, ginseng and gingko side effects

bleeding

kava side effects

oral/lingual involuntary movement

echinecea

tongue numbness
altered taste

st johns wort

xerostomia

natural effects on LA

Kava kava and st johns wort increase effects

cinnamon effects on dental

decrease antibiotics
tetracycline 80%

alternative natural antibiotics

green tea
thyme
wintergreen
hops
horseradish