Exam 2 Flashcards
Classifications of periodontal diseases and condition
- gingival diseases
- chronic periodontitis
- aggressive periodontitis
- periodontitis as a manifestation of systemic disease
- necrotizing periodontal disease
- abscess of the periodontium
- periodontitis associated with endodontic lesions
- developmental or acquired deformities and conditions
gingivitis vs periodontitis
gingivitis: reversible tissue damage, no apical migration of JE
periodontitis: irreversible tissue damage, apical migration of JE
Pseudopocket
gingival pocket fake pocket no bone loss deepening of gingival sulcus because of swelling or enlargement medications and disease will affect this
acute
lasts for short period of time, something happens then goes away, edema
edema
extra fluid in connective tissue that results in swollen tissue
Chronic
extended period of time, something happens and then keeps happening, getting worse, body tried to repair tissue by building collagen, fibrotic gingiva
fibrotic gingiva
isn’t red
It is chronic
Hard to probe subgingival
It is pink because it has been like this for a while
Smoked for a long time (you would see this)
This isn’t healthy
Probably wont bleed, usually isn’t painful
not really reversible
Looks swollen, pink, and fibrous
the two types of gingival diseases (the etiology)
- plaque induced
2. non-plaque induced
plaque induced gingival disease
most common, blunted, bleeding, gram negative for a few days of not removing (24-48 hrs)
generalized
most or all the teeth
more than 30%
localized
specific and tell you where, it can be anything but the whole mouth
(less than 30%)
papillary inflammation
papilla
marginal inflammation
papilla and marginal
diffuse inflammation
papilla, marginal, and further down
how to educate/treat pt that has inflamed gingiva
Monitor OHI, teach OHI, base line data, systemic disease (preventing from healing properly)
Poor debridement, poor OHI, systemic
Tell me about OHI, check debridement, concern that there is a systemic disease that is causing the gingiva from preventing properly.
coalesce
come together
cyanotic
blue/purple
plaque induced gingivitis modified by local factors
plaque is happening but crowding, diastama, restoration that has a chip, tooth that developed chipped, ortho treatment make the plaque worse
plaque induced gingivitis modified by systemic factors
hormones, pregnant, birth control
biofilm is the problem but the systemic disease makes it worse
pregnancy gingivitis
, pyogenic granuloma (forms as a result of inflammation, pregnant tumor, usually maxilla, 2nd and 3rd trimester, will bleed like crazy, will resolve when pt is not pregnant, pyogenic tissue. Started from biofilm and it is important to floss and brush even if it bleeds, it is painful to the patient
anti seizure drugs
Dilation
gingival hyperplasia
plaque induced gingivitis modified by medication
Biofilm is the problem, gingival hyperplasia, Drugs cause hyperplasia biofilm exacerbate (make worse) the gingivitis, These drugs can cause excessive accumulation of connective tissue in many other tissues in the body.
anti seizure drugs
immunosuppressive drugs
cardiac drugs
immunosuppressive drugs
Cyclsporine
cardiac drugs
procardia
plaque induced gingivitis modified by malnutrition
Vitamin C Deficiency
The gingiva becomes very hemorrhagic and swollen and the condition can progress to a more advanced periodontitis with extensive bone loss and tooth loss.
non plaque induced gingivitis
not common no biofilm these cause gingivits: Streptococcal infections of the throat and oral tissues in young children Syphilis Gonorrhea
Necortizing Ulcerative gingivitis
Necrotizing – to die Ulcerative – lesion Loss of epithelial tissue NUG no bone loss fusiform bacteria and spirochetes "trench out" punched out IDPs covered with a white necrotic pseudo membrane fetor oris (bad odor) acute infection painful Poor nutrition, not enough sleep, alcohol and drug use, under stress NUG is common on a college campus My gums hurt so bad, I can’t brush: NUG Tired, not feeling right, fever, lymphonapothy
Treatment to NUG
Remember patient is in pain
Debridement: ultra sonic, usually not much calculus
OHI: talk about
Systemic antibiotics: depending on symptoms , antimicrobial mouth rinse
materalic odor
Primary herpetic gingivostomatitis
primary herpes infection 1st exposure to herps viral infection children General malaise (tried, flu like) Vesicle formation present which may coalesce (come together) into ulcerative lesions Odor, but no distinctive fetor oris Treatment is palliative (fluids, pedisure) pt doesn’t want to eat Blister Wide spread pain not the normal
non plaque induced gingivitis (genetic origins)
gingival enlargement
idiopathic
just happens
idiopathic
no reason
gingival manifestation of systemic condition
Gingival enlargement with the absent of local factors we are looking for other reasons
Blood dyscrasias (outside the number limit of normal):
Acute leukemia: hemorrhagic and swollen gingival tissues far more pronounced than what would normally be expected from the amount of plaque and calculus present.
This is a very life threatening disease
gingival manifestation of dermatologic condition
Immune related
White appearance
Plaque has nothing to do with it
Usually on skin
lace like pattern
Lichen Planus: a chronic immune related disease
affects skin and mucous membranes
Wickham’s striae
Topical steroids have been used to tx but no known cure.
Benign Mucous Membrane Pemphigoid (cicatricial pemphigoid):Chronic vesiculobullous disease
Blistering and sloughing of surface epithelium.
Might be an autoimmune reaction disease similar to Lichen Planus.
More common in older individuals and females
Bulla up to 10 mm in size
Vesicle
blister
Nikolskys sign
taking a cotton roll and wipe it along the tissue, a layer comes off and a blister forms
desquamative gingivitis or gingivosis
autoimmune
painful erosive lesions
topical steroids and systemic steroid therapy may help
desquamative
Sheading layers of tissues
Traumatic lesions
Hurt the tissue
Eat hot pizza
Damage to the gingival tissue by trauma is common
Pizza burns, chemical burns such as with aspirin placed on the gingiva for pain relief, cuts from chicken bones or crusty breads or potato chips etc…
Some traumatic lesions if severe enough can lead to advanced recession
foreign body reactions
Localized painful lesions with sudden onset
tongue pricing
periodontal disease
Loss of connective tissue attachment
Loss of crestal alveolar bone. This loss of alveolar bone occurs through bone resorption (breaking down)
Bacteria and their byproducts break down the interface between the Sulcular epi and cause detachment of the JE and CT
Pockets deepen as a result of collagen breakdown in the gingival CT by enzymes such as collagenase.
Bacteria release a number of chemotactic substances that increase the flow of neutrophils in the gingival sulcus.
Neutrophils react with bacteria, producing suppuration
Periodontal case type with letter A
systemic disease that affects periodontal disease
Periodontal case type 1
pd: 1-4 mm
bone: no bone loss (1-2 mm from CEJ)
Mobility: WNL
CAL: 0mm
Periodontal case type 2
pd: 4-5 mm
bone: early (3-4 mm from CEJ)
Mobility: WNL/ class 1
CAL: 1-2mm
Periodontal case type 3
pd: 5-7 mm
bone: moderate (4-6 mm from CEJ)
Mobility: class 1-2
CAL: 3-4 mm
Periodontal case type 4
pd: 7+ mm
Bone: severe (6+ mm from CEJ)
Mobility: class 1-2
CAL: 5+ mm
Chronic Periodontitis
Bone loss that progresses slowly in a predominantly horizontal fashion.
Adults, children, and adolescents
Accumulation of plaque and calculus**
Most common
***May be associated with smoking, stress and systemic factors
may be localized or generalized
~can be in state or exacerbation or quiescence
~most reliable to determine an active state is document CAL
(Bio film is causing it- How to host is responding to it, it may make it worse)
~bone loss over years
what is CAL?
refers to the position of the periodontal attached tissues at the base of a sulcus or pocket. Clinical attachment level is measured from a fixed point (usually the CEJ) to the attachment.
estimation
exaverbation
activity
quiescence
no activity
chronic periodontitis: CAL is more important than probing depth…..But why is the probing depth significant ??
~ Bacteria is building up and no one is able to clean it
chronic periodontitis: How do radiographs aid the assessment?
~ 1-2 mm from the bone shown on a radiograph
chronic periodontitis: can you treat as RDH?
~ yes except when the condition is getting worse and you do not do anything about it. Supervised neglect (could be sued), at least refer and if they do not go that is not RDH’s fault.
- Always probe, 3mo recall, OHI
chronic periodontitis: bacteria
P. gingivalis is probably the most common , also T forsythia, P intermedia, F nucleatum, and AA.
Chronic periodontitis:
- states
- determines states
- time period
- %
- most prevalent in
- other info
~can be in state or exacerbation or quiescence
~most reliable to determine an active state is document CAL
(Bio film is causing it- How to host is responding to it, it may make it worse)
~bone loss over years
~ 5-20% of adults in US
~ adults, may affect children or adolescents
~destruction is consistent with local factors
~subgingival calculus is frequently found
~variable microbial pattern
~slow to mod. progression with periods of more rapid progression
~classified on the basis of extent and severity
~associated with local predisposing factors
~may be modified by systemic disease
~may be modified by stress and tobacco.
chronic periodontitis: bacteria
P. gingivalis is probably the most common , also T forsythia, P intermedia, F nucleatum, and AA.
chronic periodontitis: treatment
~removal of biofilm and calculus
~OHI, perio charting, films, antimicrobial, antibiotics, quad scaling, local anesthesia
~Not going to matter is a systemic disease is going to make this worse
Localized Aggressive periodontitis
Rapid destruction
Similar bacteria as chronic perio
Seen in family members, generations
No systemic disease and is not responding to treatment
less than 20 yrs (juvenile)
low levels of plaque accumulation or inflammation around the affected teeth
**Max/mand anterior teeth and first molars
More common young females
AA involved
Scaling and root planning with or without antibiotics. In some cases surgical therapy to treat osseous defects.
just happens
adult teeth
usually 10 years old
Post localized Aggressive periodontitis
A category describing Localized Aggressive which has stopped or significantly slowed. Severe bone loss around incisors and 1st molars,
Probably a late diagnosis or JP rather than a different disease
Generalized Aggressive periodontitis
~ ages: 20-30 ~ rapid bone loss ~ gingival inflammation ~ fiery red tissue va
Generalized Aggressive periodontitis
~ ages: 20-30
~ rapid bone loss of all or most teeth
~ gingival inflammation
~ fiery red tissue
~ varying amounts of biofilm and calculus
~ Bone loss and CT loss can occur over weeks or months, may have a genetic component, as well as an altered neutrophil (PMN) chemotaxis disorder.
~ comes and goes
Generalized Aggressive periodontitis treatment
elimination of local etiology usually surgery in combination with systemic antibiotics
Refractory periodontitis
Despite appropriate normal treatment, the perio condition of the patient continues to worsen and is not arrested.
Either single or multiple sites.
Bacteria involved seem to be very resistant to normal therapies. Could also be a host response deficiency.
Resistant to treatment
Chronic and aggressive can be resistant treatment
Refractory periodontitis
Despite appropriate normal treatment, the perio condition of the patient continues to worsen and is not arrested.
Either single or multiple sites.
Bacteria involved seem to be very resistant to normal therapies. Could also be a host response deficiency.
Resistant to treatment
Chronic and aggressive can be resistant treatment
periodontitis as a manifestation of systemic disease
~systemic condition is causing the problem and increase pt risk
~ modify or amplify the host response (change or increase)
~immune system can not fight it off
~examples: Down’s syndrome, Leukemia, AIDS, Papillon-Lefevre syndrome, Chediak-Higashi syndrome
down syndrome
~periodontitis as a manifestation of systemic disease
~Genetic
~Mental retardation
~Abnormal PMN function (don’t have first responders if you have down syndrome, chemotaxis is also altered)
~Chemotaxis altered therefore PMNs can’t get there
Chemotaxis
Movement of PMNs to the site for where it should be helping
Leukemia
~periodontitis as a manifestation of systemic disease
~ Gingival tissue becomes swollen, glazed and spongy
~Cancer of blood cells
HIV/AIDS
~periodontitis as a manifestation of systemic disease
~ linear gingival erythema (along margin, 2-3mm in width)
~immunocompromised
erythema
red
Papillon-Lefevre syndrome
~periodontitis as a manifestation of systemic disease ~loss of primary teeth by age 4 ~loss of permanent teeth by age 14 ~Genetic disorders ~By the age 15 teeth are all gone, rare ~ not common
Chediak-Higashi syndrome
~periodontitis as a manifestation of systemic disease ~ not common ~immune system ~decrease in phagocytes ~Genetic disease
phagocytes
eat bacteria and kill it
Osteoprosis
~periodontitis as a manifestation of systemic disease
~holes in the bones/ weaken bone/ elderly/ estrogen/ menopause ~Post menopausal women late 40s/50s ~Estrogen is no longer being made. Estrogen makes our bones strong
~Having to stay in bed b/c they aren’t being weight baring
~Steroid use – anti inflammatory
~Link between skeletal and alveolar bone loss
~Does not cause perio!!!
~Mostly mandible
~Bisphonates
~Not normal
Osteoprosis
~periodontitis as a manifestation of systemic disease
~holes in the bones/ weaken bone/ elderly/ estrogen/ menopause ~Post menopausal women late 40s/50s ~Estrogen is no longer being made. Estrogen makes our bones strong
~Having to stay in bed b/c they aren’t being weight baring
~Steroid use – anti inflammatory
~Link between skeletal and alveolar bone loss
~Does not cause perio!!! but there could be some bone loss of the alveolar bone
~Mostly mandible
~Bisphonates
~Not normal
Tobacco use
~Direct impact on periodontal disease (heat in mouth)
~Tissue become dry and mouth becomes dry
~Heat and dry cause vasoconstriction (lack of blood flow) because smoke contains cytotoxic and vasoactive components
~When pt stops smoking pt starts bleeding within 4-6 weeks (isn’t constricted anymore)
~Byproducts of smoke get into sulcus and act as an irritant
~ risk factor for perio (increase attachment loss, increased tooth loss)
~ diminished neutrophil function (doesn’t fight infection) and impaired fibroblast function and a reduced capacity of the periodontal tissues to repair themselves.
~fibrotic tissue
Has Periodontal disease and now at risk for other conditions such as
Diabetes
Cardiovascular
Pre-term babies
Diabetes Mellitus
Type I: insulant
Type II: insulant resistant
Controlled vs. uncontrolled
HB1C 7
FPG 126
Stress affects blood glucose
Diabetic that is control not a greater risk for perio
Uncontrolled puts at risk for perio and makes perio worse
Even if it is Controlled there are periods of time that it is not controlled
The goal of treatment is to control blood glucose level
Poor wound healing
Poor nutrition
Bacteria loves sugar
increased blood glucose
Glucose in crevicular fluid
Reduced PMN’s…1st line of defense (poor wound healing)
2-3 times greater risk for developing perio
what to ask a diabetic pt
what are your levelsdid you eatwhat typemedicationsdid you take the medicationswhen did you take the readings of levels
Cardiovascular disease
Systemic inflammatory response
Inflammation within arteries
C reactive proteins – marker for inflammation
Link between perio and cardiovascular disease
Pre-term babies
less than 37 weeks
low birth weight
Prostaglandins (destroy bone, hormone like structure from in __)-> osteoclasts
Already have too many prostaglandins and will cause pre mature baby aka low birth weight babies
There is a link between perio mouths and low babies weight babies
Uterus contracts from more prostaglandins
Pre-term babies
less than 37 weeks
low birth weight
Prostaglandins (destroy bone, hormone like structure from in __)-> osteoclasts
Already have too many prostaglandins and will cause pre mature baby aka low birth weight babies
There is a link between perio mouths and low babies weight babies
Uterus contracts from more prostaglandins
Necrotizing Ulcerative Periodontitis
- how is it different than NUG
NUP
Usually associated with an immune compromised disorder such as HIV.
The only difference is that bone is lost
Abscess of the periodontium
Acute: an acute localized purulent infection of the periodontium.
Perio pocket becomes occluded and an infection is allowed to become localized into an acute infection in the adjacent tissues.
Rapid bone loss can occur with pain and swelling.
Blister like lesions -> circumscribed/ fluctuant (when you push it, it comes back) , filled with puss-> neutrophils are dying and give off pus, can but acute or chronic, periodontal abscess -> rapid bone loss,
Abscess of the periodontium
- Perio pocket becomes occluded and an infection is allowed to become localized into an acute infection in the adjacent tissues.
- Rapid bone loss can occur with pain and swelling.
- Blister like lesions -> circumscribed/ fluctuant (when you push it, it comes back), filled with puss-> neutrophils are dying and give off pus, can but acute or chronic, periodontal abscess -> rapid bone loss
fistula
draining abscess
gross scaling
supra scaling (bad because you may miss the calculus underneath) -> causes a periodontium abscess
Acute Abscess of the periodontium
-Acute: an acute localized purulent infection of the periodontium.
-usually associated with deep pocket
-fistula
-pain
gross scaling
-tx: Radiographic analysis
Repair potential is great because of an acute phase reaction.
Film will help but first probe (a really deep pocket) quick bone destruction
Treat-> debride, local, might be surgically cut to making into a fistula(pus will come out), possibly antibiotics
Usually painful
Chronic Abscess of the periodontium
Clinically appears like an acute abscess…patient has no pain
Can be fistulaed / and be filled (goes back and forth)
Gingival abscess
Similar to periodontal abscess except only contained in the soft gingival tissues
Usually caused by invasion of a foreign body forced into the gingival sulcus
No bone or attachment loss.
less of a concern
popcorn gets stuck
Pericoronitis
Tissue over tooth (usually third molar)
Operculum -> tissue of the most distal tooth
Infection starts under the tissue
Is in pain
Debride the area (doesn’t always need a flap, but may)
Irrigator (antimicrobial)
Makes them feel better until get oral surgernt removes it
Palative treatment
Fever -> antibiotics
Flap of tissue distal to the 3rd molar
TREATMENT- consists of opening tissue via a flap and careful debridement of the pocket of infected area. No antibiotics are given unless there is evidence of facial cellulites (generalized area of inflammation) or if the patient has a fever.
palative treatment
treat the symptoms
Endodontic abscess
Very difficult to distinguish from a perio abscess in terms of symptoms. The facial pain and tenderness to the tooth is similar.
If pt has heat sensitivity almost always periapical -> nerve is being affected (pulp)
Tooth gets pushed up out of occlusion (just a few mm) that’s why it hurt to eat and tap on
Pulpitis- decay, bad root canal,
Radiographic analysis shows a round radiolucency at the apex of the tooth. This can be called a periapical abscess.
Etiology:
caries, traumatic fracture of the tooth , or the trauma of a dental procedure.
Drainage of the abscess is similar to the perio abscess.
Microorganisms colonize the pulp, produce toxins, cause pulp cell death and the bacteria and their products exit the apical foramen of the tooth causing localized apical abscess formation
tx: root canal therapy (RCT) (Taking out the nerve, fill with material, pt should not have pain, discolor, easier to break)
comparing periodontal and endodontic abscess
Periodontal:
type of pain- constant, localized, severe, sharp
vitalitly- vital
Radio image- bone loss but no apical lesion
Endodontic
type of pain- intermittent (comes and goes), hard to localized, extremely severe
vitalitly- usually nonvital
Radio image- apical radiolucency common
combined perio-endo lesion
Infection spread from the pulp to the periodontium or vice versa.
Difficult to determine what caused what. Symptoms are similar to individual abscesses.
Radiographs shows both bone loss and a periapical lesion.
Treatment involves treating the endo lesion first with a RCT and then treat the perio.
Usually has a crack in root
Don’t know what causes what
Endo first then perio
This is common
Peri-implant mucositis
inflammation around implant without bone loss
A hole is put into alveolar bone, they can get infected.
don’t probe implants because can damage the seal around the implant
No bone loss
Just imflammation
Peri-implant mucositis
inflammation around implant without bone loss
A hole is put into alveolar bone, they can get infected.
don’t probe implants because can damage the seal around the implant
No bone loss
Just imflammation
Peri-implantitis
Implant is infected
Bone loss
Use plastic
Implant has lost the bone that is holding it in place
systemic antibiotics
-slow down periodontal disease
AA
Inhibit collagenase activity
Tetracycline
doxycycline
-Metronidazole or flagyl (no AA, generalized aggressive)
- Penicillin/ amoxicillin (still may be effective against periodontal pathogens, but less effective than in the past due to resistance of bacteria against it.)
-Augmentin (amoxicillin and clavulanic acid) shown to be very effective in refractory periodontitis cases
-Clindamycin and ciprofloxacin useful against more aggressive types of perio disease including refractory and generalized aggressive case type diseases
-Synergistic effect
-Amoxicillin and metronidazole in combination have also been shown to effective in Localized aggressive periodontitis (JP) and against A.A.
systemic antibiotics
-slow down periodontal disease
AA
Inhibit collagenase activity
Tetracycline
doxycycline
-Metronidazole or flagyl (no AA, generalized aggressive)
- Penicillin/ amoxicillin (still may be effective against periodontal pathogens, but less effective than in the past due to resistance of bacteria against it.)
-Augmentin (amoxicillin and clavulanic acid) shown to be very effective in refractory periodontitis cases
-Clindamycin and ciprofloxacin useful against more aggressive types of perio disease including refractory and generalized aggressive case type diseases
-Synergistic effect
-Amoxicillin and metronidazole in combination have also been shown to effective in Localized aggressive periodontitis (JP) and against A.A.
What do we use to assess the periodontal status of pt
Probe depth Radiographs CAL Mobility Furcation's BOP Recession Mucogingival involvement (Perio chart)
When assessing pt what order should you think of
Gather information, a complete picture of what is causing the periodontal problem, write up a treatment plan
MEDICAL:
What is the purpose of taking a medical history?
Taking of vital signs are important because?
base line of information. safety treat the pt. correction with perio and debates, smoking, HIV/AIDS, preg. Medical clearance (infection endocarditis, Coumadin because it is a blood thinner, renal disease -> dialysis and a port.
checking blood pressure, pulse and respiration
Dental history:
If the pt comes in with a chief complaint (why the pt comes in) you deal with that first!!! When it is not pain deal with other concerns (like a pt with perio that wants white teeth)
gathering any information to help with assessment and treatment
Clinical exams include
Extra oral Intra oral Oral mucosa Oral hygiene Periodontal and dental assessments, including pocket depth , width of attached tissue, recession, mobility, suppuration, plaque and calculus presence, color, size, shape, texture, consistency
Contributing factors of bone loss
- calculus
- over hang
- food impacted
over hang
not in line with the root surface (hard to floss, can’t floss, food gets caught) this is a contributing factor to get bone loss
Types of staining
Bacterial and calculus staining
Brown staining called Tannin staining- found in coffee, tea, fruits and wines; can denature proteins of the pellicle
Chlorhexidine staining
Black staining caused by chromogenic bacteria causing black pigmentation
Green staining- stained remnants of the enamel cuticle in children
The difference between intrinsic and extrinsic staining
peridontal assessment
-signs/symptoms
-inflammation (first clinical signs would be papillary/marginal)
-destruction of periodontal tissues
- signs of disease (BOP (active), bone loss, odor (active, perio breath, because bacteria living and dying in pockets)
past perio
erythematons
red
edematms
inflammation (edema)
Probing
The periodontal pocket depth is the measured distance between the gingival margin and the base of the gingival sulcus
Line angle to line angle (middle reading)
Parallel to the tooth (in the same plane)
Walking stroke
PCP UNC – up to 12 mm
Williams – 10 mm
Probing
The periodontal pocket depth is the measured distance between the gingival margin and the base of the gingival sulcus
Line angle to line angle (middle reading)
Parallel to the tooth (in the same plane)
Walking stroke
PCP UNC – up to 12 mm
Williams – 10 mm
Recession
Free gingival margin in relationship to the cementoenamel junction (CEJ).
The FGM can be at or slightly coronal to the CEJ,
The FGM can be significantly coronal to the CEJ,
The FGM is apical to the CEJ. Recession
When the FGM is apical to the CEJ resulting in exposure of a portion of the root surface this is termed gingival recession
CEJ to GM
It occurs from mechanical trauma, ortho, particle (clasps)
Connective tissue had been loss – recession
Some times the scaling can cause recession because the inflammation of the gingiva will decrease when the calculus is removed
Root sensitivity
Frenum too high – pulls on tissue causing recession (frenum pull)
Dentinal tubules exposed – sensitive to air
Age- there might be some recession due to the aging process because of how long they have been brushing their teeth.
“long in the tooth” – teeth look long because they have recession
Chewing tabacco
Generalized recession: after ortho (because the teeth have to be moved in the bone)
CAL
Add inflammation
Subtract recession
It is an estiment – the stability of the JE
If it is moving apically there is disease activity
Probe reading might be CAL if the gingival tissue is where it should be
If the gingival tissue is higher (inflamed) than where it should be then you subtract
Add recession to the pocket depth
Bleeding
Presence of bleeding has been shown to be an indicator of disease progression
Bleeding = plaque formation
Suppuration can be detected with a probe or by gentle pressure expressing pus from the pocket
active disease
Suppuration
pus (purulent)
tooth mobility
All teeth have a slight mobility
Pathologic mobility should be noted
The more severe the bone loss, generally the more mobile
Mobility is measured with the handles of 2 metal instruments placed on each side of the tooth and gently rocked back and forth
3 mobility poor prognosis
Gently rock it back and forth – this will make it easier
2 got trouble, 3 really bad trouble
Mucogingival involvement or defect
discrepancy in the relationship between the free gingival margin and the mucogingival junction
Common conditions may be the result of:
gingival recession, resulting in inadequate or diminished attached gingiva
Probing depths extending to or beyond the mucogingival junctions into the alveolar mucosa
Anatomical variations that complicate the management of these conditions, including a high frenum attachment pulling the gingival margin away from the tooth
Most common problem with mucogingival involvement: once infection gets past JE the infection becomes more diffuse
Calculating the width of attached gingiva
BOARDS!
Will the tooth and the bone support a restoration (bridge, proclant fused to metal crown)
Subtract MGJ and PD
By dentist for restortative
Festoon
life safer like
exostosis
extra bone
Primary trauma from occlusion
Excessive forces on a normal healthy periodontium
Clenching/ grinding, rotated teeth, spaces
secondary trauma from occlusion
Normal forces on a compromised periodontium (exhibiting bone loss from previous periodontal disease)
Already have perio and focus are causing the excessive movement
attrition
flattened incisal/ occulsal edges
demineralization
biofilm
cervical findings
abfraction
abnormal occlusal forces
usually 1 tooth in quad
usually pre molar
v-shaped
Secondary pathologic migration of teeth
Usually accompanied by mobility and rotation of the teeth.
Caused by occlusal forces against a weakened periodontium.
Teeth have to be pushed out of the way to move, they do not move on their own.
teeth have already been weaken by perio
pathologic migration
Teeth start to flare out because of trauma from bite
Perio allows this to happen because the support is already being broken down
PDL is weaken
Furcation
nabers probe
Dental assessment
Evaluation for caries via visual, tactile, and radiographs
Look for overhangs, overcontoured restorations and undercontoured restorations that can hurt plaque control
Poorly fitting crown margins
Poor proximal contacts, open contacts, tight contacts
Anomolies in tooth form, cementicles, enamel pearls, lateral development grooves
abfraction
abnormal occlusal forces usually 1 tooth in quad usually pre molar v-shaped wedging at CEJ micro fractures in enamel by destructive occlusal forces
Dental assessment
Evaluation for caries via visual, tactile, and radiographs
Look for overhangs, overcontoured restorations and undercontoured restorations that can hurt plaque control
Poorly fitting crown margins
Poor proximal contacts, open contacts, tight contacts
Anomolies in tooth form, cementicles, enamel pearls, lateral development grooves
Anything that is going to complicate perio
decay
crown margins
lateral grooves
tooth wear
erosion
abrasion
attrition
parafunctional habits
clenching grinding biting or chewing lips, cheeks, tongue fingernail biting tooth pick biting pipe clenching (using your teeth when not eating)
Radiographic analysis
FMX, horizontal and vertical bitewing, periapical
Radiographs are a 2 dimensional picture of a 3 dimensional object
3-D Imaging: 3 dimensional CT scans: greater detail and accurate measurements
Bony changes; we know where health is, 1-2mm apical to CEJ
lamina dura
bundle bone that lies adjacent to the periodontal ligament, lining the tooth socket. The lamina dura surrounds the tooth socket and provides the attachment surface with which the Sharpey’s fibers of the periodontal ligament perforate. On an x-ray a lamina dura will appear as a radiopaque line surrounding the tooth root. An intact lamina dura is seen as a sign of healthy periodontium.
densities of bone
..
widening of pdl
..
CEJ discrepancy
..
supra bony
horizontal
above the alveolar crest
infra bony
vertical bone loss
below the alveolar crest
trauma
