Perio Final Flashcards
Most common chromosomal anomaly in humans, affecting about 5,000 babies born each year and more than 350,000 people in the United States
Trisomy 21
Genetic condition caused by an extra chromosome of the 21st chromosome (47 instead of 46)
Trisomy 21
Generalized early periodontitis, begins in the deciduous dentition and continues in the adult dentition
Trisomy 21
Prevalence and severity of perio is extremely high when compared to either their siblings or other mentally challenged individuals
Trisomy 21
Where are the most frequent sites of perio destruction in pts with Trisomy 21?
Molars
Incisors
The roots of the lower incisors are characteristically short which, in combination with the loss of bone, predisposes to premature tooth loss
Trisomy 21
Delayed eruption of both primary/permanent dentitions, microdontia, macroglossia
Trisomy 21
Molecular biology research has underlined the
important role of several cell-cell adhesion
receptors on the neutrophil surface; emphasizing
that defects in numbers of these receptors may
lead to increased susceptibility to infectious
disease
Leukocyte-adhesin deficiency syndrome
Associated w/ perio, oral ulcers, and chronic necrotic skin lesions
Leukocyte-adhesin deficiency syndrome
An inborn error of metabolism with highly variable clinical severity caused by loss-of-function mutations in the gene encoding tissue nonspecific alkaline phosphatase (TNSALP)
Hypophosphatasia (HPP)
Decreased serum alkaline phosphatase and severe loss of alveolar bone and premature loss of the deciduous teeth, particularly in the anterior region
Hypophosphatasia (HPP)
Mutated Gene CTSC
Papillon-Lefevre syndrome
Encodes for cathepsin C, key activator of serine proteases in immune cells
Papillon-Lefevre syndrome
Autosomal recessive, characterized by the presence of hyperkeratotic skin lesions
Papillon-Lefevre syndrome
Exhibits diffuse palmar and plantar keratosis
Papillon-Lefevre syndrome
Severe generalized periodontitis, commonly before puberty with early loss of deciduous and permanent teeth
Papillon-Lefevre syndrome
Teeth are lost in order of eruption and as yet there is no general agreement on the success of dental therapy
Papillon-Lefevre syndrome
Associated with complete edentulism early in life
Papillon-Lefevre syndrome
Chemotaxis association
Papillon-Lefevre syndrome
LYST gene lysosomal trafficking regulator protein affecting phagocytosis
Chediak-Higashi syndrome
Autosomal recessive trait associated with severe periodontitis
Chediak-Higashi syndrome
Neutrophil chemotaxis and bactericidal functions are abnormal in these patients
Chediak-Higashi syndrome
Immune system abnormalities, bleeding abnormalities, and multiple infections
Chediak-Higashi syndrome
C1R and C1S serine proteases of the complement cascade
Ehrlers-Danlos syndrome
Inherited CT disorders exhibiting joint hypermobility (joints that stretch further than normal), skin hyperextensibility (skin that can be stretched further than normal), and tissue fragility
Ehrlers-Danlos syndrome
Autosomal dominant and reclassified into 13 sub-types on the basis of inheritance and clinical presentation
Ehrlers-Danlos syndrome
Which types of Ehrlers-Danlos syndrome have increased susceptibility to periodontitis?
IV and VIII
Which type of Ehrlers-Danlos syndrome is associated with fragile oral mucosa and blood vessels?
VIII
Severe generalized periodontitis with an early onset
Ehrlers-Danlos syndrome
Children exhibit severe inflammation of
gingiva and complications include arterial or GI ruptures
Ehrlers-Danlos syndrome
Clinical term not a diagnosis; lab procedures necessitate a full diagnosis
Desquamative gingivitis
Nikolsky sign
Desquamative gingivitis
Blister formation when pressure is applied to the skin or mucosa with vesiculobullous disorders
Desquamative gingivitis
Systemic inflammatory autoimmune disease production of anti-citrullinated protein antibodies leading to synovial joint inflammation and destruction
Rheumatoid arthritis
Number of missing teeth is 4x greater in pts with this disease
Rheumatoid arthritis
P gingivalis expresses PPAD enzyme leading to ________ production
ACPA
A. actinomycetmecomitans leads to hypercitrullination of what cells?
Neutrophils
DNA of bacteria such as P. gingivalis detected in the synovial fluid of pts with what disease?
Rheumatoid arthritis
What induces the formation of pro-inflammatory cytokines?
Dysbiosis
Can consider periodo as an extra-articular source increased auto antibodies in what disease?
Rheumatoid arthritis
Perio and precancerous cells can lead to what type of cancer?
Colorectal
Travels through blood and infects tumor cells via attachment to a sugar molecule on their surface
Fusobacterium nucleatum
Associated with periodo, tonsillitis, appendicitis and preterm labor
Fusobacterium nucleatum
Infection in tumor cells of pancreatic , esophageal or colorectal cancer increases resistance to chemo and causes an inflammatory cytokine storm, which can lead to metastasis of the cells accelerating progression
Fusobacterium nucleatum
Previously Aggressive
Localized Juvenile Periodontitis (LJP)
Refractory Periodontitis
World Task Force diagnosis
-Aggregatibacter actinomycetemcomitans
-Inherited defect of neutrophil functions including: impaired chemotaxis, phagocytocis, and killing of bacteria
-Possibly due to a lytic enzymatic release against pathogens of primed neutrophils to debridement so less remains for chemotaxis and defense
-Strong genetic component
-Smoking component as well
LJP (localized juvenile perio)
Identified initially w/ Pubescent Females of African Descent but some studies afterwards found a stronger genetic component in
Caucasians
LJP
Some immunological marker differentiation
LJP
Responds well to treatment if caught in time
LJP
First molars and any incisor typically but anywhere is possible if generalized
LJP
Measures actual positives correctly identified (% of population that has a condition)
Sensitivity
Measures the actual negatives correctly identified (% of population that does NOT have a condition)
Specificity
BOP has _______ specificity, _______ sensitivity
high specificity; low sensitivity
What accounts for 1/3 of all dental emergency visits and is very painful?
Perio abscess
What disease?
Edematous
Lymphadenopathy
Fever
Increased tooth mobility/extrusion
Exudate/suppuration
Isolated deep PDs
Perio abscess
The epithelial tissues can reattach to the root of the tooth, whereas bacteria and debris remain in the apical aspect of the pocket. With the coronal portion of the pocket occluded, drainage is impaired and an abscess may result
Perio abscess
What is mandatory when diagnosing a perio abscess?
Differential diagnosis
What is the tx for a perio abscess?
Drainage via socket or open SRP
What medications are prescribed for a perio abscess?
PenVK 500 mg
Doxycycline 100 mg
What 2 lesions should you rule out before diagnosing a perio abscess?
Endo PA lesion
Lateral canal lesion
What are the 3 complications of perio abscesses?
Cellulitis
Airway patency
Sinus infections
What is imperative after treating a perio abscess?
Post-op care
What is the post-op care after treating a perio abscess?
RTC 1-2 days, then weekly to evaluate
Which 2 bacteria are involved in perio abscess?
P gingivalis
P intermedia
A biopsy of a perio abscess reveals invasive ________ present in pocket epithelium into adjacent CT
fungi
____________ microbes predominate perio abscesses
Anaerobic
If your pt has 3mm of CAL, but pocket depths are 3mm or less, do they have active perio disease?
No
What are the 2 necrotizing perio diseases?
Necrotizing ulcerative gingivitis (NUG)
Necrotizing ulcerative perio (NUP)
Both NUG and NUP may be manifestations of underlying systemic problems such as what?
HIV
What factors, other than systemic considerations, appear to be predisposed to the development of NUG and NUP?
Cig smoking
Emotional stress
Which diseases have the following clinical signs and symptoms?
Interproximal necrosis/ulceration
History of soreness/bleeding when brushing/eating
Pseudomembrane covering a “punched out” papilla
NUG
NUP
The extent and degree of involvement of NUG and NUP varies considerably from…
One papilla to entire gingiva
NUG or NUP?
On the basis of clinical findings
Onset of the disease is sudden
Severe pain around the teeth and gingiva (“My
entire mouth hurts”)
NUG
NUG or NUP?
Pain is more intense around the sites of ulceration (elicited upon brushing or when eating)
Gingiva bleeds and most often spontaneously
Spicy foods, hot or cold drinks or alcoholic beverages may be intolerable
NUG
Also called “Trench mouth” or Vincent’s Disease
NUG
What are the 4 systemic signs and symptoms of NUG?
Lymphadenopathy
Fetor oris (bad breath)
Fever
Malaise
What are the following a differential diagnosis of?
Acute gingivitis
Primary herpetic gingivostomatitis
Recurrent apthous stomatitis
Desquamative gingivitis
Infectious mononucleosis
Streptococcal or staphylococcal pharyngitis
Acute leukemia
Agranulocytosis
Secondary/Tertiary stage syphilis
NUG
What disease?
Fusospirochetal disease always appears to be superimposed onto existing tissue damage
ANUG
What disease?
Concluded that neither spirochetes nor fusobacteria could be excluded as the etiologic agents
ANUG
What 4 zones contain spirochetes in ANUG?
Bacterial zone
Neutrophil rich zone
Necrotic zone
Spirochetal infiltration zone
Which zone of ANUG?
Most superficial zone, consists primarily of a mass of bacteria of various sizes and shapes, including a few spirochetes
Bacterial zone
Which zone of ANUG?
Underlies the Bacterial zone
Neutrophil rich zone
Which zone of ANUG?
Many leukocytes with a marked predominance of neutrophils; spirochetes found btwn leukocytes
Neutrophil rich zone
Which zone of ANUG?
Contains disintegrating tissue cells, many spirochetes of the intermediate and large type and a few other bacteria which are probably fusiforms
Necrotic zone
Which zone of ANUG?
Tissue components appear well preserved, but are infiltrated with spirochetes of various sizes; no other bacteria are found in this zone
Spirochetal infiltration zone
Spirochetes can be found in ___________ tissue ahead of other bacterial types
non-necrotic
T/F: There is no marked difference in the relative infectivity of bacterial debris, injected into experimental animals, from the normal gingival sulcus, the periodontal pocket, or areas of papillary necrosis associated with ANUG
True
What is responsible for the development of ANUG?
Decreased host resistance
(rather than increased bacterial virulence)
What are the 8 local predisposing factors of ANUG?
Gross neglect
Overcrowding
Recent exts
Food stagnation
Mouth breathing
Calculus
Smoking
Emotional stress
T/F: Fatigue and local trauma, along with physical debility and lowered resistance play a role in ANUG
True
What is an important etiologic factor of ANUG?
Pre-existing gingivitis
What is directly correlated to the severity of ANUG?
Tobacco
What is the characteristic flora of NUG directly related to?
Altered host response
Very young pts with measles, protozoal infection, and malnutrition have increased risk of what?
NUG
How do you treat NUG?
Control acute bacterial phase
Educate pt in plaque control
Eliminate predisposing factors
Early + vigorous local tx during acute phase
Antibiotics only when systemic complications prevail
T/F: When treating NUG, drugs should never be considered a substitute for scaling and debridement
True
What should you do at the first visit when seeing a pt with NUG?
- Remove as much calc, plaque, and debris as possible with ultrasonic instrument
- Educate pt how to remove plaque with new toothbrush
- Prescribe ABs if fever or lymphadenopathy
- Instruct specific home care
What is the home care for NUG?
- Rinse w/ 0.12% CHX 2x/day
- Soft, bland diet
- Drink lots of water
- No smoking or drinking
- Rest
- Rinse mouth after eating
- Brush teeth
- Return to office in 24 hrs
What should you do at the 2nd visit when seeing a pt with NUG?
- Check OH, review plaque control
- Continue removing calc, plaque, debris
- Careful SRP and flush w/ warm water
- Polish
- Tell pt to return after 24-48 hrs
What should you do at the 3rd visit when seeing a pt with NUG?
- Check OH, review plaque control
- Continue removing calc, plaque, debris
- If tissues haven’t responded -> evaluate for systemic factors and refer for med consult; continue seeing pt every 24-48 hrs
- If you see improvement, tell pt to return in 7-10 days
What should you do at the 4th visit when seeing a pt with NUG?
- Check OH, review plaque control
- Continue removing calc, plaque, debris
- Reinforce OH
- Definitive SRP
- Polish
- Evaluate for further perio tx
Self-limiting disease that usually resolves within 10 days to two weeks
NUG
If symptoms persist, a complete medical evaluation (physician referral) is indicated for possible systemic factors
NUG
What do you do in the subsequent visits after treating a pt with NUG?
- Correction of residual defects
- Reinforce OH
- Refer for psych or med consult if disease recurs regularly
Which diseases?
The most severe inflammatory periodontal diseases caused by plaque bacteria
Run an acute course
Rapidly destructive and debilitating
Necrotizing gingivitis (NG)
Necrotizing perio (NP)
Necrotizing stomatitis (NS)
Which diseases?
Represent various stages of same disease process
Necrotizing gingivitis (NG)
Necrotizing perio (NP)
Necrotizing stomatitis (NS)
Which disease?
Diagnosis is applied only to conditions confined to gingival tissue and where there is no loss of attachment
Necrotizing gingivitis (NG)
Which disease?
Most often, the disease results in loss of attachment
Necrotizing perio (NP)
Which disease?
Diagnosis is applied only where lesion is confined to periodontal tissues (gingival, PDL, alveolar bone)
Necrotizing perio (NP)
Which disease?
Further progression to include tissue beyond mucogingival junction
Necrotizing stomatitis (NS)
Which disease?
Ulcerated and necrotic papillae/gingival margins
Necrotizing gingivitis (NG)
Which disease?
Initial lesion often seen interproximally at crest of a few interdental papillae; often appears in areas of pre-existing chronic gingivitis
Necrotizing gingivitis (NG)
Which disease?
Results in characteristic “punched-out” appearance
Necrotizing gingivitis (NG)
Which disease?
Ulcers are covered by a yellowish-white or greyish slough termed “pseudomembrane” (a misnomer); no coherence
Necrotizing gingivitis (NG)
Which disease?
Ulcers consist of fibrin and necrotic tissue with leukocytes, erythrocytes and masses of bacteria
Necrotizing gingivitis (NG)
Which disease?
Removal of sloughed material results in bleeding and ulcerated underlying tissue becomes exposed
Necrotizing gingivitis (NG)
Which disease?
Progression results in sequestrum formation w/ loss of small or large portions of alveolar bone; evident in HIV/immunicompromised pts
Necrotizing perio (NP)
Which disease?
Sequestrum initially is not moveable, but after some time becomes loosened and can be removed w/ forceps
Necrotizing perio (NP)
Which diseases?
Varying degrees of swelling of lymph nodes, fever, and malaise
Necrotizing gingivitis (NG)
Necrotizing perio (NP)
Necrotizing stomatitis (NS)
Which diseases?
Varying affect on OH and nutritional intake, contributing to severity of disease process and outcome of proposed tx
Necrotizing gingivitis (NG)
Necrotizing perio (NP)
Necrotizing stomatitis (NS)
Which disease?
Initial punched-out defects at top of interdental papillae of mandibular central incisor region
Necrotizing gingivitis (NUG, ANUG)
Which disease?
Often results in a major loss of interdental tissue, including alveolar bone
Necrotizing periodontitis (NP)
Which disease?
Caused by interaction btwn host and fusospirochetal bacteria
ANUG
Which disease?
Number of spirochetes is proportional to amount of inflammation and necrosis
ANUG
Which disease?
Punched out gingival margin and necrotizing condition
ANUG
Which disease?
Pseudomembrane that peels off, leaving raw areas; primarily only the marginal gingiva is affected
ANUG
Which disease?
Rare in children
No definite duration, but usually 10-14 days
No demonstrated immunity
No contagion
ANUG
Which disease?
Starts w/ necrotic lesions at 1 or more interdental papillae and progresses to max. extent within a few days
ANUG
Which disease?
In some 3rd world countries, ANUG-like lesions can expand beyond gingiva and progress to life-threatening infections
Cancrum oris (NOMA)
Which disease?
Ulcers affect the gingival margin but NOT primarily the interdental papillae
Primary herpetic gingivostomatitis
Which disease?
A circular ulcer affecting the 2nd premolar gingiva is indicative of the diagnosis
Primary herpetic gingivostomatitis
Which disease?
Caused by HSV-1 and sometimes HSV-2; common among children and young adults
Acute herpetic gingivostomatitis
Which disease?
Manifests as painful vesicular lesions that burst to form shallow ulcers w/ smooth margin and red halo
Acute herpetic gingivostomatitis
Which disease?
Lesions bleed less readily on pressure than do lesions of NUG
Acute herpetic gingivostomatitis
Which disease?
Tx is primarily supportive, but moderate-severe cases may need anti-viral drugs like Acyclovir
Acute herpetic gingivostomatitis
T/F: Presribing ABs is appropriate for treating Acute herpetic gingivostomatitis
FALSE!!!
Which disease?
Diffuse erythema leaves slightly depressed oval or spherical ulcer
Acute herpetic gingivostomatitis
Which disease?
Diffuse involvement of the gingiva; may include buccal mucosa + lips
Acute herpetic gingivostomatitis
How long does Acute herpetic gingivostomatitis last?
7-10 days
Is Acute herpetic gingivostomatitis contagious?
YES
What does an acute episode of Acute herpetic gingivostomatitis result in?
Some immunity
What disease?
Earliest symptom = most coronal portion of papilla is destroyed by necrosis from col outward; defects are covered by whiteish pseudomembrane
NUG
What disease?
First pain may be experienced before any ulcerations are clinically visible
NUG
ANUG is best treated in the early, ____________ stage
reversible
What disease?
Complete destruction of papilla between canine and premolar; uneven involvement
NUG
What disease?
White patches + erosive alterations primarily affected attached gingiva
Mild herpetic gingivostomatitis
What disease?
May have occurred secondary to trauma, such as severe toothbrush abrasion
Mild herpetic gingivostomatitis
What disease?
Pt has good OH, very little plaque, and minimal marginal inflammation despite disease
Mild herpetic gingivostomatitis
What disease?
Lack of OH, plaque retention caused by ortho leads to gingivitis, which becomes infected w/ this disease
Herpetic gingivostomatitis
What disease?
Severe gingivitis present before infection; pt my have fever and swollen lymph nodes
Severe herpetic gingivostomatitis
What disease?
Looks similar to ANUG, but vesicles are present
Severe herpetic gingivostomatitis
What disease?
Found on children who suck their thumbs and dentists
Herpetic whitlow
Inflammation of the gingiva in relation
to the crown of an incompletely erupted tooth
Pericoronitis
Where does pericoronitis most frequently occur?
Mandibular 3rd molar
Erupted 3rd molars that are crowded or close to the ascending ramus, due to anatomy of the area, may lack any
form of ___________ gingiva.
keratinized (attached)
What disease?
In the acute stage, the pt may not be able to bite properly because the swollen tissue extends over the occlusal surface of the partially impacted 3rd or fully erupted 2nd molars
Pericoronitis
What disease?
Pain can radiate to neck, throat, floor of mouth; associated lymph nodes may be enlarged and tender to palpation; fever
Pericoronitis
What disease has the following tx?
For acute lesions:
Flush area with warm water to remove debris and exudate.
Flush the area with an antimicrobial after gently elevating the flap.
ABs are prescribed in severe cases.
If flap is swollen, an incision is made in an anterior posterior direction to establish drainage
Periocoronitis
T/F: Preventively, all pericoronal flaps should be removed
True
Name the 6 systemic factors most associated with the etiology and/or progression of perio
Diabetes
Meds
Immunosuppressive disorders
Environmental conditions
Hematologic disorders
Genetic disorders
General symptoms include the classical triad: Polidypsia, Polyuria and Polyphagia
Diabetes
In diabetes, what accounts for most of the vascular changes seen in diabetic patients such as retinopathy, nephropathy, and angiopathy? (all represent alterations in the basal membrane of the vessels)
Hyperglycemia
___________ __________ results in a reduction in defense mechanisms and increased susceptibility to infections leading to destructive periodontal disease
Uncontrolled diabetes
Signs and symptoms include:
Cheilosis and tendency toward drying and cracking, burning sensations, decreased salivary flow and alterations in the flora
Diabetes
Increased anaerobic flora including AA, P gingivalis, P intermedia, and C rectus
Diabetes
Increased susceptibility to infection due to polymorphonuclear leukocyte deficiencies resulting in impaired chemo taxis, defective phagocytosis or impaired adhesion
Diabetes
What are the acute dental emergencies? What should you always have nearby?
Low circulating blood glucose (pt may sweat, shake, tremble, not be able to speak)
Always have glucose!
A calcineurin inhibitor, used as an
immunosuppressant medication. It is a natural product. Taken by mouth or by injection for RA, psoriasis, Crohn’s disease, nephrotic syndrome, and in organ transplants to prevent rejection. It is also used as eye drops for keratoconjunctivitis sicca (dry eyes)
Ciclosporin
What is phenytoin sodium (dilantin) replaced w/ tegretol used for?
Seizures
What is an antihypertensive calcium antagonist (calcium channel blockers) used for?
Hypertension
Angina
What group of drugs cause drug-induced gingival enlargements?
Membrane ion channels
What is a disfiguring side effect of anti-convulsants, calcineurin inhibitors, and calcium channel blocking agents?
Drug-induced gingival overgrowth (DIGO)
DIGO leads to an overproduction of ___________
collagen
What category?
Phenytoin sodium (Dilatin)
Anticonvulsant
Which drug?
Onset of gingival overgrowth is 3 months after; 50% of users develop these lesions
Phenytoin sodium (Dilatin)
Which category?
Nifedipine
Antihypertensive calcium antagonist
Which drug?
Manages angina and hypertension; gingival overgrowth is clinically and histologically similar to that seen in Phenytoin
Nifedipine
Which drug?
Onset of gingival overgrowth is 3 months after; 30% of users develop these lesions
Ciclosporin
Which drug?
Also used to deal with RA or diabetes type 1
Ciclosporin
Which drug?
Blocks Ca2+ channels of T helper cells and NK cells; leads to accumulation of collagen
Ciclosporin
Long term ___________ therapy can lead to osteoporosis
Prednisone
____________ has shown to impair collagen and mucopolysaccharide synthesis of bone
Hydrocortisone
What causes a modification in the host’s response to plaque and is largely confined to soft tissues and manifests as an increase in chronic gingivitis?
Pregnancy
Severity of gingival redness, swelling, bleeding and exudation increased during what months in pregnancy?
Months 2-8
What increases with gingival overgrowth during pregnancy, and leads to an increase in quantity/quality of anaerobic microflora?
Pseudo pockets
What oral path mass is associated with pregnancy?
Pyogenic granuloma
T/F: There can be fluctuations in gingivitis with phases of the menstrual cycle
True
Often accompanied by increased gingival inflammation and this heightened response to plaque has been attributed to the concentration of circulating sex hormones
Puberty
What is associated with the following oral lesions?
Linear gingival erythema
ANUG
ANUP
Necrotizing stomatitis affecting gingiva + bone
HIV
What cell count is used as a marker in HIV?
CD4+
What are 2 superimposed infections seen with HIV?
Candidiasis
Herpes
What is oral hairy leukoplakia associated with?
EBV
Drug regime failure w/ HIV pts
T/F: There is a direct relationship between gingival bleeding and CD4+ count in HIV pts
FALSE
In HIV pts, what happens as the CD4+ count decreases?
Attachment loss gets worse
When a pt quits smoking, when can you remove “smoking” from their chart/perio diagnosis?
After 1 yr free of smoking
What disease?
Differential diagnosis is leukemia and multiple myeloma
Plasma cell (B cell) gingivitis
What disease?
Due to reaction to essential oils in toothpastes (cinnamon)
Plasma cell (B cell) gingivitis
Name the 2 quantitative leukocyte disorders
Neutropenia
Agranulocytosis
Name the 2 qualitative leukocyte disorders
Chemotaxis
Phagocytic
Malignant forms exhibit ulceration and necrosis of marginal gingiva; associated w/ bleeding and involvement of attached gingiva; bone loss may occur in deciduous dentition
Neutropenia
Severe disease in number of circulating neutrophils in peripheral blood vessels
Neutropenia
May be a rxn to specific drugs, radiation, or severe infection
Neutropenia
Fluctuation of cellular production levels of bone marrow stem cells; autosomal dominant
Cyclic neutropenia
In acute form, generalized enlargement is apparent; gingival bleeding is common; may related to thrombocytopenia
Leukemia
Gingival swelling due to infiltration by leukemic cells is a feature of what disease?
Acute monocytic leukemia
What cells dictate healing and inflammation status?
Neutrophils
Platelet aggregation + leukocyte migration
Hemostasis
Neutrophil + macrophage migration; phagocytosis
Inflammation
Epithelial migration; osteoid formation; angiogenesis
Proliferation/Regeneration
Increased tensile strength of matrix
Remodeling
What disease?
Decreased neutrophil phagocytic activity
Type 1 diabetes
What disease?
Decreased neutrophil apoptosis
Type 2 diabetes
What diseases?
Decreased neutrophil chemotaxis
Increased neutrophils in periodontium
Type 1 and 2 diabetes
What causes the following?
Increased neutrophil hyperactivity
Increased neutrophil release of proinflammatory cytokines
Increased respiratory burst/oxidative stress, causing gingival destruction
Smoking
T/F: Disease in the tooth affects the periodontium and vice versa
True
Lesions of the periodontal ligament and adjacent alveolar bone may originate from infections in what places?
Periodontium or pulp
Which 3 anatomical pathways connect endo and perio tissues?
Apical foramen
Accessory canal
Exposure of dentinal tubules (ex: perio, SRP, enamel-cementum disjunction)
Where on the tooth are most accessory canals found? Where else can accessory canals be found?
Apical 1/3
Some also found in furcation region
The classification for perio-endo lesions is based on what 3 things?
Etiology
Diagnosis
Prognosis
Endo lesion w/ secondary perio involvement
Endo lesion
Perio lesion w/ secondary endo involvement
Perio lesion
What type of lesion?
Characterized by necrotic pulp and localized osseous destruction
Primary endo lesion
What type of lesion?
Excellent prognosis for reattachment
Primary endo lesion
What type of lesion?
Pulp necrosis and secondary periradicular disease may produce destruction of periodontal tissues with formation of a sinus-like tract through the periodontium
Primary endo lesion
What type of lesion?
Fistulation thru apex or lateral canal may cause furcation involvement
Primary endo lesion
What are the 2 ways endo abscesses drain into the sulcus?
Extraosseous fistulation
PDL fistulation
Pulp disease can cause ___________ pathosis
periradicular
Bone loss and/or drainage through the sulcus due to pulp disease can mimic _______
perio
What type of lesion?
Existing endodontic lesion with secondary periodontal involvement due to plaque and calculus accumulation beginning at the cervical area
Primary endo lesion w/ secondary perio involvement
Pulpal infection may cause a tissue destructive process that proceeds from the apical or furcal region of a
tooth toward the gingival margin
Retrograde perio
Infection spreads from the gingival margin toward the root apex
Marginal perio
What type of lesion?
Lesion caused by periodontal disease. Periodontitis gradually progresses until the apical region is reached
Primary perio lesion
What type of lesion?
Characterized by vital pulp and generalized bone loss
Primary perio lesion
What type of lesion?
Local factors are:
Plaque
Calculus
Developmental defect (palato-gingival groove)
Primary perio lesion
What type of lesion?
Prognosis for reattachment is questionable
Primary perio lesion
What type of lesion?
Primary periodontal lesion leading to exposure of a lateral canal to the oral environment with the resulting pulpal infection and necrosis
Primary perio lesion w/ secondary endo involvement
What type of lesion?
Could be the result of periodontal procedures in very deep lesions where the vasculature (apical or lateral) is severed by an instrument
Primary perio lesion w/ secondary endo involvement
What type of lesion?
This lesions occurs where an endodontically induced periapical lesion exists on a tooth that is also periodontally involved
True combined lesion
What type of lesion?
Radiographically the two entities meet and merge
somewhere along the root surface
True combined lesion
The microorganisms associated with periodontal lesions also may be capable of producing necrosis of pulp cells through the action of their _________ products, __________ enzymes, or other mechanisms
metabolic; destructive
What do the following cause?
Palato-gingival grooves
Periodontal Therapy (S/RP)
Root anomalies (microcracks)
Trauma induced root resorption
Fractures
Perforations
Over-instrumentations
Debris extrusion
Perio endo lesions
Low incidence in maxillary centrals and laterals
Palato-gingival grooves
Due to trauma, necrotic pulp, injury to cementum and periodontium
Trauma induced root resorption
What direction is a fractured tooth typically?
M-D
What direction is a vertically fractured root typically?
B-L
Fracture from external (occlusal) load
Fractured tooth
Fracture from internal load
Vertically fractured root
During RCT and preparation for the insertion of posts, instrumentation can accidentally cause what? What gets damaged?
Root perforation; PDL is damaged
What is associated with the following symptoms?
Increased mobility
Increased probing depth
Loss of fibrous attachment
Suppuration
Root perforation
T/F: Unless root planing is invasive (either significantly deep layers of dentin removed, or severance of apical vessels), it is doubtful perio tx results in significant pathologic changes in the pulp
True
What type of lesion?
Acute, sharp pain
Endo
What type of lesion?
Chronic, dull, tolerable pain
Perio
Which tx is done first, endo or perio?
Endo is always 1st
What type of lesion? What is the tx?
Periapical bone loss
Drainage through the sulcus
Pulp test negative
Rapid onset
Inadequate root canal
Periodontal probing yields narrow, isolated pocket
Endo
Endo tx
What type of lesion? What is the tx?
Necrotic Pulp
Periodontitis with plaque and calculus
Pulp test negative
Increase in pocket depth and attachment loss
Rx evidence of pulp and periodontal disease
Endo lesion w/ secondary perio involvement
Endo tx, then perio tx (closed)
What type of lesion? What is the tx?
History of disease progression/therapy
Deep pockets
Attachment loss
No evidence of pulpal disease
Pulp test positive
Perio lesion
Perio tx
What type of lesion? What is the tx?
Deep pockets
Extensive attachment loss
Pulp disease: increase pain, pulp test negative
Rx evidence
Perio lesion w/ secondary endo involvement
Endo tx, then perio tx
What type of lesion? What is the tx?
Etiologic factors present for both conditions
Generalized periodontal destruction that connects to periapical lesion
Pulp test negative
Root Fracture
True combined lesion
Endo tx, perio tx, ext?
What bacteria?
Gram -
Anaerobic
Non-motile
Rod
P gingivalis
T forsythia
What bacteria?
Virulence factors = tissue invasive (epithelium), collagenase enzyme production, endotoxin, keratinase, trypsin-like proteolytic enzyme, fibrinolysin, Hydrogen sulfide
P gingivalis
What bacteria?
“Keystone” pathogen; central to disease progression even in low numbers
P gingivalis
What bacteria?
Subverts host immune system, which alters plaque composition
P gingivalis
Which bacteria plays a role in RA?
P gingivalis
What bacteria?
Produces trypsin-like proteolytic enzyme
T forysthia
What bacteria?
High affinity for crevicular epithelium; invades epithelial cells
T forysthia
What bacteria?
Gram -
Anaerobic
Spirochete (motile)
T denticola
What bacteria?
Has trypsin-like proteolytic activity
T denticola
What bacteria?
Strong association w/ severe adult perio and recurrent perio
T denticola
What bacteria?
Tissue invasive in ANUG
T denticola
