Periodontal Diseases and Conditions Flashcards
(88 cards)
1
Q
Periodontal Disease: Incidence, major risk factors
A
- 20% of 14-17yo in the US are found to have attachment loss of at least 2mm at one or more sites. The number and severity of affected sites increase steadily with age, demonstrating that chronic periodontitis often begin in adolescence.
- Chronic periodontitis responds well to oral hygiene measures and can more easily be arrested in its early stages when attachment loss is minimal and deep pockets have not developed.
- Smoking is a major risk factor in periodontitis, and smoking is increasing among adolescents, particularly females.
2
Q
Aggressive Periodontitis
A
- Rare, rapidly progressing forms of periodontitis also affect children and adolescents.
- Both periodontitis as a manifestation of systemic disease and aggressive periodontitis affecting children who are otherwise healthy occur in the pediatric population.
- Rapid attachment and bone loss with familial aggregation, phagocyte abnormalities and hyper-responsive macrophage phenotype
3
Q
LAP in permanent dentition: Characteristics
A
- Formerly called localized juvenile periodontitis, is characterized by the loss of attachment and bone around the permanent incisors and first permanent molars.
- Permanent incisors and first permanent molars and no more than 2 other teeth.
- Distinctive radiographic appearance. Rapid attachment loss, occurring at 3x the rate of chronic disease. Inflammation is not as extreme as that occurring in periodontitis associated with systemic disease, such as neutropenia, but both inflammation and plaque accumulation are often greater than those found in the typical teenager.
- Usually detected in early adolescence, but retrospective examination of earlier radiographs has sometimes revealed undetected disease in the primary dentition. This suggests that LAP of permanent dentition and LAP of primary dentition are the same disease entity, differing only in the age of onset or detection.
4
Q
LAP in permanent dentition: Prevalence, etiology
A
- Prevalence: 1%. Most commonly occurring in the African American population.
- In some cases, appears to be inherited as an autosomal dominant trait and LAP has been linked to a neutrophil chemotactic defect. LAP may progress to generalized aggressive periodontitis or remain localized.
- Linked to high numbers of Aggregatibacter actinomycetemcomitans and successful treatment correlates well with eradication of the bacteria.
- No evidence of systemic disease, some populations (Brandywine) is associated with specific gene on chromosome 4, higher in African Americans
- AA and bacteroides species the most highly virulent strains***
- Functional defects reported in neutrophils from patients with LAgP ***
- Anomalies in chemotaxis, phagocytosis, bactericidal activity, and superoxide production
- Molecular markers of LAgP with low numbers of chemoattractant receptors and low GP 110***
5
Q
LAP in permanent dentition: Treatment
A
- Treatment: Local measures in combination with systemic antibiotic therapy and microbiological monitoring.
- Metronidazole alone or in combination with amoxicillin appears to be more effective in arresting disease progression. Localized surgical intervention is necessary to manage residual effects.
- Tx: tetracycline (staining!), tetra with metronidazole, metronidazole and amox***
- With surgical and non-surgical root debridement, maintenance every 4 months
6
Q
Generalized aggressive periodontitis
A
- Adolescents and teenagers.
- In young adults, formerly called rapidly progressive periodontitis.
- Affects the entire dentition and is not self-limiting. Heavy accumulations of plaque and calculus, and inflammation may be severe.
- NOT associated with high levels of A. actinomycetemcomitans; microbiological profile is closer to that of chronic disease.
- Manage aggressively with local therapy and systemic antibiotics
7
Q
LAP in primary dentition: Characteristics, associations, etiology, who does it typically affect? Where does it manifest?
A
- Characterized by localized loss of attachment in the primary dentition.
- Manifests in the molar area, where localized, usually bilaterally symmetric loss of attachment occurs.
- Most commonly occurring in the African American population.
- Usually accompanied by mild to moderate inflammation. Heavier than average plaque deposits may be visible, calculus may be present
- Commonly diagnosed during the late primary dentition or early transitional dentition.
- May progress in the permanent dentition and is probably the same disease entity, differing only in the age of onset or diagnosis.
- Believed to be the result of a bacterial infection combined with specific but minor host immunologic defects.
- Some cases are associated with systemic genetic diseases.
8
Q
LAP in primary dentition: Treatment
A
- Treatment:
- Antibiotics with local debridement
- Tetracyclines are *contraindicated* because of potential staining developing permanent teeth.
- Metronidazole is antibiotic of choice.
9
Q
Acute Necrotizing Ulcerative Gingivitis: Dental management
A
- Local debridement (ultrasonic scaling)
- NSAIDs for pain
- Penicillin or metronidazole for systemic involvement
10
Q
Acute Necrotizing Ulcerative Gingivitis/Periodontitis: Clinical features, peak incidence
A
AKA Vincent’s infection, pyorrhea, or trench mouth
- Characterized by rapid onset of painful gingivitis with interproximal and marginal necrosis and ulceration.
- Fever, lymphadenopathy, malaise, fiery red gingiva, extreme oral pain, hypersalivation, unmistakable fetor oris
- Punched out, ulcerated, and covered with a grayish pseudomembrane
- May progress into necrotizing ulcerative periodontitis in immunocompromised individuals (increased stress; HIV-infected patients).
- Peak incidence in late teens and 20s in developed countries
- Common in young children in less developed countries.
- This multifactorial disease has a bacterial population high in fusiform bacillae, Prevotella intermedia and spirochetes.
11
Q
Necrotizing Ulcerative Gingivitis/Periodontitis: Predisposing factors
A
- Predisposing factors:
- Malnutrition
- Viral infections
- Stress
- Lack of sleep
- Smoking
12
Q
Necrotizing Ulcerative Gingivitis/Periodontitis: Bacterial association
A
High levels of spirochetes and Prevotella intermedia
13
Q
Necrotizing Ulcerative Gingivitis/Periodontitis: Treatment
A
- Treatment:
- Local debridement and irrigation provides rapid resolution
- Antibiotic therapy with penicillin or metronidazole indicated with elevated temperature
- Stress-reduction
- Rest
Partial loss of interdental papillae can be expected despite normal healing.
14
Q
Plaque-induced gingivitis: Features
A
- Gingival inflammation
- No loss of attachment or bone
- Reversible
15
Q
Plaque-induced gingivitis: Prevalence
A
- Low in early childhood
- Peaks during puberty
- 60% of teenagers have gingival BOP (Handbook)
- Gingivitis 73% in 6-11yo and raises with age
- Adolescence is more 50-90%
- Gingivitis less in girls than boys, probably related with oral hygiene
16
Q
Plaque-induced gingivitis: Etiology
A
- Plaque-dependent
- Individual susceptibility variable
- Reactivity gradually increases with age
- May be related to steroid hormones
- Puberty
- Pregnancy
- Menstruation
- Oral contraceptives
- Local factors may contribute
- Crowding
- Ortho appliances
- Mouthbreathing
- Eruption
- Calculus (~10% of children, ⅓ of teens have calculus)
17
Q
Plaque-induced gingival enlargement: Clinical features
A
- Enlargement of interdental papilla and/or marginal gingiva.
- Ranges from pale and fibrotic to red and friable.
- May be generalized or localized.
18
Q
Plaque-induced gingival enlargement: Etiology
A
Prolonged exposure to plaque
19
Q
Plaque-induced gingival enlargement: Common local contributory factors
A
- Mouth breathing
- Ortho appliances
20
Q
Plaque-induced gingival enlargement: Dental management
A
- Thorough OH
- Electric TB may help
- Gingivectomy or gingivoplasty may be necessary
21
Q
Drug-induced gingival enlargement: Drugs
A
- Phenytoin (dilantin) - anti-epileptic
- Cyclosporin (immunosuppressant)
- Calcium channel blockers (diltiazem, nifedipine, amlodipine)
22
Q
Drug-induced gingival enlargement: Clinical features
A
- Starts as painless enlargement of interdental papilla and marginal gingiva
- Fibro-epithelial growth
- May progress to cover crowns
- Related to plaque-control
- Does not occur in edentulous areas
- Regresses and may disappear after cessation of drug tx
23
Q
Drug-induced gingival enlargement: Treatment
A
- Replace with alternate drug if possible
- Professional prophylaxis and thorough OH
- Daily use of CHX may help
- Gingivectomy or gingivoplasty
24
Q
Pyogenic granuloma
A
Pregnancy tumor
- Painless localized gingival enlargement
- Blue-red color
- Occurs in pregnancy
25
**Gingival abscess:** Features, onset, dental management
* Localized, painful lesion of marginal gingiva or interdental papilla
* Onset: Sudden
* Bacterial infection following gingival trauma, typically caused by embedded foreign object
* Dental management:
* Debridement, irrigation, establishment of drainage
26
**Pericoronitis:** Clinical features
* Inflammation of gingiva covering partially erupted tooth
* **Most common around erupting 3rd molars**
* Food trap, environment conducive to bacterial growth
* Pericoronal flap becomes inflamed and swollen
* Enlarged flap traumatized by occlusion = very painful
27
**Pericoronitis:** Dental management
* Debridement
* ABX therapy for systemic involvement
* CHX irrigation
28
**Vitamin C-deficiency gingivitis:** Clinical features
* Edematous, spongy gingiva
* Clinical appearance of non-specific gingivitis
* Impaired wound healing
29
**Vitamin C-deficiency gingivitis:** Dental management
* Tx of underlying deficiency
* Plaque control
30
**Diabetes and Chronic Periodontitis:** Clinical features
* Increased incidence of gingivitis
* Increased risk and earlier onset of periodontitis (10-15% of teens)
* Poor metabolic control appears to increase risk of periodontitis
* Plaque and calculus levels comparable to normal controls
31
**Diabetes and Chronic Periodontitis:** Dental management
* Plaque control
* Scaling and root planing
32
**Hypophosphatasia + Periodontal Disease:** Clinical features
* Genetic disorder
* **Early loss of primary teeth occurs in almost all reported cases.**
* **Five levels of severity:**
* **Perinatal (lethal)**
* **Infantile**
* **Childhood**
* **Adult**
* **Odontohypophosphatasia**
* Phenotypes range from severe bone abnormalities leading to neonatal death, to isolated premature loss of deciduous teeth (odontohypophosphatasia) – early loss of primary teeth may be the first clinical sign in mild forms.
* Abnormal cementum formation leads to early loss of primary teeth.
* Teeth are exfoliated with intact roots, usually before root formation is complete.
* Teeth lost in order of eruption.
* Most likely to affect primary incisors but may affect additional teeth.
* **Pulp chambers may be abnormally large.**
33
**Hypophosphatasia + Periodontal Disease:** Etiology
Deficient or defective tissue non-specific alkaline phosphatase (TNSALP)
34
**Hypophosphatasia + Periodontal Disease:** Diagnosis
* Low serum alkaline phosphatase (normal values vary with age, so normal control values must be adjusted for age).
* Increased phosphoethanolamine in urine or elevated pyridoxal phosphate in serum.
* Deficient or defective cementum by histologic examination.
* Characteristic defects on radiographic examination of bones.
35
**Hypophosphatasia + Periodontal Disease:** Dental prognosis
* In odontohypophosphatasia permanent dentition may be normal.
* Poor dentition reported in more severe forms.
36
**Hypophosphatasia + Periodontal Disease:** Systemic treatment
Enzyme replacement therapy, Asfotase Alpha, approved for perinatal, infantile, and juvenile-onset hypophosphatatsia.
37
**Hypophosphatasia + Periodontal Disease:** Dental management
Supportive therapy to address concerns and prevent potential long-term consequences of early tooth loss.
38
**Leukocyte Adhesion Defect (LAD) + Periodontal Disease:** Clinical features
* Rare AR defect
* Leukocyte surface glycoprotein defect resulting in poor leukocyte adherence.
* Oral manifestation of LAD is generalized periodontitis in primary and young permanent dentition.
* Severe generalized periodontitis refractory to treatment.
* Frequent respiratory, skin, ear, and other ST bacterial infections.
* Stem cell transportation can be curative.
39
**Leukocyte Adhesion Defect (LAD) + Periodontal Disease:** Dental management
* Thorough OH
* ABX therapy
* Extraction of affected teeth
40
**Papillon-Lefevre Syndrome + Periodontal Disease:** Etiology, Clinical features
* Rare genetic disorder
* Clinical features:
* Palmar and plantar hyperkeratosis
* **Attachment and bone loss resulting in premature loss of primary and permanent teeth**
* Inflammation can be severe
* May involve ***Aggregatibacter actinomycetemcomitans*** infections
41
**Papillon-Lefevre Syndrome + Periodontal Disease:** Dental management
* Thorough OH
* ABX therapy and extraction of affected teeth, with variable success
42
**Down syndrome + Periodontal Disease:** Prevalence, Clinical features
* Prevalence is **60-100% in those under 30yo**
* **May be noted in primary dentition**
* **Mandibular incisors** most often affected
* Susceptibility to periodontitis appears to be due to innate immune system abnormalities
43
**Down syndrome + Periodontal Disease:** Dental management
* Thorough OH
* Periodontal tx based on periodontal dx
44
**Chediak-Higashi syndrome + Periodontal Disease:** What is it?
* Rare, AR
* **Oculocutaneous albinism, photophobia, nystagmus, peripheral neuropathy**
* Severe gingivitis, periodontitis
45
**Neutropenia + Periodontal Disease:** Etiology
* Decreased circulating neutrophils
* Many possible forms of neutropenia, including **acquired** and **congenital**, with chemotherapy-induced and immune disorders being among the most common.
* Can be temporary (e.g. when neutrophils are destroyed fighting a viral infection).
* Variable degree of increased susceptibility to infection, including periodontal disease.
46
**Neutropenia + Periodontal Disease:** Periodontal signs
* Severe gingivitis with ulcerations
* Attachment loss and alveolar bone loss
* Early loss of primary teeth
* Severe periodontal disease in permanent dentition
* H/o other ST infections
47
**Neutropenia + Periodontal Disease:** Diagnosis
Decreased WBC differential count.
48
**Neutropenia + Periodontal Disease:** Dental management
* Thorough OH, ABX therapy, extraction of affected teeth.
* Periodontal tx based on periodontal dx.
* **Systemically administered granulocyte colony stimulating factor (G-CSF) to treat underlying cause.**
49
**Langerhans Cell Histiocytosis** (formerly histiocytosis X) **+ Periodontal Disease**
* Group of disorders with variable symptoms resulting from **abnormal proliferation and dissemination of histiocytic cells of the Langerhans system**.
* **~10% show oral involvement.**
* Bone lesions may produce **“floating teeth".**
* Gingival swelling.
* Dx by biopsy
50
**Acute Leukemia + Periodontal Disease**
* Gingival enlargement due to infiltration with leukemic cells may be presenting symptom, particularly of **acute myeloid leukemia (AML):****Gingiva appears hyperplasia, edematous, bluish red.**
* **Petechiae or mucosal ulcerations** may be present with any form of leukemia.
* **Initial dx by CBC**
51
Mucogingival defects
* Pocket depth exceeds width of attached keratinized gingiva.
* Lower incisor most common location.
* In children, defect may result from **labial positioning of tooth erupting through band of attached gingiva.**
52
Localized areas of gingival recession ("stripping")
* Usually due to labial malposition of tooth.
* Most common in lower incisors.
* May be difficult to clean.
* May produce mucogingival defect.
53
Pseudo-recession
* Recession-like appearance (uneven gingival margin location) w/o root exposure.
* **Distinguish from true recession by locating CEJ.**
54
Factitious Injury
* Most common in children and adolescents.
* May be seen in children with developmental delay.
* May result in recession defect.
55
High labial frenum attachment
* May exacerbate stripping and mucogingival defects in the mandible.
* May be cosmetically objectionable in maxilla.
* Papillary penetrating frenum is associated with midline diastema.
56
**Developmental or Acquired Deformities or Conditions:** Treatment
* Narrow band of attached gingiva can be maintained with good plaque control.
* Gingival graft may be needed to create anatomic contours conducive to good plaque control.
* Frenectomy may be indicated to remove frenum.
* Use of laser surgery may allow procedure to be performed w/o LA and may provide less painful post-op course. If ortho is indicated, surgery is usually postponed until after lingual repositioning of lower incisors or closing of maxillary midline diastema.
57
**Clinical Periodontal Exam:** Bone loss
Interproximal crest *should* be 1-2mm apical to the CEJ on BWX
58
**Clinical Periodontal Exam:** Attachment loss
* Attachment level determined by subtracting distance from CEJ to FGM from probing pocket depth (PPD) (distance from FGM to bottom of the pocket).
* Measured at 6 sites of tooth.
* More difficult to determine in younger patients because CEJ is usually below FGM.
* Due to inaccuracies in measurement, loss or gain of 2mm or more clinically meaningful.
59
**Clinical Periodontal Exam:** Mucogingival Problems
* To determine width of attached gingiva locate mucogingival junction and measure to FGM.
* Note sites with \<1mm of attached gingiva.
60
**Clinical Periodontal Exam:** Periodontal screening and recording (PSR)
* System designed for easier and faster screening of periodontal health for adults.
* Uses probe with colored band **3.5-5.5mm.**
* If band is even partially submerged, a complete periodontal exam is indicated.
* Can be used in children and adolescents, but erupting teeth give false positives.
61
**LAP in primary dentition:** Etiologic factors
* Leukocyte chemotactic defect
* Cementum defect
* Usually but not always associated with *A. actinomycetemcomitans*
62
**LAP in primary dentition:** Dental management
* Little data
* SRP
* ABX therapy: Amoxicillin and metronidazole for 7-10 days OR azithromycin for 3-5 days
63
What % of LAP in permanent dentition is preceded by bone loss in primary dentition?
50%
64
**LAP in permanent dentition:** Prevalence
0.2% in whites, 2.6% in blacks
65
**LAP in permanent dentition:** Etiology
* Aggregatibacter actinomycetemcomitans* in most but not all cases
* **Defects in neutrophil chemotaxis and phagocytosis, over-reactive monocyte response, genetic defects in gene coding IgG2.**
66
**LAP in permanent dentition:** Dental management
* SRP followed by systemic ABX after completion of mechanical tx
* **Amoxicillin and metronidazole for 7-10 days OR azithromycin for 3-5 days**
* Local antibiotic therapy not effective
* Surgical correction of defects
* Regenerative therapy
67
What are the three types of aggressive periodontitis?
* LAP in primary dentition
* LAP in permanent dentition
* Generalized LAP
68
**Generalized Aggressive Periodontitis:** Features and Treatment
* Generalized attachment loss in permanent dentition in persons under 30yo, heavy accumulation of plaque
* Probably the result of progression of LAP
* Smoking is a risk factor
* Treatment same as LAP (Handbook)
* Tx: debridement and antibiotics not successful, need labs to identify specific pathogens
* Premature exfoliation of primary teeth
* **Non-mobile, facultative anaerobic, gram negative rods: porphyramonous gingivalis and treponema\*\*\***
* **Alteration of IgG\*\***\*
69
Periodontal disease: Prevalence
* Gingivitis very common in children, perio is less common in young children
* 0.2-0.5% periodontal attached loss in children
70
Differences between gingiva with childhood vs adults
* Cementum is more thin and dense than adults
* PDL is wider and has fewer and less dense fibers per unit area
* Less developed net of collagen fibers than in adults in gingiva
* Lamina dura is thinner
71
What bacteria are involved with generalized aggressive periodontitis?
**Non-mobile, facultative anaerobic, gram negative rods: porphyramonous gingivalis and treponema\*\*\***
72
Periodontitis may be a manifestation of what systemic diseases
* Hypophosphatasia
* Leukocyte adhesion defect
* Papillon-LeFevre syndrome
* Down syndrome
* Chediak-Higashi syndrome
* Neutropenia
* Langerhans cell histiocytosis (formerly histiocytosis X)
* Acute leukemia
73
What are developmental or acquired periodontal deformities or conditions?
* Mucogingival defects
* Localized areas of gingival recession ("stripping")
* Pseudo-recession
* Factitious injury
* High labial frenum attachment
74
**Clinical Periodontal Exam:** Gingival inflammation
* Signs
* Color change
* Edema
* Bleeding on gentle probing
* Gingival crevicular exudate
* Gingival Index (GI) widely used to assess gingival health
75
**Clinical Periodontal Exam:** Plaque accumulation
* Several indices have been used to quantitative plaque levels
* Most include assessment of portion of surface covered by plaque
76
Manifestation of systemic disease: with eruption of primary teeth up to the age of 4-5yo
* Localized or generalized, neutrophil with abnormality, leukocyte deficiency.
* Bacteria: *Aa, Prevotella intermedia, Eikenella corrodens, Capnocytophaga sputigena*
* Papillon-Lefevre syndrome (hyperkeratosis of soles of hands and feet), hypophosphatasia (alkaline phosphatase), cyclic neutropenia, Down syndrome, leukocyte adherence deficiency (LAD), agranulocytosis, _NOT_ diabetes
* Tx: Surgical debridement and antibiotics
77
Necrotizing Perio Diseases: NPD
* Tx: Local debridement, oral hygiene, follow up, if febrile then metronidazole and penicillin
* Most significant findings is interproximal necrosis and ulceration with pain, rapid onset of gingival pain
* **High levels of spirochetes and P. intermedia**
* **Predisposition:**
* **Malnutrition, stress, viral infections, lack of sleep, stress, and systemic diseases\*\*\***
* Pts with NPD can be febrile, if febrile then give antibiotics (metronidazole an penicillin)
78
High levels of what bacteria are present in necrotizing perio diseass?
**High levels of spirochetes and P. intermedia**
79
Necrotizing ulcerative gingivitis (NUG)
Bacterial accumulations in individuals with lowered host resistance.
* Responds rapidly to the reduction of bacteria by personal plaque control and professional debridement
* If lymphadenopathy or fever with oral symptoms - systemic antibiotics may be indicated
* Chemotherapeutic rinses - beneficial in initial treatment stages
* After acute inflammation of lesion is resolved - additional intervention to prevent recurrence or correct soft tissue deformities
80
Necrotizing ulcerative periodontitis (NUP)
Rapid necrosis and destruction of the gingiva and periodontal attachment.
* Gingival bleeding and pain.
* Extension of NUG in individuals with lowered host resistance.
* In HIV (+) and (-) individuals (true prevalence is unknown).
* Management:
* Debridement with irrigation with antiseptics (povidone iodine), antimicrobial mouth rinses (chlorhexidine) and administration of systemic antibiotics.
* HIV-immune deficiency - severe loss of periodontal attachment that does not necessarily present clinically as an ulcerative lesion.
* Linear gingival erythema (LGE, not an acute disease) - In some HIV-infected individuals, does not respond to conventional scaling, root planing, and plaque control (antibiotic therapy should be used in HIV-positive patients with caution - can induce opportunistic infection).
81
*Primary herpes simplex virus type I (herpetic gingivitis)*
* Oral manifestation: Gingivitis
* By the time these patients present, usually febrile, in pain, and w/ lymphadenopathy.
* Diagnosis from clinical appearance of the oral soft tissues, and can be confirmed by viral culture (not routine).
* **Tx: Palliative therapy**
* **Self-limiting and usually resolves in 7-10 days**
* **Systemic antiviral therapy (Acyclovir)** for immunocompromised patients with herpetic gingivitis
82
**Gingival enlargement** (overgrowth of gingiva)
* May result from chronic gingival inflammation
* Exaggerated in patients with **genetic or drug-related systemic factors (anticonvulsants, cyclosporine and calcium channel blocking drugs)**
* Patients taking **phenytoin** – overgrowth may be minimized with oral hygiene and professional maintenance.
* Root debridement – does not return the periodontium to normal contour → complicates ability to clean the dentition & causes esthetic and functional problems.
* Surgical recontouring –postoperative management is important.
* Benefits may be lost due to rapid proliferation during post-therapy phase
* **Recurrence is common with drug-induced gingival overgrowth.**
* Consult patient’s physician - alternative drug therapy, if not → repeated surgical and/or non-surgical intervention.
83
Primary objective of periodontal therapy
Halt disease progression and to resolve inflammation by reducing etiologic factors below the threshold capable of producing breakdown to allow repair of the affected region.
Regeneration of lost periodontal structures can be enhanced by specific procedures (many variables responsible for complete regeneration of the periodontium are unknown and research is ongoing in this area)
84
Scaling and root planing
* Reduction of clinical inflammation, microbial shift to a less pathogenic subgingival flora, decreased probing depth, gain of clinical attachment, and less disease progression
* Technically demanding and time-consuming
* Some sites still do not respond
* Factors may limit the success of treatment: root anatomy (concavities, furrows etc.), furcations, and deep probing depths
* Re-evaluation to determine the treatment response after several weeks
* Sites that continue to exhibit signs of disease, consider:
* Daily personal plaque control not adequate - additional instruction and motivation and/or the use of topical chemotherapeutics (mouthrinses, local drug delivery devices) may be indicated
* Anatomical factors can limit effectives or limit the ability to perform personal plaque control (deep probing depths, root concavities, furcations) may require additional therapy including surgery
* Host response and systemic conditions (diabetes, pregnancy, stress, AIDS, immunodeficiencies, and blood dyscrasias) may not respond well to therapy controlling local factors - control the contributing systemic factors
85
Gingival inflammation response to dental plaque is modified by
Gonadotropic hormone
Insulin
86
Microbiology of gingivitis
* Actinomyces*
* Capnocytophagia*
* Leptotrichia*
* Selenomonas*
87
Systemic factors that can increase gingivitis
Pregnancy + diabetes
88
Medications approved to control **_SUPRA_**gingival, NOT subgingival plaque
* Thymol, menthol, eucalyptol, methyl salicylate
* Chlorhexidine gluconate
* Triclosan
