Cementum Dentin Alveolar bone Pulp Not enamel – this is epithelial tissue

Cementum Dentin Alveolar bone • Pulp Not enamel – this is epithelial tissue

perio final Flashcards by Amanda L

support and contour of free ging

attaches encircles tooth at the “neck”

Circular gingival fiber

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support of gingiva

attaches gingiva to cementum

Dentogingival

Dento=cementum

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Anchors tooth to bone

attaches cementum to periosteum

dentoperiosteal

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attaches gingiva to the bone (periosteum)

alveologingival

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keeps teeth in alignment, protects interprox bone , connect teeth

Transseptal (interdental)

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Many cells
Little extracellular matrix
Internal/external basal lamina
No blood supply

Gingival Epithelial Tissues

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Few cells
Mostly extracellular matrix
Strongropelikefibers
Rich blood supply

Gingival Connective Tissue (Lamina Propria)

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Cementum
Dentin
Alveolar bone
Pulp
Not enamel – this is epithelial tissue

Cementum
Dentin
Alveolar bone • Pulp
Not enamel – this is epithelial tissue

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Fibroblasts
Cementoblasts
Osteoblasts

(makes collagen)
(makes cementum)
(makes bone)

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Cell-to-cell connection
Two neighboring epithelial cells together
Found in gingival epithelium
Like snap closure on a jacket

Desmosome

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Originates from the cementum and runs apically to insert into the alveolar crest.
Resists lateral movement of the tooth and keeps tooth in its socket.
The first fibers to be formed before tooth eruption has occurred

Alveolar crest

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Collagen fibers from the PDL
Insertion into cementum & alveolar bone
Inserts into the hard tissues at 90 degrees
The angulation increases its strength

Sharpey’s Fibers

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Originates from cementum and runs at right angles and inserts into bone.
Opposes lateral forces.
The second fibers to be formed as soon as the first tooth-to-tooth contact has occurred

Horizontal

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Found in the middle third of the root api to the horizontal fibers; originates from cementum and runs coronally and diagonally into bone.
Absorbs occlusal forces.The most abundant and thus the principal attachment of the tooth.

Oblique

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Originates from cementum of the apex of the root, spreading out apically and laterally into bone.
Resists tipping of the tooth.
One of the last fibers to form.

Apical

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From the crest of the interradicular septum extending to the cementum in the furcation area.
Resists the forces of luxation (pulling out) and tipping.
.Lost when bone is destroyed in the furcation area in disease.

Interradicular

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Connect epithelial cell to basal lamina connection

* Found in gingival epithelium

Hemidesmosome

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Base of the sulcus
Joins gingiva to the tooth
• Nonkeratinized
• Similar to SE, it is vulnerable.
• More permeable than the OE or SE
• Attaches the gingiva enamel and/or cementum
• JE provides a seal at the base of the pocket
• JE also is a protective barrier
• Between the plaque biofilm and the underlying
connective tissue
• High rate of cell turnover

JunctionalEpithelium(JE)

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Cover outer surface of Free & Attached gingiva
From the crest of the GM to MGJ
Wavy boundary junction with the connective tissue (in health)
Epithelialridgesconnectwiththecollagenfibersinthe connective tissue
May be keratinized or parakeratinized

Oral Epithelium (OE)

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Lining of the sulcus
Thin and nonkeratinized
Vulnerable to stresses
Junction to the connective tissue is smooth
Permeable, allows fluid flow à GCF

Sulcular Epithelium (SE)

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Connective tissue attachment + Junctional Epithelium
CT (1.07mm) + JE (0.97mm) =
• Important when fabricating restorations
• It must not invade this

Biologic Width
BW (2.04mm)
Should be at least 3mm on a radiograph only!

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Loss of radicular bone including marginal bone

Dehiscence

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• Loss of radicular bone but not marginal bone
VS

• A “window” of bone resorbed on radicular surface

Dehiscence

Fenestration

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Forms before tooth eruption
No cementocytes
Covers coronal half to 2/3 of root • Thinnest at CEJ
Mostly Sharpey fibers
Thickness 30 – 60 μm

Acellular

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``` At apical 1/3 • Forms faster than acellular • Has cementocytes • Continues to form after tooth eruption • Less calcified • Thickness 150 – 200 μm ```

Cellular

* Forms before tooth eruption * No cementocytes * Covers coronal half to 2/3 of root • Thinnest at CEJ * Mostly Sharpey fibers * Thickness 30 – 60 μm

Acellular cementum

``` the cementum At apical 1/3 • Forms faster than acellular • Has cementocytes • Continues to form after tooth eruption • Less calcified • Thickness 150 – 200 μm ```

Cellular cementum

• Three microscopic interfaces @ CEJ 1. Overlap 2. Meet 3. Gap

60% 30% 10%

• cells that do removal of mineralized material and organic matrix of bone

* Osteoclasts: | * C = “Consume”

• creation of bone matrix

* Osteoblasts: | * B = “Build”

* CN V: Trigeminal nerve * Division II – * Division III –

to the maxilla • Afferent to the mandible • Afferent & Efferent

• Spongy • Lattice-like • Between Cortical bone & Alveolar bone proper Formed around tooth to form support for the Alveolar bone proper

Cancellous Bone

``` • Hard outer wall of jaws • On facial & lingual aspects • Surrounds alveolar bone proper • Gives support to socket • Not radiographically seen • Alveolar crest most coronal part of this Cortical bone ```

Cortical bone

measured from a fixed point—the CEJ—to the base of the sulcus or periodontal pocket Refers to the position of the attached periodontal tissue at the base of the pocket or sulcus

Clinical Attachment Level (CAL)

measured from the gingival margin to the base of the sulcus or periodontal pocket

probing depths

Long-lived, out of control inflammatory response • Continues for more than few weeks • Destroy healthy tissue and cause more damage than the original problem – overzealous immune system • Classic warning signs are absent • Problems go unnoticed by patient • Clinically, pain is often absent

Chronic Inflammation

- Short-term & normal process - Increased movement of plasma and leukocytes from the blood to injured tissues - Shows five classic signs of acute inflammation 1. Heat 2. Redness 3. Swelling 4. Pain 5. Loss of function

Acute Inflammation

Body sends host defense components to site of infection | In an attempt to heal and eliminate pathogens

Inflammatory Response

• Within minutes after cleaning, acquired pellicle forms over tooth surface • Acquired pellicle composed of salivary glycoproteins Allows for free-flowing microbes to stick to the pellicle

Stage 1: Initial Attachment

What stage: - Microbes able to withstand hydrodynamic forces - Predominantly gram + cocci - Attains permanent attachment - Attached microbes produce substances to attract others - Coaggregation - When genetically different bacteria become attached to one another

Stage 2: Permanent Attachment

- Self-protective matrix formation - Firmly attached bacteria secrete protective matrix -Extracellular protective matrix - Consists of proteins, glycolipids, and bacterial DNA - Protected against host immune response - Chronic disease established

Stage 3: Maturation Phase I

- Mushroom shape microcolonies form - Attached to the tooth by a narrow base - Specific species grow at an accelerated rate - Biofilm becomes thicker, forming on top of each other - Fluid channels form within the matrix - Carries nutrients to the microbes & disposes waste - Cell to cell communication occurs among each other

Stage 4: Maturation Phase II

what Stage of biofilm Microbes disperse from colony to spread to other surfaces

Stage 5: Dispersion

Condition in which a purulent oozes from the gingival surface when pressed.

gingival suppuration | pus

``` recession = + Enlargement= - ```

Determining attachment loss and inflammation

Recession that dosnt extend to the mucogingival junction with no periodontal bone loss in the interdental areas

Millers class 1

Recession that extends to/ beyond the mucogingival junction/ no interdental bone loss

Millers class 2

Recession extends to beyond the mucogingival junction, with some periodontal attachment loss in the interdental area or malpositioning of the teeth

Millers class 3

Recession that extends to or beyond mucogingival junction with severe bone loss and soft tissue loss interdentally/ with malpositioning of teeth

class 4

process whereby microorganisms irreversibly attach to and grow on a surface and produce extracellular polymers that facilitate attachment and matrix formation.

Biofilm formation

• Present @ birth • Not antigen specific Does NOT improve with repeated exposure to pathogen

• Innate

• Develops throughout life • Antigen specific • Lag time between infection and response • Memory develops which may provide lifelong immunity to reinfection

• Adaptive

to defend the life of the individual by identifying foreign substances in the body and developing a defense against them.

Prime Purpose of Immune System

* Also called neutrophils * Rapid responders * 1st line of defense against infection * Capture & destroy * Short-lives (dies after engorged with bacteria) * Attracted to bacteria by chemotaxis * Digests bacteria by using lysosomes * Perio pathogens most effectively destroyed by PMNs

PMN

* when in bloodstream =? * when in tissues =? * Slower to arrive than PMNs * Surround & destroy bacteria * Long-lives, seen in chronic inflammation

Monocytes | Macrophage

Antibodies Otherwise known as immunoglobulins (Ig) Five major classes IgM

IgD IgG IgA: found in saliva! IgE

part of the body's immune system. They help the body fight infection and other diseases.

White blood cells (WBC) Types of white blood cells are granulocytes (neutrophils, eosinophils, and basophils), monocytes, and lymphocytes (T cells and B cells).

• Small, and they reorganize & control invaders

Lymphocytes | WBC

``` when in bloodstream when in tissues • Slower to arrive than PMNs • Surround & destroy bacteria • Long-lives, seen in chronic inflammation ```

- Monocyte: | - Macrophage:

-Makes antibodies and releases them into bloodstream Y-shaped proteins that bind

B-Lymphocytes (B-Cells) ``` One end to antigen, other to B-Cell Helps B-cell kill antigen Can change to two types of B-Cells: Plasma B-Cells Memory B-Cells ```

Intensifies the response of the B cells and the macrophages to the bacterial invasion. This further stimulate immune response

T-Lymphocytes (T-Cells) | T-cells produce cytokines

....travel via bloodstream 2. Near the infection site, ....push their way between the thin layer of epithelial cells and enter the connective tissue (extravasation) 3. This process = transendothelial migration

Migration of Leukocytes to Infection Site

• Process where leukocytes 1. Enter the connective tissue 2. Are attracted to the infection site • Because of biochemical compounds released by invaders

Chemotaxis

process by which a cell uses its plasma membrane to engulf a large particle, giving rise to an internal compartment

Phagocytosis

Which inflammatory process? 1. Blood vessels in infection site become more permeable 2. PMNs arrive first at site 3. PMNs release cytokines to facilitate response 4. Liver produces C-reactive proteins (CRP) 5. If body succeeds in getting rid of infection, tissue will heal, immune cells leave area with no damage to tissues

Acute Inflammatory Process

• Dysfunction of the resolution pathway which is supposed to shut down the inflammatory response after initial response • Result: 1. Perio tissues do not heal 2. Chronic, progressive and destructive, nonresolving inflammation

Periodontal Disease

Signs and symptoms during chronic inflammation may disappear entirely or partially during period of remission

Remission •

• Signs and symptoms may recur with all of their severity in an active period called exacerbation

• Exacerbation

* Initial lesion * Early lesion * Established lesion * Advanced lesion

4 Histologic Stages in Periodontal Disease Development

What stage? Bacteria colonize near GM: initial location of biofilm • GCF increases in volume as response to bacteria presence • Vascular dilation à PMN migration • Clinically, tissue looks healthy • Host response by PMNs successful if most bacteria is destroyed • Body can repair any damage at this point • If bacteria is not controlled, early gingivitis develops

Initial Lesion: Bacterial Accumulation

* Biofilm matures, bacterial toxins penetrate the JE * Increase vasculature/permeability, more PMNs move in * PMNs release cytokines that cause localized destruction of CT * Macrophages recruited at this point, release more cytokines * Clinically: edema and redness at GM seen * Initiation of good self-care can disrupt biofilm for complete health to return * IF immune system fails to shut off this host response à lesion progresses to established gingivitis

Early Lesion: Early Gingivitis

What stage of gingivitis ? • Biofilm extends subgingivally • Disrupts attachment of the most coronal of the JE attachment • More stimulation of the immune system • More PMNs, macrophages, and lymphocytes • Plasma cells now produce large # of antibodies to assist • This host response end up getting healthy CT destroyed • JE loses attachment to root surface and transforms into pocket epithelium which is thinner & more permeable

Established Lesion: Established Gingivitis

Clinically all features of gingivitis are accentuated • Good self-care vital at this point to reverse destruction • In some pts, if bacterial infection not controlled à periodontitis

Established Lesion: Established Gingivitis continued

Biofilm spreads laterally as well as apically along the root • Chronic inflammation causes harm on periodontium • PMNs & macrophages cause destruction of CT and PDL • Macrophages produce byproducts that destroy alveolar bone • Gingival pocket à Periodontal pocket • Destruction caused by host response overwhelms any tissue repair attempt • Clinically, periodontal pocket detected, bone loss, furcation involvement, possible mobility depending on extent • Changes are irreversible

Advanced Lesion: Periodontitis

* Changes in color, contour, and consistency of gingival tissues * Can be observed clinically * 4-14 days after biofilm accumulation in sulcus

Gingivitis ``` Progression of Gingivitis • Tissue damage is reversible • Body can repair the damage • Gingivitis can persist without progressing into periodontitis! • This depends on the person ```

Acute vs. Chronic Gingivitis

* Acute gingivitis * Lasts for short period of time * Tissues appears swollen * Due to fluid in the gingival connective tissues * Chronic gingivitis * Lasts for longeràmonths or years! * Can result in more fibrotic tissue

``` • JE located belownormal (apically) • SE of pocket thickens • Small SE ulcerations expose inflamed underlying CT • Collagen destruction in area of inflammation • Alveolar bone destruction • Permanent destruction of PDL Cementum becomes exposed to the biofilm ```

``` Periodontitis Characteristics • Apical migration of JE • Loss of connective tidsue • Loss of alveolar bone • Tissue damage irreversible v ```

* Inflammation spreading: * Into gingival CT * Into the alveolar bone * Into the PDL * Inflammation spreads like this because it’s the path of least resistance * Usually results in suprabony perio pocket

Horizontal Bone Loss Pathway

Inflammation spreading: • Into gingival CT • DIRECTLY into PDL space • Into alveolar bone • Occurs when crestal PDL are weak and no longer act as an effective barrier against inflammation • Usually results in an infrabony perio pocket

Vertical Bone Loss Pathway

• Bowl-shaped defect in interdental bone • The picture is showing how a crater is affecting roots of two adjacent teeth • Craters can happen in only one tooth as well Results in difficulty in cleaning interdental surfaces

Osseous Crater

• Site that shows continued destruction • Site that shows stable attachment over a period of time Probing depths & radiographs only show past destruction

* Active disease site | * Inactive disease site

a periodontal pocket in which the bottom is coronal to the underlying bone.

suprabony pocket horizontal bone loss

a periodontal pocket in which the bottom is apical to the level of the adjacent alveolar bone.

infrabony pocket vertical bone loss

Periodontal Health

* Free from inflammatory perio disease * Absence of symptoms such as: * BOP * Erythema * Edema * Symptoms * Attachment loss * Bone loss

Periodontal health on an intact periodontium

healthy

Periodontal health on a reduced periodontium in a nonperiodontal patient

Clinical gingival health on a reduced periodontium is characterized by an absence of bleeding on probing, erythema, edema and patient symptoms in the presence of reduced clinical attachment and bone levels.

* No loss of perio tissue (past or present) =? | * Past hx of reduced perio tissue but no current activity of =?

Intact periodontium | Reduced periodontium

• Return of periodontitis that was previously arrested • Anyone with prior hx is at risk Happens especially with noncompliant pt

• Recurrent

* Return of periodontitis but with an unknown etioogy * Happens despite: * Good home care * Compliant to recommendations

• Refractory ``` Tx for Refractory Periodontal Disease • Review OH • SRP • Systemic or local antibiotics • Removal of hopeless teeth • Correcting local factors • Surgery • Frequent maintenance ```

* Necrosis of the gingival tissues, PDL and alveolar bone * Rapidly escalates & produce periodontal attachment loss within days * Involved interdental areas separated into one facial papilla and one lingual papilla with necrotic depression between them * Craters formed with the separation * Once craters are formed, PDL and Bone become destroyed

Necrotizing Periodontitis (NP) Other Names of NPD • Trench mouth • Acute necrotizing ulcerative gingivitis (ANUG) • Necrotizing ulcerative gingivostomatitis

• Limited to gingival tissues • No bone loss

Necrotizing Gingivitis (NG)

• Rare and most extensive of NPD • Associated with severe immunocompromised med system • Most distinguishable feature: • Bone denudation extending to alveolar mucosa • May result in oral-antral fistula & osteitis (inflammation of bone) • Immediate consult to oral pathologist, OMFS, and physician • Severe necrosis • Extends beyond gingiva to other parts of the oral cavity: tongue, cheeks, palate Most severe and rarest among the necrotizing perio disease

Necrotizing Stomatitis

Initial Appointment • Comprehensive medical hx • Gentle removal of pseudomembrane with cotton pellets • Limited supragingival instrumentation • Stay supragingival, preferably with ultrasonic instrument • May need topical anesthesia • Subgingival instrumentation can extend the infection! • Chlorhexidine rinse 2x daily or hydrogen peroxide:water (1:1) every 2-3 hrs for few days • Analgesic such as NSAID (ibuprofen) for pain relief • Advise to return in about 2 days for a checkup of the symptoms • Tell pt that tx is not complete when the pain stops

Treatment of Necrotizing Gingivitis: 1st Visit

* 2nd Appointment (about 2 days after 1st visit) * Subgingival instrumentation usually can be started * Pay attention to systemic symptoms * Encourage continued self-care * Smokingcessation * Stress reduction * Nutrition

Treatment of Necrotizing Gingivitis: 2nd Visit

* Third appointment (about 5 days after initial appointment) * Patient should be symptom free * Complete subgingival instrumentation * Further pt self-care counseling * Depending on systemic symptoms, antibiotics may be necessary * Make appt for comprehensive clinical assessment * Toaddressanypossibleunderlyingperiodisease * Pt needs to be reevaluated in about 1 month

Treatment of Necrotizing Gingivitis: 3rd Visit

Acute =? Chronic =?

A=Rapid, painful, lack of spontaneous draining | C= Slow, may not feel, sinus tract

• Involves tissues around crown or partially erupted tooth • Inflammation called pericoronitis • Flap (lid)of tissue covering tooth is called operculum • May have trismus-limited opening May have elevated temperature

Pericoronal

• Affects deeper structures as well as gingival margin | Occurs at site of pre-existing periodontitis

Periodontal

* Local anesthesia * Drain pus * Perio instrumentation • Warm saline rinses * Schedule follow-up * If needed: * Adjust pt’s occlusion • Rx antibiotics by DDS * Schedule follow-up

Gingival/Periodontal

* Local Anesthesia * Drain pus * Perio instrumentation * Irrigate operculum with saline * Warm saline rinse * Evaluate 3rd molar extraction * If needed Rx antibiotics by DDS

Pericoronal

``` • Compromised host immune response (immunosuppressed) • HIV • Poor oral self-care • Emotional stress • Increased level of personal stress • Inadequate sleep (fatigue) • Alcohol abuse • Drugabuse Smoking • Poor nutrition, low protein intake • Overall poor nutrition (college students) • Pre-existing gingivitis or trauma • Avg age is young adult • 22-24 yrs old • But can occur at any age ```

Etiology & Predisposing Factors for NPD

• Begins at coronal part of implant • Implant becomes mobile when it is in final parts of the disease • If mobile implant has signs of osseointegration loss, it is in failure. Shouldn’t be mobile if healthy! • Radiographic signs: • Vertical destruction of crestal bone around implant • Bottom portion of implant can still show osseointegration • May be wedge-shaped defects around implant

Peri-Implantitis

``` Risk Factors for Peri-Implant Failure • Poor biofilm control • Past hx of periodontal disease • Smoking • Residual cement Biochemical overload ```

Tx of Failing Implants • Nonsurgical perio instrumentation • Use of antiseptics • Local/systemic antibiotics • Flap surgery

``` • Plaque-induced gingivitis • “Peri-implant gingivitis” • No loss of bone • Reversible if biofilm removed • 80% patients 50% of implant sites ```

• Peri-implant mucositis

* Periodontitis in soft & hard tissues surrounding osseointegrated implant * Progressive bone loss * Biofilm-induced inflammation * 6-47% prevalence * May progress in nonlinear and accelerating pattern

• Peri-implantitis

• Epithelium adaps to titanium abutment post Barrier between the implant and the oral cavity; the soft tissue around an implant • Sulcular epithelium surrounds the implant abutment post

biological seal

Osseointegration

• Direct contact of bone with implant surface • You NEED proper osseointegration for implant to be successful • Osseointegration successful if: • No mobility • No inflammation of tissues • No discomfort during function • No increased bone loss

* Possible to eliminate certain ....factors * Faulty restoration * Possible to compensate for some that cannot be eliminated easily * Improve home care around local crowded teeth

Local Contributing Factors

• Possible to eliminate ...risk factors • Smoking IF factors cannot be eliminated, improve the balance by increasing home care or professional care ``` Such as: • Tobacco use • Diabetes mellitus • Leukemia • HIV • Stress • Osteoporosis • Hormonal variations • Medication side effect ```

Systemic Contributing Factors

Patients with well-controlled diabetes have no more periodontal disease than those without diabetes Patients with poorly-controlled diabetes more likely to develop periodontitis Patients with diabetes AND smoke 20x more likely to experience severe periodontitis than nondiabetics

TRUE

• Papilla reacting strongly to the biofilm • Tumor forms on the interdental gingiva or GM • Non-cancerous Not usually painful

Pyogenic Granuloma - usually in pregant PT

Glucose level at appointment time Target range = 80 to 120 mg/dL Increased risk of infection = 180–300 g/dL Unacceptable range = greater than 300 mg/dL

Finger-Stick

Fungle infection on corners of mouth

Cheilosis

• If self-care good, usually no problem • Usually in pts with hx of gingivitis • Inflammation of gingiva increases even in just small amounts of plaque Inflammation increases in 2nd & 3rd trimesters due to elevated estrogen create exaggerated response to biofilm

Pregnancy 2nd trimester associated with increased Prevotella intermedia levels • P. intermedia uses estrogen as a substitute for natural growth factor! • Elevated progesterone increase capillary permeability & dilation àincrease gingival exudate & edema • Elevated progesterone & estrogen suppress immune response to biofilm

Glucose level at appointment time Target range = 80 to 120 mg/dL Increased risk of infection = 180–300 g/dL Unacceptable range = greater than 300 mg/dL

Finger-Stick

The goal for most individuals with diabetes is a glucose level less than 7%. High susceptibility to infection occurs when the glucose level is above 8%.

HbA1c HbA1c monitors blood glucose over a period of time • More accurate in determining monitoring than finger stick

* Increase in hormones result in: | * Increased blood circulation to gingival tissues • Increased sensitivity to local irritants (biofilm)

Puberty • Puberty gingivitis occurs equally in males/females

* Inflammation increases in 2nd & 3rd trimesters due to elevated estrogen create exaggerated response to biofilm * 2nd trimester associated with increased Prevotella intermedia levels * P. intermedia uses estrogen as a substitute for natural growth factor! * Elevated progesterone increase capillary permeability & dilation àincrease gingival exudate & edema * Elevated progesterone & estrogen suppress immune response to biofilm

Pregnancy • If self-care good, usually no problem • Usually in pts with hx of gingivitis • Inflammation of gingiva increases even in just small amounts of plaque

* Make sure pt’s immune system is okay * ANC (absolute neutrophil count) >1000 * If less than 1000 prophylactic antibiotic needed * Platelets = 50,000 * Viral load or CD4 count does not directly impact dental care * Low CD4 count is reflection of advanced disease * Chance of opportunistic infections such as candidiasis higher

HIV/AIDS & the Dental Hygienist

* Decreased level of hormones result in oral changes * Dry mouth/burning sensation * Altered taste * Bone loss may be exacerbated * Menopausal gingivostomatitis * Gingiva that bleeds easily * Abnormal pale, dry and shiny, erythematous appearance

Menopause & the Dental Hygienist • Talk to pt about osteoporosis risk • Emphasize self-care to avoid perio problems • If pt taking bisphosphonates, have pt be aware of oral side effects, especially with IV bisphosphonates

* Most dramatic & clinically obvious * Overgrowth usually begins in the papillary area * Enlarged papillae can cover the anatomical crown * Three major classes of Rx: * Anticonvulsants * Immunosuppressants * Calcium channel blockers

Drug-Influenced Gingival Overgrowth

Xenograft refers to a graft taken from a human other then the PT receiving the graft

FALSE | Xenograft= someone else Alien

Esthetic crown lengthening surgery results in longer clinical crowns for the teeth

TRUE

When removing sutures following a periosurgical procedure, the suture knot should always be pulled through the tissue

FALSE

One of the indications for periodontal surgeries to provide acsses for improved perio dontal instrumentation

TRUE

The term healing by repare means that the architecture and function of lost tissue is completey restored

FALSE

One relative contraindiction for periodontal surgery can be high risk for dental caries

TRUE

``` • Inflammation of the lungs • Two-types • Community-acquired • Outside hospital setting • Hospital-acquired • During stay in hospital/long term • Perio disease/poor OH may be associated with hospital-acquired ```

Pneumonia

drugs that help prevent or slow down bone thinning (osteoporosis).

Bisphosphonates

* Irregular surface always covered with plaque biofilm * Surface harbors bacteria * More calculus, more plaque biofilm * Difficult/impossible for pt to clean * Calculus near perio tissues

Calculus • Supragingival & Subgingival calculus • 70-90% inorganic (mainly calcium phosphate) • 10-30% organic (biofilm, dead WBC)

1 Attached to pellicle • Most common on enamel surface • Removed easily 2 Attached to tooth irregularity • In cracks in tooth surfaces, grooves on tooth • Difficult to remove 3 Attached directly to tooth surface • Interlocked with inorganic crystals of tooth • Difficult to remove

Calculus on Different Surfaces

* Can be surgically removed * CEP * Flat triangular projection of enamel * Spherical shape enamel projection on root

Cervical Enamel Projection/Enamel Pearl

An important serum marker for CVD and possibly periodontitis • Produced during acute inflammation • Successful periodontal therapy could decrease this

C-Reactive Protein

• NO evidence of CAL or bone loss over 5 years • Heavy biofilm deposits but low level of tissue destruction • Modifiers: • Nonsmoker • Normoglycemic patient (non-diabetic)

Grade A: Slow Rate

``` • 2mm or more of CAL over 5 years • Tissue destruction exceeds expectations based on biofilm accumulation • Modifiers: • Smokers 10+ cigarettes a day • HbA1c 7% and greater in diabetic pts ```

Grade C: Rapid Rate

• Less than 2mm of CAL or bone loss over 5 years • Tissue destruction meets expectations given biofilm accumulation in mouth • Modifiers: • Smokers <10 cigarettes a day • HbA1c <7% in diabetic patients

Grade B: Moderate Rate

What stage? Severity • Interdental CAL of 1-2mm at site of greatest loss • Radiographic bone loss extending to coronal 1/3 of root • No tooth loss due to periodontitis (pt hx) * Complexity of Management * Max probing depth of 4mm or less * Mostly horizontal bone loss

Stage I Periodontitis (Mild)

what stage? • Severity • Interdental CAL of 3-4mm at site of greatest loss • Radiographic bone loss extending to coronal 1/3 of root • No tooth loss due to periodontitis (pt hx) * Complexity of Management * Max probing depth of 5mm or less * Mostly horizontal bone loss

Stage II Periodontitis (Moderate)

What stage? • Severity • Interdental CAL greater or equal to 5mm at site of greatest loss • Radiographic bone loss extends to mid 1/3 of root • Tooth loss due to periodontitis of 4 or more teeth * Complexity of Management * Max probing depth of 6mm * Vertical bone loss of 3mm or greater * Class II or III furcation involvement * Moderate alveolar ridge defect complicating implant placement

Stage III Periodontitis (Severe)

what Stage? • Severity • Interdental CAL of greater or equal to 5mm at site of greatest loss • Radiographic bone loss extends to mid 1/3 of root • Tooth loss due to periodontitis of 5 or more teeth • Complexity of Management • Max probing depth of greater than 6mm • Masticatory dysfunction/occlusal trauma • Tooth mobility > Class II • Less than 20 remaining teeth

Stage IV Periodontitis (Severe)

* Halitosis * Dry mouth * Staining * Perio disease * Cancer

Oral Problems with Smoking

• Affects both the immune & inflammatory system • Smokers with decreased signs of inflammation due to impaired blood flow • Impaired neutrophil function • May decrease antibody production

Impact on Immune System

Impact on Bone Metabolism • Associated with greater bone destruction • Nicotine may suppress osteoblasts • May alter normal bone remodeling

smoking

< 30% | >= 30%

localized generlized

Eliminate inflammation in periodontium • Attempt to restore periodontium back to health • Combination of professional care & patient’s self-care • It is the first recommended approach to control perio infections

What is NSPT? ``` Also Known As... • Initial perio therapy • Initial therapy • Phase I therapy • Soft tissue management ```

1 Minimize bacterial challenge to patient 2 Eliminate/control local factors for perio disease 3 Minimize impact of systemic factors for perio disease 4 Stabilize the attachment level

4 Goals of NSPT | After Professional Tx Has Been Rendered

* Customized OHI * Periodontal instrumentation (Scaling/Root Planing) * Eliminate local factors * Correction of systemic factors * Smoking, Diabetes * Re-evaluating periodontal response * 4-6 week reevaluation after initial NSPT * Recare typically in 3 months as perio maintenance

Tx Plan Example: Stage I/II, Grade A Periodontitis

* Customized OHI * Periodontal instrumentation (Scaling/Root Planing) * Eliminate local factors * Correction of systemic factors * Reevaluation periodontal response * 4-6 week reevaluation after initial NSPT * Is surgery needed?

Tx Plan Example: Stage III/IV, Grade B/C

* Preventive only! * Removal of biofilm, calculus, and stains from exposed and unexposed surfaces of the teeth by scaling and polishing as a preventive measure for control of local irritants

Oral prophylaxis

Removal of calculus, debris, biofilm and byproducts from tooth surface and gingival pocket to tx inflammation • This includes scaling, root planing, surgical debridement

• Periodontal debridement

• There is NO new bone, cementum or PDL formed at the site • Vulnerable for perio diseases Probing depth reduction

Long Junctional Epithelium

• Minimize recurrence & progression of periodontal disease • Reduce the incidence of tooth loss • Increase likelihood of detecting & treating other oral conditions Expected outcome: maintain the dentition throughout the life of the patient

Goals of Periodontal Maintenance

1.) Return of disease in patient who has been successfully been tx in the past • See typical reasons for recurrence in past slide 2.)Disease is resistant to therapy even with appropriate tx and great effort by the patient/clinician

Recurrent Periodontitis

* Most are relative contraindications * Relative contraindications * Conditions that may surgery inadvisable for some when the condition/situations are severe or extreme * Patients with: * Certain systemic diseases * Totally noncompliant with self-care * High risk for caries * Unreliastic expectations of the outcomes of surgery

Perio Surgery Contraindications

1 Healing by repair 2 Healing by reattachment 3 Healing by new attachment 4 Healing by regeneration

Wound Healing After Surgery

• Healing of a wound by formation of tissues that do not precisely restore the original architecture or original function of a body part • E.g. Formation of a scar after a healing of a cut • Healing of the peridontium by repair = long junctional epithelium after perio instrumentation • This does not duplicate the original perio tissues • NO new bone, cementum or PDL formed

Healing by Repair

Healing when epithelium & connective tissues are newly attached to tooth root where periodontitis has destroyed this area/attachment New attachment occurs in area damaged by disease Reattachment occurs in absence of disease

Healing by New Attachment

Regrowth of the precise tissues that were present before the disease caused damage to the area With surgery, regeneration is possible but cannot be regenerated predictably in all sites with current techniques.

Healing by Regeneration

``` 1st stage Occurs when wound margins are closely adapted • Ideal situation in perio surgery but doesn’t happen often ```

Primary Intention of wound closur

Wound margins are not in close contact • Granulation tissue must form to close the space • Many in perio surgery involve healing by this

Secondary Intention

Wound left open with intent of surgically closing later | • Doesn’t pertain to perio surgery

Tertiary Intention

``` To gain access to tooth roots • Tissue lifted long enough for whatever procedure • E.g. Calculus removal • Afterwards tissue sutured back in original place ```

Flap for Access | Modified Widman

``` • Creates a longer clinical crown • By removing gingival & alveolar bone from necks of teeth • Two types: • Functional crown lengthening • When there is decay below the GM • Esthetic crown lengthening • Improve appearance of teeth related to excess gingiva ```

Crown Lengthening ``` • Flap elevated for access to bone • Bone recontoured • Tissue sutured back in place • Healing is more apical position on the root than before • Example here: aesthetic ```

Potential for new bone to develop after bone graft

Osteogenesis

• Grafting materials to form a framework to guide the | formation of new bone within it

Osteoconduction

Grafting material cells converted into bone-forming cells | to form new bone

Osteoinduction

Bone from patient’s own body (e.g. exostoses, edentulous ridge) • Has the most osteogenic potential

Autograft

Bone taken from another human (e.g. cadaver bone)

Allograft

• Bone from another species (e.g. bovine)

Xenograft

• Synthetic material (e.g. calcium phosphate)

Alloplast

``` 1.) Does not dissolve in body fluids • Must be removed by clinician • Silk 2.) Designed to dissolve over time • Does not normally need removal • Some does not dissolve well in saliva • Plain & Chromic gut • Vicryl ```

Nonabsorbable Absorbable

1-Form of oral tablet or capsule/ Antibiotics 2- Placement of chemical agent in perio pocket where it can contact biofilm on teeth or in the sulcus • Mouthrinses • Antibiotic adjuncts

Systemic Topical

has properties that make them favorable for use in periodontitis • Administered orally (and topically – to be talked about in a bit) • Higher concentration in GCF • Effective against A.acetomycetemcomitans • Inhibit action of collagenase • Enzyme responsible for breakdown of periodontium

Tetracycline

Doxycycline Hyclate Gel

``` Atridox=Brand name • Brand name: Atridox • Tetracycline derivative • Gel into the periodontal pocket • Two syringes: liquid & powder • Mix together into one syringe • Injected into the pocket • Gel solidifies when in contact with GCF • Adjunct to SRP for local periodontitis • Same Adverse Rxns and Contraindications as Minocycline ```

• Brand name: PerioChip • Gelatin chip containing 2.5mg of CHX • Inserted into pocket • May be used in pockets 5mm or greater • Upto 8 chips can be inserted in 1 visit • Depending on the size it may need to be cut into size • Chip dissolves in the pocket over 7-10 days • Can be replaced at 3 month recare visit • No risk of antibiotic resistance since it’s not an antibiotic

Chlorhexidine | Gluconate Chip

``` Minocycline hydrochloride microspheres • Arestin • Doxycycline hyclate gel • Atridox • Chlorhexidine gluconate chip • Periochip ```

Examples of Controlled-Released Agents

``` • Brand name: Arestin • Powder microsphere form • Broad-spectrum • Tetracycline derivative • Microspheres dissolve after 5-7 days • Adjunct to SRP in patients with localized periodontitis ```

Minocycline Hydrochloride Microsphere

Only by Rx (Peridex, Paroex, Perioguard) • 0.12% concentration only in the United States • Proven to reduce gingivitis • Reduce severity of gingivitis by about 50% with proper use • Bactericidal agent against gram + and – bacteria • Disrupts cell walls of bacteria • Has low level of toxicity • Has good substantivity • Binds to hard & soft oral tissues

Chlorhexidine Gluconate

* Mouth irritation * Extrinsic tooth staining * Brown * Xerostomia * Taste changes * Unpleasant or unusual taste * Metallic taste * Increases SUPRAGINGIVAL calculus formation

Chlorhexidine Gluconate: Side Effects

``` Common active ingredient in many mouthrinses • Essential oils include: • Thymol • Menthol • Eucalyptol • Methylsalicylate • Available OTC • Some have ADA seal for use against gingivitis • Can help control biofilm • Less expensive than CHX ```

Mouthrinses with Essential Oils Side Effects • Burning sensation • Bitter taste • Drying of mucous membrane

perio final Flashcards

(180 cards)