1

DBCS 329 SGL Study Guide Ted Harmasinski Case 31 Objectives

PREPARED BY: The D2 Class

Pathology 1. Discuss the etiology, epidemiology, pathophysiology and treatment for Acute Bacterial

Sialadenitis. Explain why alcohol and coffee consumption could contribute to this problem. Sources:

Current Medical Dx & Tx Chapter 8. Ear, Nose, & Throat Disorders (Lawrence R. Lustig, MD, Joshua S. Schindler, MD)

Tintinallis Emergency Medincine Section 12. Pediatrics Chapter 118. Neck Masses in children

(Osama Y. Kentab, Nadeemuddin Qureshi)

What is Sialadenitis?

Acute bacterial sialadenitis in the adult most commonly affects either the parotid or submandibular gland. It typically presents with acute swelling of the gland, increased pain and swelling with meals, and tenderness and erythema of the duct opening. Pus often can be massaged from the duct.

Ductal obstruction, often by an inspissated (dried up) mucous plug, is followed by salivary stasis and secondary infection. The most common organism recovered from purulent draining saliva is S aureus.

The causative organism is usually S aureus or Streptococcus, as well as gram negative and anaerobic bacteria it is considered to be polymicobial in origin

o (Gram-negative bacilli include pigmented Prevotella, Porphyromonas, and Fusobacterium)

Careful examination reveals swelling over the angle of the mandible and the face

Sialadenitis often occurs in the setting of dehydration or in association with chronic illness. Underlying Sjgren syndrome may contribute.

In the setting of acute illness, a severe and potentially life-threatening form of sialadenitis, sometimes called suppurative sialadenitis, may develop

Treatment consists of intravenous antibiotics such as nafcillin (1 g intravenously every 46 hours) and measures to increase salivary flow, including hydration, warm compresses, sialagogues (eg, lemon drops), and massage of the gland.

Epidemiology

The incidence of community-acquired acute bacterial sialadenitis is unknown. However, 0.01% to 0.02%

of patients admitted to hospital and 0.02% to 0.04% of post-surgical patients develop this condition.

Chronic recurrent sialadenitis occurs 10 times more frequently in adults than in children, with an age

range of 40 to 60 years in adults and 4 months to 15 years in children.

2. Discuss the etiology, epidemiology, pathophysiology and treatment for sialolithiasis. Sources:

o Lalwani, Anil K.. Current diagnosis & treatment in otolaryngology head & neck surgery. 2nd ed.

New York: McGraw-Hill Medical, 2008. Print.

o Tintinalli, Judith E., and J. Stephan Stapczynski. Tintinalli's emergency medicine: a comprehensive study guide. 7th ed. New York: McGraw-Hill, 2011. Print.

2

Pathophysiology/Etiology

Saliva contains minerals aggregates of mineralized debris in the duct form sialoliths

These salivary duct stones contain primarily hydroxyapatite, calcium phosphate, and/or calcium carbonate.

These aggregates form a nidus, promoting calculi formation, salivary stasis, and eventually obstruction.

Recurrence of sialoliths is about 20%. Correcting risk factors can decrease recurrence rate.

Risk factors:

Long illnesses with DEHYDRATION

Gout

Diabetes

HTN

Xerostomia

If obstruction is not relieved, local inflammation, fibrosis, and acinar atrophy may ensue

Other complications include salivary stasis, acute infection (acute suppurative sialadenitis), and abscess formation

Epidemiology

Men>women, 30-60 yrs old most common

Submandibular gland (Whartons duct) most commonly affected (80-90%) because of its more viscous secretion, its longer, ascending course, and its higher content of calcium and phosphate. 10-20% are found in the parotid and they are rarely found in the sublingual and minor salivary glands.

Clinical Features

Recurrent swelling and pain in the gland, exacerbated when eating. Swelling may subside after an hour

Prolonged obstruction can lead to acute infection and increasing pain and erythema of the gland

Pt may report occasional sand-like foreign bodies in the mouth

Radiographs may reveal radioopaque stones Diagnosis

Diagnosis is clinical

A stone may be palpated within the duct or gland

A conservative course of tx shold precede imaging studies

Imaging studies include x-rays, sialography, and/or CT and MRI scans Tx

Conservative tx: treatment with analgesics, antibiotics (if there is concurrent infection), massage, and sialogogues such as lemon drops. Palpable stones in the distal duct may be digitally milked from the duct.

Ductal papilla can be dilated with ease. Graded lacrimal probes are used serially, and the stone is expressed.

If the stone is too large, a more invasive intraoral procudre is done under local or general anesthesia. The duct is cannulated and an incision is made over the stone to allow extraction. No closure of the incision is made.

Symptomatic stones embedded in the body of the gland may necessitate surgical excision of the gland

3. Discuss the etiology, epidemiology, pathophysiology and treatment for parotid pleomorphic

adenoma. Discuss why treatment could lead to palsy. Sources: Dr. Gordons Salivary Gland Pathology Lecture, eMedicine: Pleomorphic Adenoma

I. BACKGROUND

Also referred to as a benign mixed tumor

3

Most common type of salivary gland tumor

Most common tumor of parotid gland

Three components: o 1) An epithelial cell component o 2) A myoepitheilial cell component o 3) A stromal (mesenchymal) component

Pleomorphic = variable appearance seen by light microscopy o Mixed epithelial (left) and mesenchymal cell components (right)

Carcinoma Ex Pleomorphic Adenoma

o Cancer may develop in 10-20% of pleomorphic adenomas if left untreated o Sudden change of size, facial nerve involvement, ulceration and pain o Usually an adenocarcinoma o 5 year survival is 24% with treatment

II. ETIOLOGY

Unknown, but the incidence of this tumor has been found to increase 15-20 years after exposure to radiation

Possibly Simian virus (SV40)

III. EPIDEMIOLOGY

Most common salivary gland tumor in both children and adults (45-75% of all salivary gland neoplasms)

Annual incidence: ~2-3.5 cases per 100,000 population

Occurs in individuals of all ages o Most common in the third to sixth decades o Average age at presentation is between 43 and 46 years

Seen more often in females than males (2:1 ratio)

4

IV. PATHOPHYSIOLOGY

Epithelial elements may be arranged in duct-like structures, sheets, clumps and/or interlacing strands and consist of polygonal, spindle or stellate-shaped cells (hence pleomorphism).

Areas of squamous metaplasia and epithelial pearls may be present.

The tumor is usually enveloped by a fibrous capsule of varying thickness and often incomplete.

The tumor often extends through these discontinuities but is not a sign of malignant transformation as it does not invade surrounding tissues.

V. TREATMENT

The most common and effective treatment: complete surgical resection

Needle biopsy is highly recommended prior to surgery to confirm the diagnosis

Radiotherapy o Physicians may feel that follow-up radiation treatment is necessary o The National Institute of Health (NIH) does not recommend radiation therapy in all cases and

suggest that it is reserved for specific patients with surgical difficulties because radiation therapy could increase the likelihood that any recurring tumors become malignant.

VI. ADVERSE OUTCOMES

The surgical risks involved in the removal of the tumor vary with the tumor itself. o A smaller, more confined tumor will be easier to remove and therefore be less likely to cause

damage to the facial nerve located nearby. o A tumor that extends to a wider area may carry heavier risk.

Bells Palsy Facial paralysis due to Lyme disease, typhoid fever, trauma, temporal bone

fracture, tumors including acoustic neuroma and herpes virus

Nerve weakness could occur for up to four months after surgery, but this generally does not require any therapy. Permanent nerve damage rarely occurs.

The possibility of infection exists with any surgical wounds, but can be treated with antibiotics.

4. Discuss the etiology, epidemiology and pathophysiology of gestational diabetes.

3-10% of pregnancies depending on population group studied

40-60% of women with GDM show no symptoms

For women who have had gestational diabetes there is a 40% chance of developing diabetes within 10 years after pregnancy.

What group is at the highest risk? Obese mothers Family history of Type II Diabetes Maternal age >35y/o Previous pregnancy with GDM Polycystic Ovary Syndrome (common female endocrine disorder) Ethnicity African American, Native American, Hispanic, Pacific Islanders, South Asia

Potential complications for offspring

Large for gestational age Macrosomia Delivery complications C-section Childhood obesity (future type II diabetes)

5

Hypoglycemia Jaundice Still birth (mother has seizure) Pre-eclampsia: characterized by high BP (>140/90) + protein in urine of pregnant women. Leads to

eclampsia seizure/coma. Low birth weight due to management with diet and medication

Pathophysiology

Exact mechanism is not know.

Pregnancy hormone and other factors are thought to be related: o Human placental lactogen (human chorionic somatomammotropin)

Hormone similar to growth hormone Present only during pregnancy Decreases maternal insulin sensitivity Interferes with insulin receptor at cell signaling level

Cortisol o Response to stress o Gluccocorticoid increases blood glucose through gluconeogenesis

Others including: estradiol, prolactin, progesterone

Possible mechanisms include : o Single Gene Mutation, Autoimmunity, Obesity and more which result in inappropriate insulin

balance.

Symptoms Increased thirst Increased Urination Blurred Vision Fatigue Nausea Vomiting Bladder Infection/Yeast Infection

Treatment Dietary intervention followed by insulin injection if diet alone does not work

Glipizide sulfonylurea increase insulin production from B-cells in pancreas by binding to K-channels on B-cells: cells cannot hyperpolarize-membrane becomes more+, leads to an influx of calciumincrease insulin secretion Metformin Decreases glucose production in liver & act as antagonist to glucagon.

Microbiology 5. Describe the polymicrobial nature of the etiology of acute bacterial sialadenitis in the parotid

gland. Source: Oral and Maxillofacial Pathology Book + Dr. Ks Lecture on Salivary Glands

Most cases of acute bacterial sialadenitis are caused by Staphylcoccus aureus, but may also rise from

streptococci or other organisms, i.e., gram-negative and anaerobic bacteria

6

According to Dr. K - Staph aureus (mixed): S. aureus colonizes around duct orifice

Treatment o symptomatic supportive care, IVF hydration and antibiotics o Augmentin, Unasyn, Cephalosporin o Clindamycin, zithromax, biaxin (not erythromycin-high resistance) o Not oxacillin or dicloxacillin (anti-staph, but high resistance) o May need surgical incision and drainage

6. Discuss the rationale for culture and sensitivity analysis for Acute Bacterial Sialadenitis. Source: Current Diagnosis & Treatment Ch.15, Dr. Flick Lecture, Dr. K Lecture

Acute Suppurative Parotid Sialadenitis Seen with changes in fluid balance: elderly, debilitated, malnourished Trauma, sepsis, surgery, fever Usually bilateral (if unilateral, R>L) Mean age = 60 Slightly more in males Staph aureus (mixed): S. aureus colonizes around duct orifice Clinical rapid onset of painful swelling; palpation shows no flow, with purulence

Start of with Empiric Antibiotic Use Predictable bacterial etiology Routine culture and sensitivity is not cost effective or beneficial Use narrowest spectrum antibiotic, less disruption of GI flora, less resistance development Least toxic and lowest side effects

Follow with Culture and Sensitivity when: Rapidly progressive infection Non-responsive infection Recurrent Infection Compromised Host Defenses

Treatment symptomatic supportive care, IVF hydration and antibiotics Augmentin, Unasyn, Cephalosporin Clindamycin, zithromax, biaxin (not erythromycin-high resistance) Not oxacillin or dicloxacillin (anti-staph, but high resistance) May need surgical incision and drainage

Antibiotics targeted against S aureus should be started immediately and continued for 710 days. Culture testing and sensitivity may be necessary to rule out abscess formation or stone (sialolithiasis) in patients who

do not improve clinically after several days of appropriate therapy.

7

Pharmacology 7. Describe Furosemide according to the pharmacology template. How would Furosemide contribute

to Acute Bacterial Sialadenitis?

Furosemide

A sulfonamide-derived loop diuretic used in the management of edema associated with congestive heart failure, cirrhosis, and renal disease

Pharmacodynamics o Competes with Cl- for the Na/K/2Cl symporter in the ascending limb of the Loop of Henle, thus

inhibiting sodium and chloride re-uptake from the filtrate Also increases excretion of Ca, Mg, bicarbonate, ammonium and phosphate

o Ion concentration increases in the filtrate and decreases in the renal medulla, resulting in less water being resorbed via osmosis and resulting diuresis

o The renal vasodilation and net decrease in blood volume from diuresis result in decreased blood pressure and help decrease tissue edema

Pharmacokinetics: o Minimally metabolized in the liver o 50-80% excreted unchanged in the urine w/in 24h, remaining via feces

Renal disease may increase the proportion cleared through the feces Adverse effects

o Excess amounts of drug may result in fluid and electrolyte depletion o Adrenal cortex may try to compensate for diuresis by releasing aldosterone which increases

sodium resorption and potassium and hydrogen excretion, may result in metabolic alkalosis o Hyponatremia, hypokalemia, hypocalcemia, hypochloremia and hypomagnesemia must be

monitored for Dental considerations:

o Diuretic properties may result in dehydration and a resulting decrease in salivary flow, which can lead to sialadenitis via a retrograde bacterial infection

o No documented issues with local anesthetic administration

Periodontics 8. Discuss the etiology, epidemiology, pathophysiology and treatment for localized severe chronic

periodontitis Source: Kacy Jos LI

Chronic periodontitis, formerly known as adult periodontitis or chronic adult periodontitis is the more

prevalent form of periodontitis.

Slowly progressing disease

However, in the presence of systemic or environmental factors that may modify the host response to plaque accumulation (i.e. diabetes, smoking, or stress) disease progression may become more aggressive

8

Most frequently observed in adults, however, it can occur in children and adolescents in response to chronic plaque and calculus accumulation

Recently defined as an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss

Periodontal pocket formation is usually a sequel of the disease process, unless gingival recession accompanies attachment loss, in which case pocket depths may remain shallow even in the presence of ongoing attachment bone loss

Clinical featuresGeneral characteristics:

Supragingival and subgingival plaque accumulation that is frequently associated with calculus formation, gingival inflammation, pocket formation, loss of periodontal attachment and loss of alveolar bone

Gingiva ordinarily is slightly to moderately swollen and exhibits alterations in color ranging from pale red to magenta

Loss of gingival stippling and changes in the surface topography may include blunted or rolled gingival margins and flattened or cratered papillae

In many patients, the changes in the color, contour, and consistency that are frequently associated with gingival inflammation may not be visible on inspection, and inflammation may be detected only as bleeding of the gingiva

Gingival bleeding, either spontaneous or in response to probing is frequently

Inflammation-related exudates of crevicular fluid and suppuration from the pocket also may be found

In some cases, probably as a result of long standing, low-grade inflammation, thickened, fibrotic marginal tissues may obscure the underlying inflammatory changes

Pocket depths are variable; both horizontal & vertical bone loss can be found

Tooth mobility often appears in advanced cases when bone loss has been considerable Diagnosis

Clinically diagnosed by the detection of chronic inflammatory changes in the marginal gingiva, presence of periodontal pockets, and loss of clinical attachment

Radiographically diagnosed by evidence of bone loss

Findings may be similar to those seen in aggressive disease. A differential diagnosis is based on the age of the patient, rate of disease progression over time, familial nature of aggressive disease, and relative absence of local factors in aggressive disease compared with the presence of abundant plaque and calculus in chronic periodontitis

Disease distribution Chornic periodontitis is considered a site-specific disease. The clinical signs of CP namely inflammation, pocket

formation, attachment loss, and bone lossare considered to be due to the direct, site-specific effects of

subgingival plaque accumulation.

It may be described as being localized when few sites (30%) around the mouth are affected.

Disease severity

Mild: more than 1 to 2 mm of clinical attachment loss

Moderate: 3-4mm of clinical attachment loss

Severe: 5mm or more of clinical attachment loss

9

Epidemiology:

Estimate of 64.7 million adults have chronic periodontitis (moderate/mild > severe)

Adults aged 65 years and older, 64% had either moderate or severe periodontitis

Highest in men, Mexican Americans, adults with less than a high school education, adults below 100% Federal Poverty Levels (FPL), and current smokers

Resources: Prevalence of Periodontitis in Adults in the United States: 2009 and 2010 from Journal of Dental

Research. www.jdr.sagepub/com

Etiology: Periodontitis is considered to be a multifactorial disease in which the normal balance between microbial plaque and host response is disrupted.

Local factors

Prior history of periodontitis need continuous monitoring and maintenance of periodontitis to prevent a reoccurrence of disease

Plaque accumulation on tooth and gingival surfaces at the dentogingival junction (considered primary initiating agent)

Increase in proportion of gram-negative organisms in subgingival plaque biofilm

Plaque accumulation is the primary initiating agent in periodontal destructionanything that facilitates plaques

accumulation or prevents plaque removal by oral hygiene procedures can be detrimental to the patient.

Plaque retentive factors

Important in the development and progression of CP because they retain plaque microorganisms in close

proximity to the periodontal tissues, providing an ecologic niche for plaque growth and maturation

Calculus is considered the most important plaque retentive factor retain and harbor plaque bacteria on its rough surface

Subgingival and/or overhanging margins of restorations

Carious lesions that extend subgingivally

Furcations exposed by loss of attachment and bone

Crowded and malaligned teeth

Root grooves and concavities

Systemic factors

While the rate of progression of plaque-induced chronic periodontitis is generally slow, in a patient with a

systemic disease the rate of destruction may be significantly increased

Diabetes

Severe periodontitis has been observed in individuals with primary neutrophil disorders agranulocytosis, neutropenia, Chediak-Higashi syndrome, and lazy leukocyte syndrome

More frequent and severe periodontitis has been observed in individuals who exhibit secondary neutrophil impairment Down syndrome, Papillon-Lefevre syndrome, and inflammatory bowel disease

10

Environmental & behavioral factors

Smokingmore attachment and bone loss, more furcation involvements, deeper pockets, more supraginigval and less subgingival calculus, and less bleeding on probing

Emotional stress associated with necrotizing ulcerative disease and influence the extent and severity of chronic periodontitis

Genetic factors

Frequently seen among family members and across different generations within a family, suggesting the possibility of a genetic basis to the susceptibility to periodontal disease

Recent studies have demonstrated a familial aggregation of localized/generalized aggressive periodontitis

No clear genetic determinants have been described for patients with chronic periodontitis, a genetic predisposition to more aggressive periodontal breakdown in response to plaque/calculus accumulation may exist

o Recent data indicate that a genetic variation or polymorphism in the gene encoding interleukin 1-alpha and interleukin 1-beta is associated with an increased susceptibility to a more aggressive form of chronic periodontitis in subjects of Northern European origin

o Recent study suggested that patient with the IL-1 genotype increased the risk for tooth loss by 2.7 times; those who were heavy smokers and IL-1 genotype negative increased the risk for tooth loss by 2.9 times; the combined effect of IL-1 genotype and smoking increased risk of tooth by 7.7 times

Pathophysiology

Increase in proportion of gram-negative organisms in subgingival plaque biofilm, with specific increases in organisms known to be exceptionally pathogenic and virulent.

Bacteroides gingivalis, B. Forsythus, and Treponema denticola are frequently associated with ongoing attachment and bone loss in chronic periodontitis

The mechanism by which attachment and bone loss occurs have not been clearly delineated, but these bacteria may impart a local effect on the cells of the inflammatory response and the cells and tissues of the host, resulting in a local, site-specific disease process.

Resources: Carranzas Clinical Periodontology, 9th Edition. Pg 398- 407

Probing depths vs. Attachment level

11

9. Discuss the etiology, epidemiology, pathophysiology and treatment of pregnancy tumors Source: Dr. Gordons PPT, Oral Pathology Book, PubMed, Dr. Ashrafis PPT

Epidemiology:

Between 0.5% and 5% of pregnant females develop pyogenic granulomas in the oral cavity o 75% of oral pyogenic granulomas occur on the gingiva o More common on the maxilla and interproximally

Pyogenic granulomas can occur at any age with a predilection for females and children, or young adults

Appears to be similar in all races

Etiology & Pathophysiology:

Unknown, but associated with trauma, hormonal influences, viral oncogenes or underlying microscopic arteriovenous malformations

It is neither infected nor a granuloma Originally thought to be caused by pyogenic organisms, thus the name

Reactive lesion due to local irritating factors Traumatic agents include gingival and periodontal irritants such as plaque accumulation,

calculus, overhanging margins, implantation of foreign material etc. Independent of their exact nature, the traumatic insults induce inflammation, followed by repair with

production of excessive granulation tissue Highly vascular proliferation that resembles granulation tissue

Numerous small and larger endothelium-lined channels are formed that are engorged with red blood cells and organized in lobular aggregates

Surface becomes ulcerated with mixed inflammatory cell infiltrates of neutrophils, plasma cells and lymphocytes

Gradual rise in development of these lesions throughout pregnancy may be related to the increasing levels of estrogen and progesterone as the pregnancy progresses

After pregnancy and the return of normal hormone levels, some of these pyogenic granulomas resolve without treatment or undergo fibrous maturation and resemble a fibroma

Treatment Options:

No treatment o Due to the risk of complications and higher recurrence rate during pregnancy, treatment should

be deferred with the exception of cases featuring excessive bleeding and ulceration, or marked functional and esthetic problems

Surgical Excision o Excision should include the removal of the base of the lesions, with extension down to

periosteum, and curettage o Extraction of associated teeth is rarely necessary

LASER Therapy o If surgery is necessary, it is preferably done after the second trimester o LASER is used over surgical excision due to the high content of vascular tissue (control of bleeding)

All obtained specimen should be evaluated microscopically to confirm the diagnosis

12

10. Explain how Scaling and Root Planing (SRP) can help control periodontal disease. Discuss why a reevaluation should be done 4-6 weeks after the SRP is performed. Source: Carranzas Clinical Periodontology

Primary objective of SRP is to restore gingival health by completely removing elements that provoke gingival

inflammation (i.e., biofilm, calculus, and endotoxin) from the tooth surface

Instrumentation has been shown to reduce dramatically the numbers of subgingival microorganisms

o Shift in composition of subgingival biofilm from one with high numbers of gram-negative anaerobes to

one dominated by gram-positive facultative bacteria compatible with health

When biofilm and calculus form on enamel, the deposits are usually superficially attached

o Scaling is sufficient to remove deposits from enamel, leaving a smooth, clean surface

Root surfaces frequently have biofilm and calculus deposits embedded in cemental irregularities

o Subgingival calculus is porous and harbors bacteria and should be removed completely

o Root surfaces exposed to biofilm are contaminated by toxic substances (i.e. endotoxins)

Scaling alone is insufficient ; portion of root surface must be removed to eliminate these deposits

o Where cementum is thin, dentin may be exposed; not intentionally, but may be unavoidable

Re-evaluation should be done 4-6 weeks after the SRP, following a period of soft tissue healing

o Need to wait for re-epithelialization of wounds otherwise bleeding on probing can be expected

o Re-evaluation at this point is to check on the progress and success of the SRP therapy

o Can decide at this point what further treatment is needed (i.e. perio maintenance, surgery etc.)

11. Define the ADA and AAP classifications.

13

14

15

12. Compare and contrast the biofilm for a patient with a healthy periodontium versus a patient with Chronic Periodontitis. How does the biofilm change after scaling and root planing? Why does it change? Source: Ashrafis Periodontal lectures and Carrazas Clinical Periodontology

Bacterial plaque is made primarily of gram-postive bacteria cocci and rods. Some bacteria are more prevalent

than others, those prevalent bacteria include: P.gingivitis, T. forsynthis, P. intermedia, F. nucleantumDuring the

later stages of plaque formation, the mass of plaque will be made up of mostly gram-negative bacteria.Primary

Colonizers: streptococci and actinomycetesSecondary Colonizers: P. intermedia, P. loescheii, Capnocytophaga

spp., F. nucleatum, Porphyromonas gingivalis

The shift in bacterial plaque goes as follows.

Gram positive to gram negative From cocci to rods to spirochetes Non motile to motile Facultative anaerobes to obligated anaerobes. Fermenting to proteolytic During the process of scaling and root planing, calculus and bacterial plaque are removed from the crown and root surfaces. This bacterial plaque includes both early and late colonizers(responsible for inflammation present in

16

periodontitis). Because the early colonizers have been removed, the late colonizing gram negative bacteria cannot return, therefore allowing the overall health of the gingiva to improve. However, if the early colonizing bacterial are allowed to return as bacterial plaque, the late colonizers can once again be present in the gingival pocket, lead to further development of chronic periodontitis.

13. List and describe at least 5 periodontal conditions that require referring a patient to a

periodontist. Source: SGL Assignment 1 Answer Handout

1. Persistent probing depths with bleeding on probing - a pocket is a risk factor for further periodontal destruction

2. Vertical defects and furcation involvement which will need regeneration procedures 3. Lack of keratinized and attached gingiva that is causing problems for the patient or for teeth that are

receiving crowns or will be abutments to partial dentures 4. Crown lengthening surgery 5. Implants 6. Ridge augmentation procedures 7. AxiUm D0170 re-eval limited problem focus:

a. Use after SRP to evaluate success of perio treatment and need for referral

Clinical 14. Describe the rationale for use of the intracoronal and extracoronal RPD attachment systems.

Sources: https://open.umich.edu/sites/default/files/1029/JShotwell-Week10.pdf, RPD manual, Dr. Organs lecture

17

Intracoronal Extracoronal

Engage vertical walls built into the crown of the abutment tooth to create frictional resistance to removal (internal or precision attachments)

Utilizes mechanical resistance to displacement by components on or attached to the external surface of an abutment tooth

Types: Hannes anchor

Interlock

Bredent

Ceka

Advantages: Occlusal forces exerted upon the abutment tooth are applied close to the long axis of the tooth

Enhance appearance of the RPD eliminate need for facial clasps

Not readily dislodged because it can only be removed in one direction

Normal tooth contour can be maintained, minimal tooth reduction necessary and the possibility of devitalizing the tooth is reduced.

Path of insertion is easier for patients with limited dexterity

Enhance appearance of the RPD (esthetic advantage)

Use this when it is not possible to create a box prep that will totally incorporate the female element into the crown

Disadvantages: Additional tooth reduction required

Increase cost of RPD

Necessitate having to remake the fixed retainer when they wear out

When used with distal extensions, add higher stresses to the abutment teeth

Not good for people with limited dexterity

Retention is reduced with wear of the retentive surfaces

The size of these attachments limits their use, especially in vital teeth or small teeth

Sufficient crown height must exist for adequate length for a positive friction fit

Increase cost of RPD

Necessitate having to remake the fixed retainer when they wear out

When used with distal extensions, add higher stresses to the abutment teeth

Make oral hygiene more difficult

Resin bonding retention is inadequate

improves the tissue response below the attachment

unfavorable stresses on the abutment teeth

15. Describe advantages and disadvantages of intracoronal RPD attachment systems.

Source: From Attachment Systems and Connectors for FPDs Dr. Organ

Intracoronal RPD Attachment systems

- Advantage o Occlusal forces exerted on the abutment tooth are applied close to the long axis of the tooth

- Disadvantage o Additional tooth reduction

16. Describe advantages and disadvantages of extracoronal RPD attachment systems.

18

17. Describe partial veneer crowns (3/4 crown) preparation principles: axial reduction, occlusal

reduction, proximal groove placement, and occlusal offset. Source: Dr. Organs Lecture

Axial reduction 3 axial walls are prepared; 1mm axial reduction; 2-5 degrees of taper/wall; chamfer finish line.

Occlusal reduction 1.5mm on centric cusp; 1.0 on noncentric cusp; minimal metal display on buccal (bevel over

buccal cusp).

Proximal grooves retention grooves are placed with 169L carbide bur; grooves must be placed into the tooth at

least to the full diameter of the bur. Should be parallel to the axis of tooth preparation in the bucco-lingual plane

and convergent toward that axis in the mesio-distal plane; occlusal portion of the groove should be located

directly across from the interproximal contact point. Recommended occluso-gingival height for a proximal groove

is 4mm; gingival floor of groove should be flat and well defined; gingival floor of the groove should be 0.5 mm

above the finish line.

There should be 90-degree angle between lingual walls of proximal grooves and the axial walls to resist lingual

displacement of restoration. Proximal flares buccal wall of the proximal groove should be flared to remove

unsupported tooth structure.

Occlusal offset V-shaped groove that extends from the proximal grooves along the buccal cusp; occlusal offset

groove is placed with inverted cone bur; provides additional bulk to ensure rigidity of the restoration.

19

18. Describe advantages and disadvantages of partial veneer crowns (3/4 crown).

Advantage of Crown Disadvantage of Crown

Conservation of tooth structure

Reduced pulpal and periodontal insult during prep

Access to supragingival margins is rather easy and allows the operator to perform selected finishing procedures

Better access for OH

Less gingival involvement than with complete coverage

Better seating of the restoration due to ease of luting agent escape

Better visibility to check for proper seating and cementation

Remaining intact tooth permits EPT testing

Less retention and resistance

Difficult prep

Some metal is displayed (poorer esthetics)

19. Describe the phases of the treatment plan when each step of the implant procedure for a Single

Tooth Implant would occur.

Surgical placement of implants occurs in Phase II of Treatment planning, while the restorative part occurs

in Phase III when all other crowns and FPD are delivered.

There are 3 steps to implant placement.

o Phase I Surgery- Placement and time to osteointegrate,

o Phase II Surgery- Assessment of osteointegration and healing abutment placed,

20

o Restorative Phase - Steps leading to restoration such as provisional, abutment selection and

prosthesis delivery.

20. Describe the importance of the ferrule effect for a tooth preparation. What is a potential adverse outcome of an inadequate ferrule effect? How can the ferrule effect be improved for a tooth preparation? Source: Dr. Organs 2012 Fall_Restoration of Teeth with RCT_TP_BB.pdf. DAOB 322.

An adequate ferrule effect is necessary to provide sufficient support from occlusal load forces. If a ferrule effect is

not obtained, there will insufficient retention for a crown and the uneven distribution of occlusal forces can cause

a vertical fracture in the root.

Ferrule effect can be improved for a tooth preparation by ensuring that there is 1.5-2.0 mm of sound tooth

structure from the core margin to the finish line. The crown should envelop the remaining sound tooth structure

to properly protect the tooth from fracture (vertical) after being prepared for a crown.

Options for improving ferrule effect include:

Crown lengthening o Must be performed after completion of RCT and provisional placement

Orthodontic extrusion/forced eruption

Alveoplasty

Placement of the finish line subgingivally

21. Describe the instructions that you would provide for the dental laboratory in your lab prescription

as to how you want #6 and #11 PFM crowns designed so that these crowns will reflect the design of your planned RPD.

Make sure there are guide planes and rest seats on the crowns