Department of Pediatric Dentistry
Lutheran Medical Center
Resident’s Name: Craig Elice Date: 7/31/2009
Article title: Treatment of Patients with Bleeding Disorders
Author(s): Patton LL, Ship J:.
Journal: Dental Clinics of North America
Volume (number): 38(3)
Date: July 1994
Major topic: Hemophilia A and B, Platelet disorders and von Willebrand’s disease
Type of Article: Review of Literature
Main Purpose: This review article summarizes the tests performed to properly evaluate patients with bleeding disorders and outlines techniques and treatment suggestions to deliver safe effective care.
Findings: A thorough medical history is necessary including systemic and oral diseases, medications, hospitalizations, operations and history of transfusions. A careful review of systems with a focus on symptoms of bleeding disorders like petechiae, ecchymosis, or hematomas, etc. Lab tests should be evaluated. These include platelet counts (normal 100k-400k cells/mm3). Below 100k, abnormal bleeding may occur. Prothrombin time (PT time) measures the effectiveness of the extrinsic pathway to control fibrin clot formation. It is most influenced by anticoagulation therapy like coumadin and heparin treatment as well as aspirin therapy. PT ranges from10-15 seconds. At 1.5x or greater, the etiology could be due to decreases in fibrinogen, prothrombin, factors V, VII or X, liver damage, or coumadin therapy. Activated partial thromboplastin time tests for intrinsic and common pathways. Normal is 25-35 seconds depending on the hospital controls with an increase being related to many of the factor deficiencies or heparin therapy. Bleeding time measures vascular and platelet phases of coagulation with increased times indicating thrombocytopenia, von Willebrands, and disorders of platelet function. Thrombin time measures clotting times after the addition of thrombin and measures fibrinogen deficiency, systemic heparin, and intravascular coagulation. Lastly a physician consult should be obtained
Dental management: Preventive procedures like good oral hygiene, diets low in sugar, fluoride etc. are essential. Keep restorative treatment as supragingival as possible. Orthodontic treatment using safe technique minimizes any bleeding. Periodontal patients requiring subgingival scaling and root planning in areas of inflammation may require medical management. In terms of endodontics, pulpotomies, pulpectomies, and root canal therapy can be accomplished without bleeding complications. In patients with severe disease, especially Hemophilia A have 11% hematoma formation after inferior alveolar block therefore block anesthesia is contraindicated until correction of hemostatic defect is achieved. Local infiltration of anesthesia in firm tissue bound to bone followed by direct pressure for 3-4 minutes is a better choice as well as periodontal injections. The authors recommend 2% Lidocaine with 1x 100,000 epinephrine as drug of choice. Acetominophen and narcotics are best for postoperative pain while aspirin and NSAID’s are contraindicated. During oral surgical procedures, minimizing trauma to the surgical site, removal of osseous fragments and granulation tissue and reapproximating tissues aids in healing. Loose primary teeth can usually be removed without medical management. Aids to clotting include use of Avitene, Oxycel, or Surgicel as well as Gelfoam. Antibiotics are often prescribed when clotting aids are used to prevent infection. Lastly hemostatic sponges like INSTAT help in early hemostasis. In severe cases, diet shold be limited to cool liquids and lead to soft pureed foods. AMICAR at 50mg/kg every 6-7 hours for 10 dayscan prevent post surgical bleeding.
Platelet disorders: Thrombocytopenia occurs when the platelet count is less than 100k cells/mm3. No clinical bleeding or surgical hemorrhage is expected at dgreater than 50k cells/mm3. Spontaneous bleeding rarely occurs until counts are at 10k- 20k cells/mm3. Chemotherapy, gold, salts, etc. may indue reversible causes of decreased platelets and usually recovers 2 weeks after removal of causal agent. Irreversible causes include leukemia, lymphoma, HIV, etc. 1 Unit of platelets contains 6000 cells/mm3 and patients usually receive 6 units per transfusion. Thrombocytopathy is a qualitative abnormality in platelet activity. Aspirin and NSAID’s as well as some rare diseases may cause this. Roving the agents and waiting 7 days for recovery is necessary. In patients with end stage renal disease, procedures can be planned the day after hemodialysis.
Inherited Coagulopathies Hemophilia A is an X-linked recessive disorder with a deficiency of Factor VIII. Severe hemophilacs withfactor at less than 1% bleed spontaneously into joints and muscles. Moderate at 1-5% bleed withmoderate trauma and mild at 6-30% of normal levels have reare spontaneous bleeding and hemorrhage with severe trauma or surgery. Patients have a prolonged aPTT and normal PTT, TT, and BT. Systemic therapy should maintain levels at 30-50% every 12 hours. In mild to moderate Hemophilia, DDAVP can be used to raise levels to hemostatic levels by causing the release of von Willebrand’s factor from storage sites in endothelial cells. Given IV, peak levels are reached in 30-60 minutes and may raise factor VIII levels 2 to 3 times. In cases of moderate to severe Hemophilia, Factor VIII concentrate is necessary using recombinant DNA or monoclonal antibody products 1 unit/kg of Factor VIII raises levels by 2% Therapeutic levels after IV push occurs within minutes with a half life of 8-12 hours. In cases with high inhibitor levels, Factor IX complex or Prothrombin complex concentrates are effective in 50-75% of the cases. Hemophilia B (Christmas disease) is X linked recessive resulting in Factor IX deficiency. It accounts for 10-15% of all hemophiliac. The desired levels of Factor for dental surgery are between 30-50%. Von Willebrand’s disease is often autosomal dominant affecting both sexes. vWF . a protein that affects adhesion of platelets to the vessel wall is deficient. Type I accounts for 70-80% and involves reduced levels of vWF and responds to DDAVP. Type II affects high molecular weight vWF, and Type III is the severe form. Factor VIII concentrates are the treatment of choice for Type II and III VW disease. Cryoprecipitate contains more vWF although it has the dangers of viral contamination.
Anticoagulants: Coumarin derease vitamin K factors (VII, IX, and X and prothrombin)) is frequently prescribed in thromboembolic diseases. It has a half life of 44 ours. Heparin is given IV and has a shorter half life. Management includes either maintaining doses andusing local hemostatic agents or decrease doses with a short-term change t Heparin while under continuous hospital care. Severe Liver Disease: Vit K deficiency can also affect the systhesis of Factors.
Key points/Summary : The dentist should get a hematology consult to determine (1) the severity of the disease, (2) the bleeding risk of the prescribed dental procedures, (3) the patients history as it relates to the response to previous surgeries, trauma, and (4) historical response to previous medical therapies.
Assessment of article: Good review article with lots of board questions. We will see Hemophilia A patients and von Willebrand’s patients in our practice in RI.
Thursday, July 30, 2009
Hemostatic System During Childhood
Resident’s Name: Joanne Lewis Date: July 31, 2009
Article title: Maturation of the Hemostatic System During Childhood
Author(s): Maureen Andrew, et al
Journal: Blood
Volume (number): 80(8)
Month, Year: October 1992
Major topic: Hemostatic system in childhood
Type of Article: Prospective cohort study
Main Purpose: To determine the normal plasma concentrations for the majority of known coagulation proteins during childhood and gain insight into the lower risk of thromboembolic complications in children.
Overview of method of research: 246 healthy children aged 1 to 16 (a minimum of four subjects at each age) who were having minor day surgery were selected to participate in the study. These children had no history of bleeding problems in the family. 29 healthy adults were also studied. A 3 mL blood sample was collected from the subjects during routine preoperative blood work. 33 components of the hemostatic system as well as bleeding times were measured.
Findings: Bleeding times were significantly prolonged during childhood; the upper limit of normal was as high as 13 minutes up to age 10, compared to an upper limit of 7 minutes in adults. Mean plasma concentrations of the vitamin K-dependent coagulation factors (II, VII, IX, X) were significantly lower in children than in adults. Mean plasma concentrations of 2 contact factors, XII and XI, were comparable with those of adults until ages 11 to 16, when they decreased slightly. Plasma concentrations of many coagulation inhibitors showed striking differences from adults.
Key points/Summary: Plasma concentrations of certain procoagulants were significantly lower at some time during childhood, while others were similar to adults. Plasma concentrations of 2 inhibitors were increased in early childhood. The bleeding time was significantly longer for children until approximately 10 years of age compared with adults. The coagulation system in children is distinctly different from that of adults, and this difference is physiologic. There is no evidence that children are at greater risk for hemorrhagic problems than adults, and the risk for thrombotic complications is considerably less that for adults.
Assessment of article: Made some good points about the fallacy of using adult norms to interpret lab values for children…..difficult to get through all the numbers.
07/31/09 Bleeding Tendancy: A Practical Approach in Dentistry
Resident: Adam J. Bottrill
Date: 31JUL09 Region: Providence
Article title: Bleeding Tendancy: A Practical Approach in Dentistry
Author(s): Garfunkel, Adi A DMD et al
Journal: Compendium
Volume #: 20 No. 9
Page #s: pp: 836-852
Year: 1999
Major topic: Bleeding disorders
Minor topic(s): Coagulation pathways
Type of Article: Topic review and summary
Main Purpose: Discussion of bleeding disorders and dental considerations
Overview of method of research: Topical summary
Findings: N/A
Key points in the article discussion: Normally, bleeding is not considered a major problem when treating patients with normal hemostatic systems. Use of anesthetic agents assists the process. Occasionally, pt’s will experience exaggerated bleeding because of a congenital or acquired hemostatic anomaly.
A. Hemostatic System:
1. Platelet aggregation (primary hemostasis)
a. hemostatic plug
b. vasoconstriction
2. Coagulation cascade (secondary hemostasis)
a. fibrin clot formation
3. Fibrinolysis
b. Note: human saliva contains plasminogen activator inhibitor. Possibly to control bleeding in the oral cavity.
B. Congenital hemorrhagic disorders:
1. hemophilia A (VIII), B (IX) are Dx at birth and not a surprise to the dentist after thorough med Hx.
2. factor XI def, VII def, von Willebrand disease may remain undetected until later in life.
C. Drugs:
1. Platelet aggregation inhibitors
a. aspirin: COX inhibitor, lasts the lifetime of the platelet increases bleeding time
b. NSAIDs: competitive COX inhibitors slightly increased bleeding time
c. ticlopidine: used in stroke patients
d. consider discontinuing NSAID’s and Aspirin at least 5 days prior to surgery and then renewing immediately after. Be especially careful with even moderate alcohol consumption
2. Antivitamin K agents
a. coumarins, dicoumarol, warfarin
b. pts with prosth heart valves or Hx of DVT or PE
b. interfere with factors II, VII, IX and X.
c. monitored by prothrombin time (PT)
d. when within normal INR (2.0-3.5) no need to stop before dental Tx.
3. Heparin etc.
a. tx of DVT or postsurgical thromboembolus prevention
b. LMW hep preserves antithrombotic effects but not anticoagulant effects. Associated with less bleeding.
D. Liver Disease:
1. Impaired production of fibrinogen, prothrombin, II, V, VII, IX, X and XI. Also, thrombocytopenia can result from portal hypertension-related splenomegaly.
2. Cirrhosis can cause increased fibrinolysis as a result of impaired clearance of plasminogen activator.
E. Dental Approach: We should be familiar with the more common blood coagulation tests.
1. Platelet count: Normal is 150-400. Less is thrombocytopenia, more is thrombocytosis. Both of these conditions are associated with increased bleeding tendancy.
2. Bleeding time: Normal is 2.5-8 minutes. Not significant indicator of post-surgical bleeding tendancy.
3. Activated partial thromboplastin time (aPTT): Normal is 25-36 seconds. Measures intrinsic and common coagulation pathways. Indicate deficiency in any of the following XII, kininogen, prekallikrein, XI (not of concern); VIII and IX (of concern).
4. Prothrombin time (PT): Normal is 11-14 seconds. Measures extrinsic and common pathway. Hi PT AND aPTT suggests deficiency in II, V or X (of concern). Hi PT with normal aPTT suggests deficiency in VII (of concern).
5. International normalized ratio (INR): Normal is 1.0-1.3. gives a standardized ratio so different labs can give similar results.
F. Applicable MHx concerns
1. Gingival bleeding with no apparent etiology
2. Petechiae and ecchymoses
3. Nasopharyngeal bleeding.
4. Cutaneous bleeding
5. Hx of post-extraction bleeding.
6. Hx of hematuria, rectal bleeding.
7. Hx of joint hematomas.
8. Prolonged bleeding in any surgical situation.
9. Previous blood transfusion.
G. Treatment: We face 3 types of pt; known, suspected, dx following tx. Adequate Hx , consultations and local measures differ depending on which one.
1. Local measures
a. pressure, sutures, gelfoam, cellulose, topical thrombin, microfibrillar collagen, fibrin glue, cyanoacrylate, thermal methods (cautery, laser, cryo), antifibrinolytic agents, epinephrine, intraligamentary anesthesia, systemic replacement of components, platelet transfusion, FFP, cryoprecipitate, factor VIII concentrate
2. Systemic use of pharmacological agents
a. antifibrinolytic agents, vasopressin,
Summary of conclusions: Dental treatment for pts with a bleeding tendancy/disorder requires a multidisciplinary approach. The article described multiple disorders and conditions along with their associated dental considerations and possible treatments.
Assessment of article: Though this article was very thorough, it was unorganized and jumbled.
Date: 31JUL09 Region: Providence
Article title: Bleeding Tendancy: A Practical Approach in Dentistry
Author(s): Garfunkel, Adi A DMD et al
Journal: Compendium
Volume #: 20 No. 9
Page #s: pp: 836-852
Year: 1999
Major topic: Bleeding disorders
Minor topic(s): Coagulation pathways
Type of Article: Topic review and summary
Main Purpose: Discussion of bleeding disorders and dental considerations
Overview of method of research: Topical summary
Findings: N/A
Key points in the article discussion: Normally, bleeding is not considered a major problem when treating patients with normal hemostatic systems. Use of anesthetic agents assists the process. Occasionally, pt’s will experience exaggerated bleeding because of a congenital or acquired hemostatic anomaly.
A. Hemostatic System:
1. Platelet aggregation (primary hemostasis)
a. hemostatic plug
b. vasoconstriction
2. Coagulation cascade (secondary hemostasis)
a. fibrin clot formation
3. Fibrinolysis
b. Note: human saliva contains plasminogen activator inhibitor. Possibly to control bleeding in the oral cavity.
B. Congenital hemorrhagic disorders:
1. hemophilia A (VIII), B (IX) are Dx at birth and not a surprise to the dentist after thorough med Hx.
2. factor XI def, VII def, von Willebrand disease may remain undetected until later in life.
C. Drugs:
1. Platelet aggregation inhibitors
a. aspirin: COX inhibitor, lasts the lifetime of the platelet increases bleeding time
b. NSAIDs: competitive COX inhibitors slightly increased bleeding time
c. ticlopidine: used in stroke patients
d. consider discontinuing NSAID’s and Aspirin at least 5 days prior to surgery and then renewing immediately after. Be especially careful with even moderate alcohol consumption
2. Antivitamin K agents
a. coumarins, dicoumarol, warfarin
b. pts with prosth heart valves or Hx of DVT or PE
b. interfere with factors II, VII, IX and X.
c. monitored by prothrombin time (PT)
d. when within normal INR (2.0-3.5) no need to stop before dental Tx.
3. Heparin etc.
a. tx of DVT or postsurgical thromboembolus prevention
b. LMW hep preserves antithrombotic effects but not anticoagulant effects. Associated with less bleeding.
D. Liver Disease:
1. Impaired production of fibrinogen, prothrombin, II, V, VII, IX, X and XI. Also, thrombocytopenia can result from portal hypertension-related splenomegaly.
2. Cirrhosis can cause increased fibrinolysis as a result of impaired clearance of plasminogen activator.
E. Dental Approach: We should be familiar with the more common blood coagulation tests.
1. Platelet count: Normal is 150-400. Less is thrombocytopenia, more is thrombocytosis. Both of these conditions are associated with increased bleeding tendancy.
2. Bleeding time: Normal is 2.5-8 minutes. Not significant indicator of post-surgical bleeding tendancy.
3. Activated partial thromboplastin time (aPTT): Normal is 25-36 seconds. Measures intrinsic and common coagulation pathways. Indicate deficiency in any of the following XII, kininogen, prekallikrein, XI (not of concern); VIII and IX (of concern).
4. Prothrombin time (PT): Normal is 11-14 seconds. Measures extrinsic and common pathway. Hi PT AND aPTT suggests deficiency in II, V or X (of concern). Hi PT with normal aPTT suggests deficiency in VII (of concern).
5. International normalized ratio (INR): Normal is 1.0-1.3. gives a standardized ratio so different labs can give similar results.
F. Applicable MHx concerns
1. Gingival bleeding with no apparent etiology
2. Petechiae and ecchymoses
3. Nasopharyngeal bleeding.
4. Cutaneous bleeding
5. Hx of post-extraction bleeding.
6. Hx of hematuria, rectal bleeding.
7. Hx of joint hematomas.
8. Prolonged bleeding in any surgical situation.
9. Previous blood transfusion.
G. Treatment: We face 3 types of pt; known, suspected, dx following tx. Adequate Hx , consultations and local measures differ depending on which one.
1. Local measures
a. pressure, sutures, gelfoam, cellulose, topical thrombin, microfibrillar collagen, fibrin glue, cyanoacrylate, thermal methods (cautery, laser, cryo), antifibrinolytic agents, epinephrine, intraligamentary anesthesia, systemic replacement of components, platelet transfusion, FFP, cryoprecipitate, factor VIII concentrate
2. Systemic use of pharmacological agents
a. antifibrinolytic agents, vasopressin,
Summary of conclusions: Dental treatment for pts with a bleeding tendancy/disorder requires a multidisciplinary approach. The article described multiple disorders and conditions along with their associated dental considerations and possible treatments.
Assessment of article: Though this article was very thorough, it was unorganized and jumbled.
Oral Manifestations with Leukocyte Adhesion Deficiency: A Five Year Study 7/31/09
LUTHERAN MEDICAL CENTER
Dental Residency Program
Literature Review Form
Resident: Murphy Date: Region: Prov.
Article title: Oral Manifestations Associated w/ Leukocyte Adhesion Deficiency: A Five Year Study
Author(s): Roberts, MW, et al.
Journal: Pediatric Dentistry
Volume #; Number; Page #s): 12:2 4
Year: 1990
Major topic: Oral manifestations of LAD
Minor topic(s): LAD and its associated infections
Type of Article: Five year case study
Main Purpose: Assess how LAD affects the oral cavity, and how to treat it.
Overview of method of research: Five year case study of a 3 yo female w/ LAD
Findings: Leukocyte adhesion deficiency (LAD) occurs when three glycoproteins are absent or defective on leukocytes, leaving patients more susceptible to bacterial infections. The three sites are Mac-1, LFA-1, and gp 150,95. These proteins help the leukocyte to adhere to and phagocyte bacterium. Without them, the leukocytes defenses are severely diminished. LAD is an autosomal dominant disease that has been mapped to chromosome 21. Homozygous patients have severe LAD, while heterozygous patients usually present as clinically healthy. People with LAD lack a necessary beta subunit, which activates and alpha subunit, which further affects immunosuppression. The earliest clinical manifestation of LAD is delayed separation of the umbilical cord, causing septicemia. Other infections occurring in people with LAD include multiple skin abscesses, recurrent ear infections, and pneumonitis. While lab results show elevated levels of granulocytes, biopsy sites of infected areas are absent of neutrophils. The most common oral finding with LAD is severe periodontitis. Other oral findings include stomatitis, ulcers, and facial cellulites. The five year case study was on a three yo old female(child’s parents were first cousins) who presented with a history of respiratory distress, fever, poor healing, recurrent skin infections, multiple abscesses without pus, and leukoctyosis. Her WBC was 10-20,000ml. After multiple diagnostic tests, it was confirmed by fluorescent cell analysis that she lacked the necessary receptors on her leukocytes. She had generalized gingival recession, increased mobility, and attachment and bone loss. The child was treated with thorough scaling and prophy. The parents were advised to brush the child’s teeth twice daily with sodium bicarbonate and to apply stannous fluoride .4% after the evening hygiene, every night. The patient was also placed on prophy. Trimethoprim, Septra, and ferrous sulfate were prescribed. Seven months later the child returned with better oral hygiene practices, but still generalized gingivitis. There was increasing bone loss associated with all of the primary teeth. OHI was reinforced and the patient was sent home. Four months later, now eleven months since the original visit, the child presented with a large, asymptomatic, facial swelling of the mandibular left molars of three day duration. Both teeth had abscesses. The area was irrigated extensively and the child was placed on more antibiotics. At six years 8 months she was diagnosed with chronic progressive periodontitis. The girl returned to the hospital 6 more times before her eight birthday with serious infections and no improvement of her periodontal disease. Every time she presented asymptomatically. The basic treatment regiment included constant antibiotic therapy and extensive oral hygiene practices, all to simply curtail the periodontal disease.
Key points in the article discussion: LAD is effectively characterized by the patients inability to respond to recurrent infections. The leukocytes have the severe functional defect which prevents them from phagocytic chemotaxis, aggregation, and adherence. When cultures were obtained from the patients periodontal pockets, the usual suspect of periodontal disease were not present(a,a, p.g, etc.). This is probably due to the problem not being with the childs bacterial count, but the inability to fight off many if not all of the opportunistic pathogens. Intense oral hygiene and constant professional care failed to arrest the periodontal disease. The child still presented with attachment and bone loss and destruction of the surrounding periodontal tissue. Antibiotics and the use of stannous fluoride .4% only suppressed the disease, with the antibiotics being more effective.
Summary of conclusions: The maintenance of healthy gum tissue depends largely on an intact immune system. You can practice the best oral hygiene in the world, but if you can’t fight the bacteria off at a basic level, it’s futile. This is what patients with LAD deal with daily. Possible treatment options include extraction of all primary teeth to attempt to get the oral tissue to a healthy baseline, bone marrow transplant, and as previously stated, constant aggressive antibiotic and OHI therapy.
Assessment of article: Good article. Very informative and detail oriented. It was a bit of a downer, essentially stating that so far, there is no concrete way to help individuals affected by this terrible disease get better. One bad thing about the article, it only mentioned patient compliance briefly. I thought they should have focused more efforts on making sure the treatment was being followed to the “T” at home.
Dental Residency Program
Literature Review Form
Resident: Murphy Date: Region: Prov.
Article title: Oral Manifestations Associated w/ Leukocyte Adhesion Deficiency: A Five Year Study
Author(s): Roberts, MW, et al.
Journal: Pediatric Dentistry
Volume #; Number; Page #s): 12:2 4
Year: 1990
Major topic: Oral manifestations of LAD
Minor topic(s): LAD and its associated infections
Type of Article: Five year case study
Main Purpose: Assess how LAD affects the oral cavity, and how to treat it.
Overview of method of research: Five year case study of a 3 yo female w/ LAD
Findings: Leukocyte adhesion deficiency (LAD) occurs when three glycoproteins are absent or defective on leukocytes, leaving patients more susceptible to bacterial infections. The three sites are Mac-1, LFA-1, and gp 150,95. These proteins help the leukocyte to adhere to and phagocyte bacterium. Without them, the leukocytes defenses are severely diminished. LAD is an autosomal dominant disease that has been mapped to chromosome 21. Homozygous patients have severe LAD, while heterozygous patients usually present as clinically healthy. People with LAD lack a necessary beta subunit, which activates and alpha subunit, which further affects immunosuppression. The earliest clinical manifestation of LAD is delayed separation of the umbilical cord, causing septicemia. Other infections occurring in people with LAD include multiple skin abscesses, recurrent ear infections, and pneumonitis. While lab results show elevated levels of granulocytes, biopsy sites of infected areas are absent of neutrophils. The most common oral finding with LAD is severe periodontitis. Other oral findings include stomatitis, ulcers, and facial cellulites. The five year case study was on a three yo old female(child’s parents were first cousins) who presented with a history of respiratory distress, fever, poor healing, recurrent skin infections, multiple abscesses without pus, and leukoctyosis. Her WBC was 10-20,000ml. After multiple diagnostic tests, it was confirmed by fluorescent cell analysis that she lacked the necessary receptors on her leukocytes. She had generalized gingival recession, increased mobility, and attachment and bone loss. The child was treated with thorough scaling and prophy. The parents were advised to brush the child’s teeth twice daily with sodium bicarbonate and to apply stannous fluoride .4% after the evening hygiene, every night. The patient was also placed on prophy. Trimethoprim, Septra, and ferrous sulfate were prescribed. Seven months later the child returned with better oral hygiene practices, but still generalized gingivitis. There was increasing bone loss associated with all of the primary teeth. OHI was reinforced and the patient was sent home. Four months later, now eleven months since the original visit, the child presented with a large, asymptomatic, facial swelling of the mandibular left molars of three day duration. Both teeth had abscesses. The area was irrigated extensively and the child was placed on more antibiotics. At six years 8 months she was diagnosed with chronic progressive periodontitis. The girl returned to the hospital 6 more times before her eight birthday with serious infections and no improvement of her periodontal disease. Every time she presented asymptomatically. The basic treatment regiment included constant antibiotic therapy and extensive oral hygiene practices, all to simply curtail the periodontal disease.
Key points in the article discussion: LAD is effectively characterized by the patients inability to respond to recurrent infections. The leukocytes have the severe functional defect which prevents them from phagocytic chemotaxis, aggregation, and adherence. When cultures were obtained from the patients periodontal pockets, the usual suspect of periodontal disease were not present(a,a, p.g, etc.). This is probably due to the problem not being with the childs bacterial count, but the inability to fight off many if not all of the opportunistic pathogens. Intense oral hygiene and constant professional care failed to arrest the periodontal disease. The child still presented with attachment and bone loss and destruction of the surrounding periodontal tissue. Antibiotics and the use of stannous fluoride .4% only suppressed the disease, with the antibiotics being more effective.
Summary of conclusions: The maintenance of healthy gum tissue depends largely on an intact immune system. You can practice the best oral hygiene in the world, but if you can’t fight the bacteria off at a basic level, it’s futile. This is what patients with LAD deal with daily. Possible treatment options include extraction of all primary teeth to attempt to get the oral tissue to a healthy baseline, bone marrow transplant, and as previously stated, constant aggressive antibiotic and OHI therapy.
Assessment of article: Good article. Very informative and detail oriented. It was a bit of a downer, essentially stating that so far, there is no concrete way to help individuals affected by this terrible disease get better. One bad thing about the article, it only mentioned patient compliance briefly. I thought they should have focused more efforts on making sure the treatment was being followed to the “T” at home.
Oral bleeding in classic hemophilia
Resident’s Name: Brian Schmid DMD Date: 7/31/09
Article title: Oral bleeding in classic hemophilia
Author(s): AL Sonis DMD. RJ Musselman DDS
Journal: Oral Surgery
Month, Year: April 1982
Major topic: Diagnosis of hemophilia in the dental setting
Type of Article: Retrospective analysis
Findings: 132 charts from three hospitals in Louisiana were chosen and reviewed for severity of hemophilia, age and manner of diagnosis and need for factor infusions secondary to bleeding episodes. 29% had mild hemophilia, 40% moderate and 31% severe. Their average age of diagnosis was 14 months, 8 months and 6 months. 13.6% of all cases were diagnosed due to persistent oral bleeding, most commonly mild hemophilia (28.6% of all mild cases). The most common site of oral bleeding was the lip frenum with 78% and the tongue 22%. Overall, 9% of factor infusions were due to persistent oral bleeding; 60% with the lip frenum, 23% the tongue, 17% the buccal mucosa and 0.5% the gingival and palate.
The diagnosis of hemophilia due to persistent oral bleeding is logical since in the first year of life, the mouth and face are the most common sites of injury and most cases of hemophilia, particularly mild and moderate, are diagnosed after an acute bleeding event. Also, it fits that even severe hemophilia is not diagnosed until after 6 months since this is the time most babies will begin to crawl, shuffle, grab and stand, giving them ample opportunity for orofacial injury. Slightly more severe trauma may be found in toddlers who are now learning to walk, albeit precipitously, and correspondingly mild hemophilia patients are most often diagnosed around 14 months. Bechner and Strauss found that only 13% of mild hemophiliacs had a major bleeding event in the first year of life, while 30.5% had experienced one by 18 months.
Key points/Summary: About 14% of all cases of hemophilia are diagnosed after a chief complaint of persistent oral bleeding, most commonly mild hemophilia. Therefore it is well within the scope of pediatric dental practice to be wary of hemophilia and to screen for it when persistent oral bleeding occurs.
Assessment of article: A thorough and well thought out article with applicable knowledge supported by good research.
Article title: Oral bleeding in classic hemophilia
Author(s): AL Sonis DMD. RJ Musselman DDS
Journal: Oral Surgery
Month, Year: April 1982
Major topic: Diagnosis of hemophilia in the dental setting
Type of Article: Retrospective analysis
Findings: 132 charts from three hospitals in Louisiana were chosen and reviewed for severity of hemophilia, age and manner of diagnosis and need for factor infusions secondary to bleeding episodes. 29% had mild hemophilia, 40% moderate and 31% severe. Their average age of diagnosis was 14 months, 8 months and 6 months. 13.6% of all cases were diagnosed due to persistent oral bleeding, most commonly mild hemophilia (28.6% of all mild cases). The most common site of oral bleeding was the lip frenum with 78% and the tongue 22%. Overall, 9% of factor infusions were due to persistent oral bleeding; 60% with the lip frenum, 23% the tongue, 17% the buccal mucosa and 0.5% the gingival and palate.
The diagnosis of hemophilia due to persistent oral bleeding is logical since in the first year of life, the mouth and face are the most common sites of injury and most cases of hemophilia, particularly mild and moderate, are diagnosed after an acute bleeding event. Also, it fits that even severe hemophilia is not diagnosed until after 6 months since this is the time most babies will begin to crawl, shuffle, grab and stand, giving them ample opportunity for orofacial injury. Slightly more severe trauma may be found in toddlers who are now learning to walk, albeit precipitously, and correspondingly mild hemophilia patients are most often diagnosed around 14 months. Bechner and Strauss found that only 13% of mild hemophiliacs had a major bleeding event in the first year of life, while 30.5% had experienced one by 18 months.
Key points/Summary: About 14% of all cases of hemophilia are diagnosed after a chief complaint of persistent oral bleeding, most commonly mild hemophilia. Therefore it is well within the scope of pediatric dental practice to be wary of hemophilia and to screen for it when persistent oral bleeding occurs.
Assessment of article: A thorough and well thought out article with applicable knowledge supported by good research.
Wednesday, July 29, 2009
Hemophilia A
Department of Pediatric Dentistry
Lutheran Medical Center
Date: 07/24/2009
Article title: Hemophilia A
Author(s): Leon W. Hoyer M.D.
Journal: New England Journal of Medicine
Volume (number): Vol 330 No 1
Month, Year: 1994
Major topic: Hemophilia
Minor topics:
Type of Article: Review of Literature
Main Purpose: Review of Everything Hemophilia A
Overview of method of research: Review of Literature
Findings:
Hemophilia has a history of being a very destructive disease, but modern therapies have significantly improved the quality of life and the lifespan of those affected. Basically, it is the absence of clotting factor VIII or having a plasma concentrate of less than .04ug per milliliter plasma. Treatment is much more than the simple prescription of factor VII concentrates. A dental examination with plans for appropriate care is recommended as an essential part of any hemophilia patient's treatment.
Key points/Summary :
- Incidence approaches 20 per 100,000 male births.
- Although and X-linked disorder, it is supposed that up to 1/3 of cases come from random deletions and are not inherited.
- The gene that codes for factor VIII is at the tip of the long arm of the X chromosome, which can be missing or mutated.
- Factor VIII circulates in a non-covalent bond with von WIllenbrand factor, which enhances synthesis of the factor.
- Factor VIII is essential for rapid cleavage of factor X--if you want more clotting science, read it.
- Clinically, it is essential to distinguish between severe presentations and mild or moderate, the later perhaps never having a bleeding episode outside of surgery or severe trauma.
- Diagnosis of hemophilia should be suspected anytime there is abnormal bleeding in male patients. The diagnosis is determined by laboratory testing (which you can read about in the article)
- The clinical hallmarks are joint and muscle hemorrhages, easy bruising and prolonged and potentially fatal hemorrhage post surgery or trauma; but no excessive bleeding after minor cuts and abrasions.
- Hemarthroses are usually first noted when a child is learning to walk, which quickly leads to limitation of motion and mild discomfort. Within hours, it becomes severe pain, joint swelling and cutaneous warmth.
- Untreated the disease process leads to hemophilic arthropathy and can lead to permanent disability.
- Bleeding can happen in other locations also including intramuscular hematomas and closed space bleeding can lead to nerve paralysis and or airway constriction.
- In the past, 25% of deaths were attributed to intracranial bleeds. AIDS would take over this high percentage of deaths during the years of tainted transfusion.
- Factor VIII plasma replacement can be achieved using human donated plasma or synthetically derived alternatives.
- Patients with some factor VIII production can benefit from Desmopressin.
- Today--1994 that is--parents can use genetic testing and amniocentesis to determine the likelihood of transmission from mother to son.
- Care is constantly improving and the article suggested that perhaps stem-cell therapy could ultimately be a cure for the disease.
Assessment of article: A great review. This article was too in-depth for our uses and it would be nice to see an update to this (which I'm sure could be researched) and see where treatment is today. This is an interesting and significant disease. If you can get through the hard science without burning out there is a lot of good relevant information.
Monday, July 27, 2009
Oral Manifestations in Patients with Aplastic Anemia 7/31/09 - Boboia
LUTHERAN MEDICAL CENTER
Dental Residency Program
Literature Review Form
Resident: Boboia Date: 7/31/09
Article title: Oral Manifestations in Patients with Aplastic Anemia
Author(s): Brennan et al.
Journal: Oral Surgery, Oral Medicine, Oral Pathology, Oral Medicine
Volume #; Number; Page #s): 92:5
Year: 2001
Type of Article: Review
Main Purpose: Characterize the prevalence and risks of oral complications in patients with aplastic anemia (AA)
What is it?
-Rare hematologic disorder characterized by a failure of hematopoietic precursor cells in bone marrow to produce adequate number of blood cells
-Pts will demonstarte signs and symptoms related decreased blood oxygen carrying capacity (fatigue, tachycardia, weakness)
-Thrombocytopenia (¯ platelets) cause tendency for bruising / bleeding
-Leukopenia (¯wbc) predisposes pts to bacterial and fungal infections that are often times fatal
Cause:
Underlying cause is unknown; some cases are associated with exposure to environmental toxins (benzene), tx. with certain drugs (chloramphenicol), or infection with certain viruses (non-A, B, C, or G hepatitis); a few genetic disorders (Faconi’s anemia) are also associated with this
Subjects and Methods: 79 patients with AA evaluated and treated from 1993 to 1999 were compared with control subjects (66 schizophrenic patients seen at the NIH dental clinic 1993 to 1999). These controls were demographically well matched to the study subjects patients having similar hospital stays (usually 2-6 months for a protocol visit); all controls did not have a known hematologic or immune deficiency; in addition the control group had dental treatment completed as inpatients.
Data collection and Definition of Oral Manifestations:
-Included a review of medical and dental charts by 3 investigators
-Dental disease was documented for cases and control subjects as follows:
1) Current and past dental health status was documented with respect to DMFT (a score of one for missing restored or diseased tooth and 0 for for healthy tooth). Max DMFT was 28 – 3rds not included
2) Because of pancytopenia in AA patients periodontal status was assessed by alveolar bone height; intpx bone height assessed from orthopantomographs
Risk factors for oral complications in AA pt group:
Cyclosporine treatment within the previous 6 months
Prednisone treatment within the previous 6 months
Disease duration
Labs: WBC, absolute lymphocyte, monocyte, and neutrophil counts, Hct, Hgb, RBC, and platelet count
Dental Management Issues:
Dental treatment was provided for cases and controls during hospitalization; the following were documented: Predental treatment prophylaxis (usually platelet transfusions or abx or both), type of dental tx., hemorrhagic episodes > 48 hrs after dental tx., Hg levels before and after exts, infections or febrile after exts, bacteremia during hospital stay.
Results:
Patients with AA have an increased chance of presenting with petechiae, gingival hyperplasia, spontaneous gingival bleeding, and herpetic ulcertations when compared with control subjects.
Petechiae: 27% - labial and buccal mucosa, ventral tongue, palate, and gingiva
Gingival hyperplasia: 16% - common on mandibular anterior teeth
Spontaneous gingival bleeding: 16% - all 4 quads
HSV ulcerations: 16% - primarily on lips
Discussion:
- Petechia hemorrhages most common finding in AA group however no independent variables (lab values, etc) were predictive of their presence
- Gingival bleeding is another very common manifestation which also did not correlate to any other independent variable – likely caused by other oral factors (plaque,etc)
Gingival hyperplasia – 34% of AA pts. treated with cyclosporine had this
HSV – a total 28% of AA pts had HSV lesions either at baseline or during tx
Periodontal disease / bone loss – no increase in risk for the AA group compared to control
Conclusions:
- AA pts. should have routine dental examinations and tx. when appropriate
- Exts or more invasive dental tx for pts with pancytopenia should be done in a hospital setting; in this study 3/10 pts undergoing exts required at least one or more infusion of platelets or packed RBC within 4 days of dental procedures; hemorrhagic events are related to the type pt procedure rather then the degree of transfusion dependence.
Assessment of article: Good study / Review
Dental Residency Program
Literature Review Form
Resident: Boboia Date: 7/31/09
Article title: Oral Manifestations in Patients with Aplastic Anemia
Author(s): Brennan et al.
Journal: Oral Surgery, Oral Medicine, Oral Pathology, Oral Medicine
Volume #; Number; Page #s): 92:5
Year: 2001
Type of Article: Review
Main Purpose: Characterize the prevalence and risks of oral complications in patients with aplastic anemia (AA)
What is it?
-Rare hematologic disorder characterized by a failure of hematopoietic precursor cells in bone marrow to produce adequate number of blood cells
-Pts will demonstarte signs and symptoms related decreased blood oxygen carrying capacity (fatigue, tachycardia, weakness)
-Thrombocytopenia (¯ platelets) cause tendency for bruising / bleeding
-Leukopenia (¯wbc) predisposes pts to bacterial and fungal infections that are often times fatal
Cause:
Underlying cause is unknown; some cases are associated with exposure to environmental toxins (benzene), tx. with certain drugs (chloramphenicol), or infection with certain viruses (non-A, B, C, or G hepatitis); a few genetic disorders (Faconi’s anemia) are also associated with this
Subjects and Methods: 79 patients with AA evaluated and treated from 1993 to 1999 were compared with control subjects (66 schizophrenic patients seen at the NIH dental clinic 1993 to 1999). These controls were demographically well matched to the study subjects patients having similar hospital stays (usually 2-6 months for a protocol visit); all controls did not have a known hematologic or immune deficiency; in addition the control group had dental treatment completed as inpatients.
Data collection and Definition of Oral Manifestations:
-Included a review of medical and dental charts by 3 investigators
-Dental disease was documented for cases and control subjects as follows:
1) Current and past dental health status was documented with respect to DMFT (a score of one for missing restored or diseased tooth and 0 for for healthy tooth). Max DMFT was 28 – 3rds not included
2) Because of pancytopenia in AA patients periodontal status was assessed by alveolar bone height; intpx bone height assessed from orthopantomographs
Risk factors for oral complications in AA pt group:
Cyclosporine treatment within the previous 6 months
Prednisone treatment within the previous 6 months
Disease duration
Labs: WBC, absolute lymphocyte, monocyte, and neutrophil counts, Hct, Hgb, RBC, and platelet count
Dental Management Issues:
Dental treatment was provided for cases and controls during hospitalization; the following were documented: Predental treatment prophylaxis (usually platelet transfusions or abx or both), type of dental tx., hemorrhagic episodes > 48 hrs after dental tx., Hg levels before and after exts, infections or febrile after exts, bacteremia during hospital stay.
Results:
Patients with AA have an increased chance of presenting with petechiae, gingival hyperplasia, spontaneous gingival bleeding, and herpetic ulcertations when compared with control subjects.
Petechiae: 27% - labial and buccal mucosa, ventral tongue, palate, and gingiva
Gingival hyperplasia: 16% - common on mandibular anterior teeth
Spontaneous gingival bleeding: 16% - all 4 quads
HSV ulcerations: 16% - primarily on lips
Discussion:
- Petechia hemorrhages most common finding in AA group however no independent variables (lab values, etc) were predictive of their presence
- Gingival bleeding is another very common manifestation which also did not correlate to any other independent variable – likely caused by other oral factors (plaque,etc)
Gingival hyperplasia – 34% of AA pts. treated with cyclosporine had this
HSV – a total 28% of AA pts had HSV lesions either at baseline or during tx
Periodontal disease / bone loss – no increase in risk for the AA group compared to control
Conclusions:
- AA pts. should have routine dental examinations and tx. when appropriate
- Exts or more invasive dental tx for pts with pancytopenia should be done in a hospital setting; in this study 3/10 pts undergoing exts required at least one or more infusion of platelets or packed RBC within 4 days of dental procedures; hemorrhagic events are related to the type pt procedure rather then the degree of transfusion dependence.
Assessment of article: Good study / Review
Sunday, July 26, 2009
Sickle Cell Anemia: A Review for the Pediatric Dentist
Resident: Tyler Roberts
Article title: Sickle Cell Anemia: A Review for the Pediatric Dentist
Author: Fonseca DDS, et al
Journal: Pediatric Dentistry
Volume #: 29(2) pages #: 159 - 169
Year: March 2007
Major topic: review of Sickle Cell Anemia
Type of article: review
Key pts/findings
Sickle Cell Anemia is characterized by a person who carries a homozygous genetic trait - a substitution of valine for glutamic acid at position 6 of the beta globin chain of adult (A1) hemoglobin. This trait affects the structure and synthesis of hemoglobin and causes general complications of painful crises, stroke, pulmonary disease, delayed growth, osteomylitis, organ damage, psychosocial dysfunction. Oral and dental manifestations include orofacial pain, paresthesia of the mental nerve, stepladder appearance of the alveolar bone on radiographs, pulpal necrosis and enamel hypomineralization.
It was originally thought that sickling of the RBC caused micro circulatory obstruction during capillary transit thus leading to a vaso occlusive crisis and manifestations of the disease. Today it is understood that sickling causes RBC adhesion to endothelium, thus leading to the formation of hetero cellular aggregates causing local hypoxia and chronic inflammation within the circulatory system.
The only available curative therapy for the disease is hemotopoeitic stem cell transplantation that must be done prior to organ dysfunction. However, most patients use anti-inflammatories and opoids to manage their conditions. Blood transfusions have also proved important in slowing the progression and easing the painful symptoms of this disease.
Patients that exhibit low risk complications can and should have outpatient dental services performed including restorations and simple extractions. Moderate to high risk patients should be treated in a fully equipped operating room. A consultation with an anesthesiologist as well as a hematologist should be obtained before hand. Lung function as well as the risk for periopertive and postoperative complications should be assessed and the possible need for blood transfusion prior to appointment should be discussed.
Pediatric dentist: restorations are preferable to Extractions. Treatment plans should be completed prior to a patient beginning bisphosphonate therapy( no case reports of ON with children on bisphosphonates have been reported to date). Local anesthetic with vasoconstrictor is appropriate. Nitrous oxide is considered safe as long as concentrations of at least 50% oxygen are administered at all times. Oral sedation can be used, try to avoid drugs that cause respiratory depression. Mild to moderate pain can be managed with NSAIDS or Acetaminophen; avoid aspirin due to Reyes syndrome. The need for prophylaxis is controversial with no consensus at this point in time. Elective surgeries such as extraction for orthodontics should be avoided if possible.
List of other oral complications: delayed eruption, dentin hypomineralization, pulp calcification's, pulpal necrosis, glossitis, gingival enlargement, mental nerve paresthesia, neuropathy, stepladder appearance of trabecullar bone, prominent zygomatic and parietal bones, thin border of the mandible, mandibular radiopaque lesions, osteomylitis, osteoporosis, malocclusion, mucosal jaundice etc
Summary: Sickle cell disease is most severe in those found with the homozygous trait. Anti inflammatories and opoids along with blood transfusions are the main forms of treatment. Complications resulting from this disease can vary and be wide spread. Dentist should always obtain a good medical history and consult with other health professionals before delivering care to these patients.
Article title: Sickle Cell Anemia: A Review for the Pediatric Dentist
Author: Fonseca DDS, et al
Journal: Pediatric Dentistry
Volume #: 29(2) pages #: 159 - 169
Year: March 2007
Major topic: review of Sickle Cell Anemia
Type of article: review
Key pts/findings
Sickle Cell Anemia is characterized by a person who carries a homozygous genetic trait - a substitution of valine for glutamic acid at position 6 of the beta globin chain of adult (A1) hemoglobin. This trait affects the structure and synthesis of hemoglobin and causes general complications of painful crises, stroke, pulmonary disease, delayed growth, osteomylitis, organ damage, psychosocial dysfunction. Oral and dental manifestations include orofacial pain, paresthesia of the mental nerve, stepladder appearance of the alveolar bone on radiographs, pulpal necrosis and enamel hypomineralization.
It was originally thought that sickling of the RBC caused micro circulatory obstruction during capillary transit thus leading to a vaso occlusive crisis and manifestations of the disease. Today it is understood that sickling causes RBC adhesion to endothelium, thus leading to the formation of hetero cellular aggregates causing local hypoxia and chronic inflammation within the circulatory system.
The only available curative therapy for the disease is hemotopoeitic stem cell transplantation that must be done prior to organ dysfunction. However, most patients use anti-inflammatories and opoids to manage their conditions. Blood transfusions have also proved important in slowing the progression and easing the painful symptoms of this disease.
Patients that exhibit low risk complications can and should have outpatient dental services performed including restorations and simple extractions. Moderate to high risk patients should be treated in a fully equipped operating room. A consultation with an anesthesiologist as well as a hematologist should be obtained before hand. Lung function as well as the risk for periopertive and postoperative complications should be assessed and the possible need for blood transfusion prior to appointment should be discussed.
Pediatric dentist: restorations are preferable to Extractions. Treatment plans should be completed prior to a patient beginning bisphosphonate therapy( no case reports of ON with children on bisphosphonates have been reported to date). Local anesthetic with vasoconstrictor is appropriate. Nitrous oxide is considered safe as long as concentrations of at least 50% oxygen are administered at all times. Oral sedation can be used, try to avoid drugs that cause respiratory depression. Mild to moderate pain can be managed with NSAIDS or Acetaminophen; avoid aspirin due to Reyes syndrome. The need for prophylaxis is controversial with no consensus at this point in time. Elective surgeries such as extraction for orthodontics should be avoided if possible.
List of other oral complications: delayed eruption, dentin hypomineralization, pulp calcification's, pulpal necrosis, glossitis, gingival enlargement, mental nerve paresthesia, neuropathy, stepladder appearance of trabecullar bone, prominent zygomatic and parietal bones, thin border of the mandible, mandibular radiopaque lesions, osteomylitis, osteoporosis, malocclusion, mucosal jaundice etc
Summary: Sickle cell disease is most severe in those found with the homozygous trait. Anti inflammatories and opoids along with blood transfusions are the main forms of treatment. Complications resulting from this disease can vary and be wide spread. Dentist should always obtain a good medical history and consult with other health professionals before delivering care to these patients.
07/31/09 Periodontal Changes Associated With Chronic Idiopathic Neutropenia
Date: 07/31/09
Resident: Jason Hencler
Article title: Periodontal Changes Associated with Chronic Idiopathic Neutropenia
Author(s): Kenneth L. Kalkwarf, DDS, MS; Dennis P. Gutz, DDS, MS
Journal: Pediatric Dentistry
Volume #3; Number 2; Page 189-195 Year: 1981
Major topic: Chronic Idiopathic Neutropenia
Background: Chronic Idiopathic Neutropenia is a relatively rare blood disorder characterized by severe decrease in circulating neutrophils. Infants and children exhibiting severe neutropenias report hx of persistent infections of the skin and respiratory tract as well as severe gingivitis, oral ulcers, and destruction of the alveolar bone. Only antibiotics have had predictable success in controlling systemic sequel.
Type of Article: Case Report
Main Purpose: Present a case report of a child exhibiting chronic neutropenia, discuss classification of such neuropenias and review dental management for children with such problems.
Overview of method of research: A four year clinical course of this patient was monitored and is presented in this paper.
Findings: Patient was a 3 ½ yo white female in no pain referred for eval and tx of her gingival condition. Med hx revealed initial problems appeared at 2 ½ wks with the development of an intense papular diaper rash. Dx was staphylococcal dermatitis and was tx with ampicillin. The rash cleared but recurred 2 wks after antibiotics discontinued. Patient also experienced many bouts of respiratory distress and frequent febrile episodes. Each clinical picture recurred with cessation of antibiotics. A bone marrow examination was consistent with congenital neutropenia. Dental findings were swollen edematous gingival with a distinct granulomatous collar at the cervical region that bled easily when manipulated. Gingival recession had occurred in the anterior areas resulting in root exposure. No caries detected. Mother noted patient complained of a sore mouth and resisted tooth brushing. Radiographs revealed significant bone loss in the anterior regions of the mouth but no caries. OHI was given and patient was put on 3 mo recare over the next 4 yrs. During the 4 yrs of observation the patient’s OH varied from fair to poor. Progressive gingival recession eventually resulted in advanced root exposure throughout the primary dentition especially in the anterior regions. Radiographic eval revealed alveolar destruction in anterior regions and furcations of primary molars. Soft tissue lesions, appearing to be aphthous ulcers were occasionally present. No radiographic caries was observed. Mandibular primary incisors were exfoliated at 5 yr 7 mo. Eruption of permanent incisors followed a normal pattern with normal alveolar support through age 7.
Key points in the article discussion: Numerous systemic conditions can result in gingival inflammation, alveolar bone loss, and mucosal ulceration. Diff Dx should include: juvenile perio, histiocytosis X, Chediak-Lefevre syndrome, acatalasia, chronic granulomatous disease, hypophosphatasia, diabetes, leukemia, and neutropenia. Neutropenic conditions in children are classified according to clinical symptoms, age of onset, duration, white cell counts, immune function, familial tendencies, and bone marrow alterations. The patient in this case was dx as chronic idiopathic neutropenia on the following basis. The clinical course of neutropenia was present from birth with no etiology, no familial tendencies discovered. Clinical symptoms consisted of persistent, recurrent infections including gingivitis, throughout the patient’s life. An interesting finding was that while periodontal destruction, gingival recession, tooth discoloration and moderate to heavy plaque accumulation were present, no evidence of carious activity was ever found. Tooth discoloration was due to intrinsic staining, probably due to antibiotics during formative periods and extrinsic staining due to plaque control attempts. Therapy modalities other that antibiotics to control recurrent episodes of infection were not successful. The lack of carious activity is difficult to explain but may be due to a relative lack of certain inflammatory cells that alters the microbial population to one incapable of initiating a carious process. At the time this article was published the exact role(s) of the neutrophil in protecting the periodontal tissues were not discovered but investigators had determined that the cell may pass through the junct epi and reside in the sulcus in a viable state. It was certainly plausible that the periodontal destruction seen in patients with chronic idiopathic neutropenia is a result of decreased neutrophil count. We now know that the neutrophil play an important role in contolling the periodontal microbiota. They are the first leukocyte to arrive at the site of inflammation and are always the dominant cell type in the junct epi and the gingival sulcus. Disorders of neutrophils are associated with invasive perio infections and aggressive periodontitis. This patient exhibited a normal eruption sequence of the perm dentition. The eruption schedule was accelerated due probably to early loss of primary dentition. It is expected that alveolar destruction around her perm teeth will occur with time. Episodes of recurrent aphthous ulcers seen in neutropenic patients do not have a clear association with the circulating neutrophil count. With better antibiotic therapy, children with hematologic disorders are surviving infections and are requiring dental tx. Although caries does not appear to be a major problem, patients with chronic idiopathic neutropenia, daily stannous fluoride gel has been recommended to reduce the possibility of tooth loss or dental infection due to carious lesion. Stannous fluoride application has also been shown to reduce plaque formation and be potentially useful in the control of early periodontitis. A strict hygiene program should be implemented for these patients. Also, maximum precautions including aseptic rinses and antibiotic coverage, prior to tissue manipulation is suggested to reduce chance of bacteremias and post op infection.
Summary of conclusions: Chronic idiopathic neutropenia is characterized by a severe decrease in the number of circulating neutrophils. Symptoms include oral ulceration, gingival inflammation, and rapid alveolar bone loss.
Assessment of article: This article presented a good background of neutropenia types and there classification. All aspects presented from this case, including neutropenic symptoms, tx, and dx would be helpful to a pediatric dentist when tx a similar patient. This article, however, may be a little outdated. It was written when the neutrophils exact role in protecting the periodontal apparatus was still unknown. At 28 yo, this article outdates some of our residents, unfortunately I am not one of them.
Resident: Jason Hencler
Article title: Periodontal Changes Associated with Chronic Idiopathic Neutropenia
Author(s): Kenneth L. Kalkwarf, DDS, MS; Dennis P. Gutz, DDS, MS
Journal: Pediatric Dentistry
Volume #3; Number 2; Page 189-195 Year: 1981
Major topic: Chronic Idiopathic Neutropenia
Background: Chronic Idiopathic Neutropenia is a relatively rare blood disorder characterized by severe decrease in circulating neutrophils. Infants and children exhibiting severe neutropenias report hx of persistent infections of the skin and respiratory tract as well as severe gingivitis, oral ulcers, and destruction of the alveolar bone. Only antibiotics have had predictable success in controlling systemic sequel.
Type of Article: Case Report
Main Purpose: Present a case report of a child exhibiting chronic neutropenia, discuss classification of such neuropenias and review dental management for children with such problems.
Overview of method of research: A four year clinical course of this patient was monitored and is presented in this paper.
Findings: Patient was a 3 ½ yo white female in no pain referred for eval and tx of her gingival condition. Med hx revealed initial problems appeared at 2 ½ wks with the development of an intense papular diaper rash. Dx was staphylococcal dermatitis and was tx with ampicillin. The rash cleared but recurred 2 wks after antibiotics discontinued. Patient also experienced many bouts of respiratory distress and frequent febrile episodes. Each clinical picture recurred with cessation of antibiotics. A bone marrow examination was consistent with congenital neutropenia. Dental findings were swollen edematous gingival with a distinct granulomatous collar at the cervical region that bled easily when manipulated. Gingival recession had occurred in the anterior areas resulting in root exposure. No caries detected. Mother noted patient complained of a sore mouth and resisted tooth brushing. Radiographs revealed significant bone loss in the anterior regions of the mouth but no caries. OHI was given and patient was put on 3 mo recare over the next 4 yrs. During the 4 yrs of observation the patient’s OH varied from fair to poor. Progressive gingival recession eventually resulted in advanced root exposure throughout the primary dentition especially in the anterior regions. Radiographic eval revealed alveolar destruction in anterior regions and furcations of primary molars. Soft tissue lesions, appearing to be aphthous ulcers were occasionally present. No radiographic caries was observed. Mandibular primary incisors were exfoliated at 5 yr 7 mo. Eruption of permanent incisors followed a normal pattern with normal alveolar support through age 7.
Key points in the article discussion: Numerous systemic conditions can result in gingival inflammation, alveolar bone loss, and mucosal ulceration. Diff Dx should include: juvenile perio, histiocytosis X, Chediak-Lefevre syndrome, acatalasia, chronic granulomatous disease, hypophosphatasia, diabetes, leukemia, and neutropenia. Neutropenic conditions in children are classified according to clinical symptoms, age of onset, duration, white cell counts, immune function, familial tendencies, and bone marrow alterations. The patient in this case was dx as chronic idiopathic neutropenia on the following basis. The clinical course of neutropenia was present from birth with no etiology, no familial tendencies discovered. Clinical symptoms consisted of persistent, recurrent infections including gingivitis, throughout the patient’s life. An interesting finding was that while periodontal destruction, gingival recession, tooth discoloration and moderate to heavy plaque accumulation were present, no evidence of carious activity was ever found. Tooth discoloration was due to intrinsic staining, probably due to antibiotics during formative periods and extrinsic staining due to plaque control attempts. Therapy modalities other that antibiotics to control recurrent episodes of infection were not successful. The lack of carious activity is difficult to explain but may be due to a relative lack of certain inflammatory cells that alters the microbial population to one incapable of initiating a carious process. At the time this article was published the exact role(s) of the neutrophil in protecting the periodontal tissues were not discovered but investigators had determined that the cell may pass through the junct epi and reside in the sulcus in a viable state. It was certainly plausible that the periodontal destruction seen in patients with chronic idiopathic neutropenia is a result of decreased neutrophil count. We now know that the neutrophil play an important role in contolling the periodontal microbiota. They are the first leukocyte to arrive at the site of inflammation and are always the dominant cell type in the junct epi and the gingival sulcus. Disorders of neutrophils are associated with invasive perio infections and aggressive periodontitis. This patient exhibited a normal eruption sequence of the perm dentition. The eruption schedule was accelerated due probably to early loss of primary dentition. It is expected that alveolar destruction around her perm teeth will occur with time. Episodes of recurrent aphthous ulcers seen in neutropenic patients do not have a clear association with the circulating neutrophil count. With better antibiotic therapy, children with hematologic disorders are surviving infections and are requiring dental tx. Although caries does not appear to be a major problem, patients with chronic idiopathic neutropenia, daily stannous fluoride gel has been recommended to reduce the possibility of tooth loss or dental infection due to carious lesion. Stannous fluoride application has also been shown to reduce plaque formation and be potentially useful in the control of early periodontitis. A strict hygiene program should be implemented for these patients. Also, maximum precautions including aseptic rinses and antibiotic coverage, prior to tissue manipulation is suggested to reduce chance of bacteremias and post op infection.
Summary of conclusions: Chronic idiopathic neutropenia is characterized by a severe decrease in the number of circulating neutrophils. Symptoms include oral ulceration, gingival inflammation, and rapid alveolar bone loss.
Assessment of article: This article presented a good background of neutropenia types and there classification. All aspects presented from this case, including neutropenic symptoms, tx, and dx would be helpful to a pediatric dentist when tx a similar patient. This article, however, may be a little outdated. It was written when the neutrophils exact role in protecting the periodontal apparatus was still unknown. At 28 yo, this article outdates some of our residents, unfortunately I am not one of them.
Thursday, July 23, 2009
Pediatric Sialolithiasis
Department of Pediatric Dentistry
Lutheran Medical Center
Date: 07/24/2009
Article title: Pediatric Sialolithiasis
Author(s): Nahieli Oded, Eliav Eli, Hasson Oscar, Zagury Ami
Journal: Oral Surgery Oral Medicine Oral Pathology
Volume (number): Vol 90 Number 6
Month, Year: 2000
Major topic: Sialolithiasis
Minor topics:
Type of Article: Case Review
Main Purpose: Review of recent pediatric sialolithiasis cases and compare findings to previous literature.
Overview of method of research: Case Report
Findings:
Pediatric Sialolithiasis is relatively common in adults, but is rare in children. Still it must be considered in the differential diagnosis of facial swelling and intermittent pain in young patients.
Review was of 15 cases followed for 3 years in an OMS clinic in Israel. The endoscope was the primary instrument used to treat and evaluate the sialoliths.
Key points/Summary :
- The main complaint is usually unilateral swelling. Most are diagnosed by imaging.
- 33% of cases had a distinguishable cause: phytobezoar, hair follicle, intraductal evagination.
- Endoscopy is very important in the evaluation and elimination of sialolithiasis.
- Predominant in males.
- Usually affects the submandibular gland.
Assessment of article: I liked this article. It has some good images (although hard to see in a photocopy) of clinical findings as well as imaging and the stones themselves. Important to be able to recognize this stuff, because patients may come to us, when others have failed them.
Gingival Enlargement Associated With a Partially Erupted Mandibular Molar 7/24/09
LUTHERAN MEDICAL CENTER
Dental Residency Program
Literature Review Form
Resident: Ray Murphy Date: 7/24/09 Region: Providence
Article title: Gingival Enlargement Associated With a Partially Erupted Mandibular Molar
Author(s): Catherine Flaitz, DDS,MS
Journal: Pediatric Dentistry
Volume #; Number; Page #s): 23:5, 3
Year: 2001
Major topic: Peripheral odontogenic fibroma (PodF)
Minor topic(s): -
Type of Article: Case Report
Main Purpose: Discuss the clinical and microscopic features of a PodF in a 13yo male.
Overview of method of research: 13yo male evaluated for soft tissue growth overlying his mandibular second molar.
Findings: A POdF is a rare tumor that exclusively exists in the soft tissues covering the tooth bearing areas of the jaws. It is described as a firm, sessile enlargement of the soft tissue with a pink, smooth, nonulcerated mucosal surface. They range in size from approx. .5cm-3.5cm. It is found throughout the dental arches with an affinity for the buccal gingival of the mandible. It typically presents as a solitary lesion. This 13 yo male patient presented with an asymptomatic fibrous overgrowth on his mandibular second molar. IOE revealed a 2cm x 1.5 cm firm, pinkish gray, smooth, dome shaped lesion arising from the posterior lingual gingival/retromolar pad. The lesion was delaying the second molar from fully erupting. Also, the maxillary second molar was displaced lingually into a cross-bite as a result of occluding on the lesion. Radiographically the second molar had normal root development and open apices. No bone involvement was noticed. EOE revealed multiple hypertrophic scars and keloids on the patients extremities. Treatment of the lesion was excisional biopsy to allow the second molar to completely erupt. Histologically, the lesion was comprised of well vascularized, fibrous connective tissue with multinucleated giant cells. There was no evidence of calcifications in the stroma. Ten months after the excision of the lesion there was no recurrence.
Key points in the article discussion: The POdF is an uncommon gingival tumor that is similar to the central odontogenic fibroma. Whether the lesion is a true neoplasm, or a reactive hyperplasia has not yet been decided. People of all ages are susceptible to PodF’s, with the largest occurrence being before the age of 20(although this may be underestimated b/c not an operculum are submitted for histological differentiation). Treatment of choice is surgical excision. While the prognosis of the lesion after excision is excellent, it’s behavior is not totally understood. Recurrence happens 38% of the time, usually within 1-4 years. It is suspected that recurrence following the first year after excision is due to incomplete removal of the entire lesion initially. Differential diagnosis is extensive, including reactive hyperplasias, hamartomas, neoplasms, irritation fibromas, POF, pericoronal hamartoma, etc. The most common gingival enlargement overylying a molar is focal fibrous hyperplasia of the operculum. The difference between an operculum and a PodF is that a PodF will hinder the complete eruption of the affected molar, an operculum does not.
Summary of conclusions: In conclusion, the PodF is a soft tissue lesion that can affect the eruption of whichever tooth it is associated with. The differential diagnosis are extensive, but a diagnosis can be narrowed down by thorough IOE and histological differentiation. Histologically, the PodF and the pericoronal hamartoma are extremely similar, which could possibly mean that they represent a clinical spectrum of the same disease, ESPECIALLY when it occurs in children. The treatment of choice is excisional biopsy to allow the affected molar to continue erupting. Following excision, normal eruption of the affected molar was noted in 95% of cases.
Assessment of article: Good article. Clinically relevant. Listed numerous differential diagnosis of PodF and why it was different. Overall a good case report.
Dental Residency Program
Literature Review Form
Resident: Ray Murphy Date: 7/24/09 Region: Providence
Article title: Gingival Enlargement Associated With a Partially Erupted Mandibular Molar
Author(s): Catherine Flaitz, DDS,MS
Journal: Pediatric Dentistry
Volume #; Number; Page #s): 23:5, 3
Year: 2001
Major topic: Peripheral odontogenic fibroma (PodF)
Minor topic(s): -
Type of Article: Case Report
Main Purpose: Discuss the clinical and microscopic features of a PodF in a 13yo male.
Overview of method of research: 13yo male evaluated for soft tissue growth overlying his mandibular second molar.
Findings: A POdF is a rare tumor that exclusively exists in the soft tissues covering the tooth bearing areas of the jaws. It is described as a firm, sessile enlargement of the soft tissue with a pink, smooth, nonulcerated mucosal surface. They range in size from approx. .5cm-3.5cm. It is found throughout the dental arches with an affinity for the buccal gingival of the mandible. It typically presents as a solitary lesion. This 13 yo male patient presented with an asymptomatic fibrous overgrowth on his mandibular second molar. IOE revealed a 2cm x 1.5 cm firm, pinkish gray, smooth, dome shaped lesion arising from the posterior lingual gingival/retromolar pad. The lesion was delaying the second molar from fully erupting. Also, the maxillary second molar was displaced lingually into a cross-bite as a result of occluding on the lesion. Radiographically the second molar had normal root development and open apices. No bone involvement was noticed. EOE revealed multiple hypertrophic scars and keloids on the patients extremities. Treatment of the lesion was excisional biopsy to allow the second molar to completely erupt. Histologically, the lesion was comprised of well vascularized, fibrous connective tissue with multinucleated giant cells. There was no evidence of calcifications in the stroma. Ten months after the excision of the lesion there was no recurrence.
Key points in the article discussion: The POdF is an uncommon gingival tumor that is similar to the central odontogenic fibroma. Whether the lesion is a true neoplasm, or a reactive hyperplasia has not yet been decided. People of all ages are susceptible to PodF’s, with the largest occurrence being before the age of 20(although this may be underestimated b/c not an operculum are submitted for histological differentiation). Treatment of choice is surgical excision. While the prognosis of the lesion after excision is excellent, it’s behavior is not totally understood. Recurrence happens 38% of the time, usually within 1-4 years. It is suspected that recurrence following the first year after excision is due to incomplete removal of the entire lesion initially. Differential diagnosis is extensive, including reactive hyperplasias, hamartomas, neoplasms, irritation fibromas, POF, pericoronal hamartoma, etc. The most common gingival enlargement overylying a molar is focal fibrous hyperplasia of the operculum. The difference between an operculum and a PodF is that a PodF will hinder the complete eruption of the affected molar, an operculum does not.
Summary of conclusions: In conclusion, the PodF is a soft tissue lesion that can affect the eruption of whichever tooth it is associated with. The differential diagnosis are extensive, but a diagnosis can be narrowed down by thorough IOE and histological differentiation. Histologically, the PodF and the pericoronal hamartoma are extremely similar, which could possibly mean that they represent a clinical spectrum of the same disease, ESPECIALLY when it occurs in children. The treatment of choice is excisional biopsy to allow the affected molar to continue erupting. Following excision, normal eruption of the affected molar was noted in 95% of cases.
Assessment of article: Good article. Clinically relevant. Listed numerous differential diagnosis of PodF and why it was different. Overall a good case report.
Palatal Blue Nevus In Children 7/24/09
LUTHERAN MEDICAL CENTER
Dental Residency Program
Literature Review Form
Resident: Murphy Date:7/24/09 Region: Prov.
Article title: Palatal Blue Nevus In Children
Author(s): Flaitz, Catherine, DDS
Journal: Pediatric Dentistry
Volume #; Number; Page #s): 23:4, 2
Year: 2001
Major topic: Palatal Blue Nevus
Minor topic(s): Other soft tissue pigmentations
Type of Article: Case Report
Main Purpose: Review a case of blue nevus(BN) in a child
Overview of method of research: N/A
Findings: Except for vascular entities, blue lesions are relatively uncommon in a child’s oral cavity. They are mostly found on the skin. In this case, a 7 yo female presented with an asymptomatic, non-blanching, smooth, bright blue oval macule measuring 7mm x 4mm on her palate. There was no history of trauma. Treatment was excisional biopsy. Histologically, there was heavily pigmented spindle shaped cells with dendritic extensions aligned parallel to the epithelium.
Key points in the article discussion: Oral nevi are farely rare, with a prevalence of .1% in the general population. The BN is the second most common type of nevi, accounting for 36% of all nevi found. BN present as a solitary blue-gray macule that’s slightly raised, less than 6mm in size, regular margins, and a smooth surface. The most common site for a BN is the palate, accounting for 75% of the cases, followed by the labial mucosa. There’s a slight female predilection, but mostly in the third and forth decades. Only 2% of BN are seen in children. While the treatment of choice is surgical excision, this pratice is somewhat controversial. It’s recommended because the lesion is constantly subjected to trauma, which makes it hard to monitor changes in size and appearance, which may mimic melanoma. While malignant transformation of BN has been implicated in children, there are no intra oral examples of this. Some risk factors of malignant transformation include a new or changing nevus, the presence of multiple nevi, fair skin, family history of melanoma, congenital nevus, and immunosuppression. Differential diagnosis of BN includes amalgam tattoo, melanotic macule, and various vascular anomalies. In terms of amalgam tattoo, a good history of trauma and past dental procedures is important.
Summary of conclusions: In summary, the BN is an extremely rare lesion seen in the oral cavity of a child. Take a good medical history to rule out other possible causes and diagnosis, and when in doubt, excise the entire lesion. This is because should the lesion turn malignant, the overall 5 year survival rate for oral melanomas is less then 15%.
Assessment of article:Good article. It was quick to the point. Easy to read. Good summary.
Dental Residency Program
Literature Review Form
Resident: Murphy Date:7/24/09 Region: Prov.
Article title: Palatal Blue Nevus In Children
Author(s): Flaitz, Catherine, DDS
Journal: Pediatric Dentistry
Volume #; Number; Page #s): 23:4, 2
Year: 2001
Major topic: Palatal Blue Nevus
Minor topic(s): Other soft tissue pigmentations
Type of Article: Case Report
Main Purpose: Review a case of blue nevus(BN) in a child
Overview of method of research: N/A
Findings: Except for vascular entities, blue lesions are relatively uncommon in a child’s oral cavity. They are mostly found on the skin. In this case, a 7 yo female presented with an asymptomatic, non-blanching, smooth, bright blue oval macule measuring 7mm x 4mm on her palate. There was no history of trauma. Treatment was excisional biopsy. Histologically, there was heavily pigmented spindle shaped cells with dendritic extensions aligned parallel to the epithelium.
Key points in the article discussion: Oral nevi are farely rare, with a prevalence of .1% in the general population. The BN is the second most common type of nevi, accounting for 36% of all nevi found. BN present as a solitary blue-gray macule that’s slightly raised, less than 6mm in size, regular margins, and a smooth surface. The most common site for a BN is the palate, accounting for 75% of the cases, followed by the labial mucosa. There’s a slight female predilection, but mostly in the third and forth decades. Only 2% of BN are seen in children. While the treatment of choice is surgical excision, this pratice is somewhat controversial. It’s recommended because the lesion is constantly subjected to trauma, which makes it hard to monitor changes in size and appearance, which may mimic melanoma. While malignant transformation of BN has been implicated in children, there are no intra oral examples of this. Some risk factors of malignant transformation include a new or changing nevus, the presence of multiple nevi, fair skin, family history of melanoma, congenital nevus, and immunosuppression. Differential diagnosis of BN includes amalgam tattoo, melanotic macule, and various vascular anomalies. In terms of amalgam tattoo, a good history of trauma and past dental procedures is important.
Summary of conclusions: In summary, the BN is an extremely rare lesion seen in the oral cavity of a child. Take a good medical history to rule out other possible causes and diagnosis, and when in doubt, excise the entire lesion. This is because should the lesion turn malignant, the overall 5 year survival rate for oral melanomas is less then 15%.
Assessment of article:Good article. It was quick to the point. Easy to read. Good summary.
Wednesday, July 22, 2009
Traumatic herniation of the buccal fat pad
Resident: Tyler Roberts
Article: Traumatic herniation of the buccal fat pad
Author: Horie. et al
Journal: Pediatric Dentistry
Volume # 23:3, pages: 249 - 251
Year: 2001
Major topic: Traumatic herniation of the buccal fat pad
Type of article: case review
Purpose: To diagnose and treat this rare truamatic lesion found most commonly in children
Kep pts/findings
The buccal fat pad consist of 4 segments: the ptergoid, buccal, superficial and deep temporal areas. It lies wedged between the masseter and the buccinator. It extends on one end from the anterior region of the masseter through to the retromolar region of the mandible. Up until the year 2000, only 31 cases of traumatic herniation of the buccal fat pad has ever been reported.
Case 1
A 10 month old reportedly fell down while holding chopsticks in his mouth. The chopsticks did not break and minimal bleeding was noted at the time of injury. On examination a laceration was found present on his right buccal mucosa, inferior and distal to the parotid papilla. From the laceration a reddish-yellow soft pedunculated mass measuring 1.0 x .5 x.5 cm was protruding. The working diagnoses was given. The treatment included irrigating and reapproximating the margins and placing 4-0 nylong sutures while under local anesthesia. An antibiotic was given for four days and in two weeks the lesion had completely healed.
Case 2
A 1 year 9 month old had fallen while holding her toothbrush in the mouth. The tooth brush was not broken and minimal bleeding was present. The following morning a large mass extended from the right buccal mucosa into the oral cavity. The pedunculated mass appeared to be reddish brown in color with the dimension of 1.5 x 1.0 x 1.0 cm. and located just inferior to the parotic papilla. The working diagnosis was given. Three days later the mass was excised at the hospital under general anesthesia. The patient recieved. 4-0 nylon sutures and was placed on antibiotics for 5 days. One month later everything appeared to be healed with no cosmetic defects.
summary of conclusions:
Almost all cases of buccal herniation of the fat pad have been due to a traumatic injury. It most frequently occurs in infants and small children under the age of 4. The site of the lesion is almost always along the oclussal table near the parotid papilla. Histologically this lesion is not capsulated and composed of mature adipose tissue. Treatment includes excision or reaprroximation of the pad depending on size. No history of recurrence has been reported after treatment.
Article: Traumatic herniation of the buccal fat pad
Author: Horie. et al
Journal: Pediatric Dentistry
Volume # 23:3, pages: 249 - 251
Year: 2001
Major topic: Traumatic herniation of the buccal fat pad
Type of article: case review
Purpose: To diagnose and treat this rare truamatic lesion found most commonly in children
Kep pts/findings
The buccal fat pad consist of 4 segments: the ptergoid, buccal, superficial and deep temporal areas. It lies wedged between the masseter and the buccinator. It extends on one end from the anterior region of the masseter through to the retromolar region of the mandible. Up until the year 2000, only 31 cases of traumatic herniation of the buccal fat pad has ever been reported.
Case 1
A 10 month old reportedly fell down while holding chopsticks in his mouth. The chopsticks did not break and minimal bleeding was noted at the time of injury. On examination a laceration was found present on his right buccal mucosa, inferior and distal to the parotid papilla. From the laceration a reddish-yellow soft pedunculated mass measuring 1.0 x .5 x.5 cm was protruding. The working diagnoses was given. The treatment included irrigating and reapproximating the margins and placing 4-0 nylong sutures while under local anesthesia. An antibiotic was given for four days and in two weeks the lesion had completely healed.
Case 2
A 1 year 9 month old had fallen while holding her toothbrush in the mouth. The tooth brush was not broken and minimal bleeding was present. The following morning a large mass extended from the right buccal mucosa into the oral cavity. The pedunculated mass appeared to be reddish brown in color with the dimension of 1.5 x 1.0 x 1.0 cm. and located just inferior to the parotic papilla. The working diagnosis was given. Three days later the mass was excised at the hospital under general anesthesia. The patient recieved. 4-0 nylon sutures and was placed on antibiotics for 5 days. One month later everything appeared to be healed with no cosmetic defects.
summary of conclusions:
Almost all cases of buccal herniation of the fat pad have been due to a traumatic injury. It most frequently occurs in infants and small children under the age of 4. The site of the lesion is almost always along the oclussal table near the parotid papilla. Histologically this lesion is not capsulated and composed of mature adipose tissue. Treatment includes excision or reaprroximation of the pad depending on size. No history of recurrence has been reported after treatment.
Highly Aggressive Brown Tumor in the Jaw Associated with Tertiary Hyperparathyroidism
Department of Pediatric Dentistry
Lutheran Medical Center
Resident’s Name: Craig Elice Date: 7/24/2009
Article title: Highly Aggressive Brown Tumor in the Jaw Associated with Tertiary Hyperparathyroidism
Author(s): Pinto LP, Cherbinim K, Salum FG, et al.
Journal: Pediatric Dentistry
Volume (number): 28(6)
Date: 2006
Major topic: Brown Cell tumor diagnosis and management
Type of Article: Case Report
Main Purpose: This case report describes a 12 year old female with an aggressive brown tumor associated with tertiary hyperparathyroidism and treated medically with calcitonin and corticosteroids.
Review of Case: Brown tumors are central giant cell granulomas which develop as a result of untreated hyperparathyroidism. The tumor affects mainly children and young adults with a female predilection. It represents less than 7% of all benign jaw lesions. The primary form of hyperparathyroidism relates of a hyperplastic or neoplastic parathyroid gland. Secondary occurs due to chronic renal insufficiency and tertiary is secondary with spread of parathyroid glands to other sites. Brown tumors occur in 1.5-1.7% of patients with chronic renal insufficiency. Treatment is focused around solving the underlying endocrine abnormatlity. The brown color is derived from hemorrhay and hemosiderin infiltration of the lesion.
The 12 yewar old female presented with right buccal lesion noted 3 months ago, and had a firm consistency. The panorex revealed a large osteolytic lesion. Blood tests revealed elevated blood creatinine levels, parathyroidhormone and alkaline phosphatase. Histology confirmed the diagnosis. Other radiographs showed lesions on the left humerus, pelvis, and right femur. Dialysis controlled the creatinine levels and a parathyroidectomy of the upper left gland reduced the PTH levels. Due to the extension of the lesions, treatment with inhaled salmon calcitonin, and intralesional triancinolone once per week was undertaken. After 12 weeks, the lesion became calcified. A renal transplant was performed and the patient is free of clinical and radiographic signs of relapse.
Discussion: In patients with renal insufficiency, PTH contrations become elevated in response to hypocalcemia, hyperphosphatemia, and vitamin D defiency. Parathyroid gland increases in size and may enlarge or develp neoplasia. In some cases partial to complete parathyroidectomy is effective in reducing PTH concenctration and treating the lesion. This study illustrates the first casein which both calcitonin and intralesional corticosteroid injections. The calcitonin blocks the effects of PTH and the corticosteroids prevent osteoclastic giant cell activity.
Key points/Summary : Brown tumors are central giant cell granulomas with an underlying parathyroid disorder. Non-surgical intervention using a combination of inhaled calcitonin and intra-lesional injections successfully treated this case
Assessment of article: Good article.
Lutheran Medical Center
Resident’s Name: Craig Elice Date: 7/24/2009
Article title: Highly Aggressive Brown Tumor in the Jaw Associated with Tertiary Hyperparathyroidism
Author(s): Pinto LP, Cherbinim K, Salum FG, et al.
Journal: Pediatric Dentistry
Volume (number): 28(6)
Date: 2006
Major topic: Brown Cell tumor diagnosis and management
Type of Article: Case Report
Main Purpose: This case report describes a 12 year old female with an aggressive brown tumor associated with tertiary hyperparathyroidism and treated medically with calcitonin and corticosteroids.
Review of Case: Brown tumors are central giant cell granulomas which develop as a result of untreated hyperparathyroidism. The tumor affects mainly children and young adults with a female predilection. It represents less than 7% of all benign jaw lesions. The primary form of hyperparathyroidism relates of a hyperplastic or neoplastic parathyroid gland. Secondary occurs due to chronic renal insufficiency and tertiary is secondary with spread of parathyroid glands to other sites. Brown tumors occur in 1.5-1.7% of patients with chronic renal insufficiency. Treatment is focused around solving the underlying endocrine abnormatlity. The brown color is derived from hemorrhay and hemosiderin infiltration of the lesion.
The 12 yewar old female presented with right buccal lesion noted 3 months ago, and had a firm consistency. The panorex revealed a large osteolytic lesion. Blood tests revealed elevated blood creatinine levels, parathyroidhormone and alkaline phosphatase. Histology confirmed the diagnosis. Other radiographs showed lesions on the left humerus, pelvis, and right femur. Dialysis controlled the creatinine levels and a parathyroidectomy of the upper left gland reduced the PTH levels. Due to the extension of the lesions, treatment with inhaled salmon calcitonin, and intralesional triancinolone once per week was undertaken. After 12 weeks, the lesion became calcified. A renal transplant was performed and the patient is free of clinical and radiographic signs of relapse.
Discussion: In patients with renal insufficiency, PTH contrations become elevated in response to hypocalcemia, hyperphosphatemia, and vitamin D defiency. Parathyroid gland increases in size and may enlarge or develp neoplasia. In some cases partial to complete parathyroidectomy is effective in reducing PTH concenctration and treating the lesion. This study illustrates the first casein which both calcitonin and intralesional corticosteroid injections. The calcitonin blocks the effects of PTH and the corticosteroids prevent osteoclastic giant cell activity.
Key points/Summary : Brown tumors are central giant cell granulomas with an underlying parathyroid disorder. Non-surgical intervention using a combination of inhaled calcitonin and intra-lesional injections successfully treated this case
Assessment of article: Good article.
Dentigerous Cysts in Primary Dentition: Report of 2 cases
Resident: Tyler Roberts
Author: Delbem et al
Journal: Pediatric Dentistry
Volume # 28:3, pages 269-271
Year: 2006
Major topic: Dentigerous cyst in children/adolescents
Type of article: case review
Kep pts/findings:
Dentigerous cyst are benign odontogenic cysts associated with the crowns of unerupted permanent teeth. They are usually single in occurrence and located in the mandible. They are the second most common type of odontogenic cyst, accounting for 49% of all cystic lesions. They are most common in male patients and frequently occur during the second or third decade of life. These lesions are usually asymptomatic and discovered at the time of routine radiographic examination. If the cyst is greater than 2cm in diameter swelling, mild sensitivity, tooth mobility and displacement may be observed. Radiographically these lesions are symmetric, well-defined, unilocular surrounding the crown of the unerupted tooth. Possible complications include: permanent bone deformation or fracture, expansive bone destruction, loss of permanent teeth, development of squamous cell carcinoma
Case 1
A 10 year old presented with swelling on the left side of his jaw. An intraoral examination revealed bulging along the cortical bone that extended from his mandibular left first bicuspid to the distal of the permanent mandibular left first molar and a radiographic lesion that appeared unilocular, radiolucent and was associated with the dental crown of the bud of the mandibular left second molar. A differential diagnosis suggested a dentigerous cyst. Marsupialization was chosen as treatment. The primary mandibular left second molar was extracted, the lesion was decompressed and a space maintenance appliance was inserted. The parents were told to irrigate the lesion with listerine solution and clean the appliance daily. A histopathologic examination revealed that the lesion was indeed a dentigerous cyst.
Case 2
An 8 year old boy, was found to have a volumetric increase of the lingual cortical plate in the region of the primary mandibular right lataeral incisor which showed prolonged retention. Radiographically a well-defined, unilocular, radiolucent lesion was present surrounding the bud of the permanant mandibular right lateral incisor. The lesion appeared to be causing root resportion of the primary lateral incisor and canine. The working diagnosis was a dentigerous cyst. Treatment included extraction of the primary mandibular right lateral incisor and primary canine as well as total enucleation of the cyst due to the small size. Stitches were placed and removed seven days later and seven months later eruptive movements of the permanent right lateral incisor was present along with new bone neoformation was visible in the area.
Summary of conclusions: Dentigerous cysts are benign and asymptomatic. Because they are common among cyst they should not be overlooked at the time of routine radiographic examination. Small cyst are most likely to undergo complete enucleation while larger cyst may require decompression for healing to take place.
Author: Delbem et al
Journal: Pediatric Dentistry
Volume # 28:3, pages 269-271
Year: 2006
Major topic: Dentigerous cyst in children/adolescents
Type of article: case review
Kep pts/findings:
Dentigerous cyst are benign odontogenic cysts associated with the crowns of unerupted permanent teeth. They are usually single in occurrence and located in the mandible. They are the second most common type of odontogenic cyst, accounting for 49% of all cystic lesions. They are most common in male patients and frequently occur during the second or third decade of life. These lesions are usually asymptomatic and discovered at the time of routine radiographic examination. If the cyst is greater than 2cm in diameter swelling, mild sensitivity, tooth mobility and displacement may be observed. Radiographically these lesions are symmetric, well-defined, unilocular surrounding the crown of the unerupted tooth. Possible complications include: permanent bone deformation or fracture, expansive bone destruction, loss of permanent teeth, development of squamous cell carcinoma
Case 1
A 10 year old presented with swelling on the left side of his jaw. An intraoral examination revealed bulging along the cortical bone that extended from his mandibular left first bicuspid to the distal of the permanent mandibular left first molar and a radiographic lesion that appeared unilocular, radiolucent and was associated with the dental crown of the bud of the mandibular left second molar. A differential diagnosis suggested a dentigerous cyst. Marsupialization was chosen as treatment. The primary mandibular left second molar was extracted, the lesion was decompressed and a space maintenance appliance was inserted. The parents were told to irrigate the lesion with listerine solution and clean the appliance daily. A histopathologic examination revealed that the lesion was indeed a dentigerous cyst.
Case 2
An 8 year old boy, was found to have a volumetric increase of the lingual cortical plate in the region of the primary mandibular right lataeral incisor which showed prolonged retention. Radiographically a well-defined, unilocular, radiolucent lesion was present surrounding the bud of the permanant mandibular right lateral incisor. The lesion appeared to be causing root resportion of the primary lateral incisor and canine. The working diagnosis was a dentigerous cyst. Treatment included extraction of the primary mandibular right lateral incisor and primary canine as well as total enucleation of the cyst due to the small size. Stitches were placed and removed seven days later and seven months later eruptive movements of the permanent right lateral incisor was present along with new bone neoformation was visible in the area.
Summary of conclusions: Dentigerous cysts are benign and asymptomatic. Because they are common among cyst they should not be overlooked at the time of routine radiographic examination. Small cyst are most likely to undergo complete enucleation while larger cyst may require decompression for healing to take place.
07/24/09 Mucoepidermoid carcinoma of the palate in a child
Resident: Adam J. Bottrill
Date: 24JUL09
Region: Providence
Article title: Mucoepidermoid carcinoma of the palate in a child
Author(s): Flaitz, Catherine M. DDS, MS
Journal: Pediatric Dentistry
Volume #: Number; Page #s): 22: 292-293
Year: 2000
Major topic: Mucoepidermoid carcinoma of the palate
Minor topic(s): Salivary gland tumors
Type of Article: Case review
Main Purpose: Discussion and differential diagnosis for salivary gland tumors
Overview of method of research: Case study
Findings: 8 y.o. white boy presented with soft tissue enlargement of the palate. Increasing in size for 9 months. Localized, submucosal nodule of Rt posterior hard palate. Mucosa smooth, intact and faintly blue. Soft, compressible and fluctuant. No mobility or displacement of adjacent teeth. No other abnormalities.
Key points in the article discussion: Due to slow growth and location, salivary gland tumor should be considered. 1st most common is the pleomorphic adenoma followed by mucoepidermoid carcinoma.
A. Mucoepidermoid carcinoma:
1. Malignant tumor occurring most frequently in the parotid gland followed by submandibular gland. When involving MINOR salivary glands, palatal region is most common.
2. Most diagnosed withw girls between age 10 and 16
3. Painless, persistent enlargement present for about a year. With Major glands or tongue involved, pain, parasthesia and difficulty with swallowing most common. Intraoral lesions are localized, fluctuant nodule with bluish or reddish smooth mucosa. Some may drain through sinus tract. Most are soft and compressible but the higher grade tumors may be firm. More aggressive tumors may exhibit ulceration, bone resorption.
4. Most pediatric tumors are diagnosed as low or intermediate grade. Present case Dx as low grade with multicystic spaces and duct-like structures in fibrous connective tissue.
5. Tx: Wide local excision with adequate, tumor-free margins. Higher grade tumors require more aggressive surgery with possible radiation or chemotherapy. Low grade: > 90% cure rate. High grade: 20-30% cure rate.
B. DDX: Abscess (more sudden with tooth symptoms), mucocele (uncommon site), hemangioma (gingival sulcular bleeding and uncommon site), neurofibroma, schwannoma.
Summary of conclusions: Though this is a rare oral lesion in children, it should be ruled out when dealing with a mucocele-like lesion on the hard palate. Tx as a mucocele may result in spread of the carcinoma. This tumor has also presented as a secondary malignancy after therapy of a more aggressive primary malignancy. In pediatric pts, these rare malignancies are MORE likely to be malignant when they arise in minor salivary glands. Prompt differential diagnosis, referral and therapy is important.
Assessment of article: A concise DDX and discussion for mucoepidermal carcinoma of the palate.
Date: 24JUL09
Region: Providence
Article title: Mucoepidermoid carcinoma of the palate in a child
Author(s): Flaitz, Catherine M. DDS, MS
Journal: Pediatric Dentistry
Volume #: Number; Page #s): 22: 292-293
Year: 2000
Major topic: Mucoepidermoid carcinoma of the palate
Minor topic(s): Salivary gland tumors
Type of Article: Case review
Main Purpose: Discussion and differential diagnosis for salivary gland tumors
Overview of method of research: Case study
Findings: 8 y.o. white boy presented with soft tissue enlargement of the palate. Increasing in size for 9 months. Localized, submucosal nodule of Rt posterior hard palate. Mucosa smooth, intact and faintly blue. Soft, compressible and fluctuant. No mobility or displacement of adjacent teeth. No other abnormalities.
Key points in the article discussion: Due to slow growth and location, salivary gland tumor should be considered. 1st most common is the pleomorphic adenoma followed by mucoepidermoid carcinoma.
A. Mucoepidermoid carcinoma:
1. Malignant tumor occurring most frequently in the parotid gland followed by submandibular gland. When involving MINOR salivary glands, palatal region is most common.
2. Most diagnosed withw girls between age 10 and 16
3. Painless, persistent enlargement present for about a year. With Major glands or tongue involved, pain, parasthesia and difficulty with swallowing most common. Intraoral lesions are localized, fluctuant nodule with bluish or reddish smooth mucosa. Some may drain through sinus tract. Most are soft and compressible but the higher grade tumors may be firm. More aggressive tumors may exhibit ulceration, bone resorption.
4. Most pediatric tumors are diagnosed as low or intermediate grade. Present case Dx as low grade with multicystic spaces and duct-like structures in fibrous connective tissue.
5. Tx: Wide local excision with adequate, tumor-free margins. Higher grade tumors require more aggressive surgery with possible radiation or chemotherapy. Low grade: > 90% cure rate. High grade: 20-30% cure rate.
B. DDX: Abscess (more sudden with tooth symptoms), mucocele (uncommon site), hemangioma (gingival sulcular bleeding and uncommon site), neurofibroma, schwannoma.
Summary of conclusions: Though this is a rare oral lesion in children, it should be ruled out when dealing with a mucocele-like lesion on the hard palate. Tx as a mucocele may result in spread of the carcinoma. This tumor has also presented as a secondary malignancy after therapy of a more aggressive primary malignancy. In pediatric pts, these rare malignancies are MORE likely to be malignant when they arise in minor salivary glands. Prompt differential diagnosis, referral and therapy is important.
Assessment of article: A concise DDX and discussion for mucoepidermal carcinoma of the palate.
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