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.

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.

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.

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.