Wednesday, January 5, 2011
Central Hemangioma: An Overview and Case Report
Resident’s Name:Murphy Program: Lutheran Medical Center - Providence
Article title:Central Hemangioma: An Overview and Case Report
Author(s): Nikhil Marwah, MDS, Archana Agnihorti BDS, Samir Dutta, MDS
Journal: Pediatric Dentistry
Year. Volume (number). Page #’s: 2006. vol 28 No 5. 460-467
Major topic: Central Hemangiomas
Minor topic(s): Differential diagnosis, treatment options, Case report
Overview of method of research: Review/Case Report
Findings:
Hemangioma is a benign tumor characterized by proliferation of blood vessels. Presentation of a central hemangioma (CH) in the maxilla or mandible is rare. The literature differs on the origin of CH. Some believe it is a reaction from endothelial proliferation, while others contend it is a hamartoma resulting from proliferation of mesoderm that differentiates and becomes vascularized. CH also may be congential in origin. However it is agreed that it is benign. Some CH exhibit large size increases and can be locally destructive. CH occurs most commonly in the mandible (usually the body, sometimes the condyle) with a male:female ratio of 1:3 with peak incidence in the second decade of life. A CH may contain fibrous CT, osseous tissue, or cavernous blood vessels. The characteristic appearance of CH is a sunburst, or soap bubble pattern.
CH is a great mimicker of other conditions. CH may be in the differential diagnosis for:
1. Osteosarcoma
2. FD
3. Central giant cell granuloma
4. Ameloblastoma
5. Multiple myelome
6. Dentigerous cyst
7. Odontogenic cyst
8. Central ateriovenous fistula (clinically)
9. Aneurysms (clinically)
10. Shunts (clinically)
Clinical Findings
A CH may show little to no evidence of any intrabony lesion. Possible symptoms are pain including referred pain to the ear, TMJ, and condyle, swelling, or throbbing, and may be present from 1 week to 10 months. Referred pain to the ear, TMJ, and condyle is possible as well.
Dental findings may include
1.Occlusal derangement
2. Displaced teeth
3. Supraeruption
4. Premature exfoliation of primary teeth
5. Early eruption of teeth.
Radiographic Appearance
Usually presents as an area of altered radiodensity, usually osteolytic, occasionally w/ central radiopaque areas and a trabecular pattern. Trabeculae are arranged as spokes of a wheel, radiating from the center to the periphery. A soap bubble, sunburst or honeycomb pattern is possible as well. Nearly any combination of lesion size, shape, location or pattern can develop, with well defined, ill defined, and scalloped margins all being possible. Due to the ambiguity of the radiographic exam of a CH, diagnosis by radiographs alone is impossible.
Histology
This is the diagnostic test for a CH. It can either be capillary, cavernous, or mixed.
Diagnosis
A biopsy is 100% necessary for proper diagnosis. However due to the vascular nature of CH, uncontrollable bleeding must be considered. Angiography is a very useful diagnostic tool, as is aspiration.
Treatment
1. Radiotherapy(500-3300 R)-Used when the lesion is inaccessible to surgery
2. Injection of sclerosing agents (Boiling H20, Na morrhuate, Na tetradecly sulfate)-Very irritating, thrombogenic
3. Surgical removal-Risky, but still used the most frequently. Sometimes surgery and embolization (occlusion of vessels feeding the lesion) are used in conjunction. The biggest concern is hemorrhaging.
Case Report
8 yo Indian boy presented with a mandibular left side swelling that had been present for 10 months. The child’s primary molar had been ext’s before the start of the swelling. It started out small, then grew for the first 5 months. The child had minor ‘tooth’ pain. The swelling was confined to the left, lateral aspect of the mandible, it was hard, nonhyperthermic, and only sensitive to deep palpation. PA’s we non descript. A panorex showed coarse trabeculations and an increased radiodensity extending from the mand. lateral incisor to the 1st molar. The tooth buds of the canine and second premolar were affected. There was a definite honeycomb appearance. Lab reports were all normal. Fine needle aspiration was done to confirm the diagnosis. The child was admitted to the hospital, declared healthy, and prepped for surgery. A submand. Incision was made from the angle of the mandible to the symphyseal area. Enbloc resection of the lesion, including 1 cm of healthy bone was performed. A nickel titanium plate was placed over the defect. Further lab tests confirmed the lesion was a CH. 8 weeks post surgery the child was healing well, and the graft was being planned.
Key points/Summary:
Diagnosis cannot be made by clinical exam and/or radiographic exam alone. The three treatment options all have their pro’s and con’s. Many factors must be taken into account before deciding which treatment is best. CH must always be considered in the DD and proper precautions must be taken in establishing the final diagnosis before any tx is initiated.
Assessment of Article: Good, thorough review of CH and it’s implications. I thought the case report was ok. Would have liked to see more pictures and radiographs and the follow up of the boy. Overall a good review.
Removal of a Complex Odontoma within a Dentigerous Cyst

Odontogenic Myxoma in the Pediatric Patient: A Literature Review and Case Report
Resident: Cho
Author(s): Harokopakis-Hajishengallis E, et al.
Journal: Pediatric Dentistry
Year. Volume (number). Page #’s: 2007. 29. 409-414.
Major topic: Odontogenic Myxoma
Type of Article: Case Report
Key points/Summary:
Myxoma: benign soft tissue or bone neoplasm that may appear anywhere in the body.
Most central myxomas occur in the jaws where they are called odontogenic myxomas (
Radiographically,
Upon gross examination,
The generally accepted treatment of
CASE REPORT
Healthy 6-year, 11-month female with unremarkable medical history, no dental caries, normal complement of teeth for her age presents on radiographic exam with bifurcation radiolucency and root resorption around #J, poorly defined radiolucency in the furcation of #J, unerupted #13 displaced superiorly.
#J was extracted and incisional biopsy performed. Microscopic exam of excised mucoid soft tissue provided histopathologic diagnosis of odontogenic myxoma. It showed stellate-shaped fibroblastic cells interspersed in matrix blue ground substance.
Upon CT, the lesion presented as a single unilocular radiolucency with well-defined scalloped borders located superior to extraction socket of #J. Adjacent to unerupted #13, it had caused buccal expansion, thinning, and convexity of the inferior floor of the maxillary sinus. The mass was surgically excised in the OR. The buccal cortex surrounding the lesion was removed and the tumor was enucleated without difficulty. #14, unerupted #12, unerupted #13, and #I were all extracted due to being inside the tumor bed or close to the tumor bed. 9 months following the lesion’s excision, the patient has shown no evidence of recurrence.
Assessment of Article: Excellent article. Learned a lot and thought that it gave a very thorough description of odontogenic myxomas.
Benign Teratoma of the Tongue in a Neonate: A Case Report and Review of the Literature
Program: Lutheran Medical Center - Providence
Article title: Benign Teratoma of the Tongue in a Neonate: A Case Report and Review of the Literature
Author(s): Shetty et al.
Journal: Pediatric Dentistry
Year. Volume (number). Page #’s: 2010. 32:3. 245-249.
Major topic: Benign Teratoma of Tongue
Overview of method of research: Case Report
Background:
Teratomas are neoplasms with the ability to grow continuously and are the most common extragonadal germ cell tumors of childhood. The cause of these neoplasms are unknown. Teratomas of the tongue are very rare and may develop from misplaced cells from the tuberculum impar.
Case Report:
A 6-week-old male presented in India for evaluation of a congenital lesion that had remained unchanged since birth. He was experiencing difficulty swallowing and breast-feeding, but no breathing problems. Clinical exam revealed a 2x1.5x1.5 cm pedunculated mass with smooth surface and normal coloring on the anterior 2/3 of the dorsum of the tongue. The patient experienced severe ankyloglossia and also polydactyly in all 4 limbs.
A team of oral and maxillofacial surgeons and pediatric dentists excised the mass under nasotracheal intubation with a circumferential incision including a few millimeters of healthy tissue. The lesion was cauterized and primary closure was obtained and a frenectomy was performed to correct the ankyloglossia. Histopathological exam revealed fibrous connective tissue, adipose tissue, mixed salivary glands, sebaceous glands, striated muscle, chondroid tissue and blood vessels and there was no evidence of malignancy.
Discussion:
Teratomas are classified into 4 different types:
1. dermoid- epidermal and mesodermal elements, most common
2. teratoid- ectodermal, mesodermal and endodermal, but poorly differentiated
3. true teratoma- 3 germ layers and differentiated
4. epignathus- highly differentiated into recognizable organs/limbs, high mortality rate
There have only been 20 documented cases of tongue teratoma since 1966. 75% experienced difficulty eating, but only 35% had problems breathing. Although the majority of cases are benign, 20% possessed histological evidence of malignancy.
Differential diagnosis: lymphangioma, hemangioma, granular cell myoblastoma, gastric mucosal cyst, lingual thyroid, thyroglossal duct cyst, ectodermal inclusion body, heterotropic gastric mucosal mucosal cyst, congenital rhabdomyosarcoma, encephalocele, glioma and neurofibromatosis.
Surgical excision is the treatment of choice and recurrence is rare.
Assessment of Article:
A well written article and good overview of teratomas, their clinical presentation, differential diagnosis and treatment.
Tuesday, January 4, 2011
01/05/2011 Molar Incisor Hypomineralization: Review and Recommendations for Clinical Management
Date: 01/05/2011
Article title: Molar Incisor Hypomineralization: Review and Recommendations for Clinical Management
Author: Williams et al.
Journal: Pediatric Dentistry-28:3 2006
Major topic: Molar incisor hypomineralization (MIH)
Type of Article: Lierature Review
Main Purpose:
Describe the diagnosis, prevalence, putative etiological factors, and features of hypomineralized enamel in MIH and present a sequential approach to management.
Background:
MIH was introduced in 2001 to describe the clinical appearance of enamel hypomineralization of systemic origin affecting one or more permanent first molars (PFMs) that are frequently associated w/ affected incisors. MIH is attributed to disrupted ameloblastic function during the transitional and maturational stages of amelogenesis. MIH’s clinical management is challenging due to the sensitivity and rapid development of caries in affected PFMs, the limited cooperation of a young child, difficulty in achieving anesthesia, and the repeated marginal breakdown of restorations.
MIH Diagnosis:
After a thorough prophy, the 4 PFMs and 8 erupted permanent incisors are examined wet for demarcated opacities, post eruption breakdown (PEB), and atypical restorations. Opacities are usually limited to the incisal or cuspal 1/3 of the crown, rarely involving the cervical 1/3. Restorations may not conform to typical caries pattern and frequently involve the cuspal or incisal 1/3 of the crown. Teeth with developmental defects of enamel may present similarly regardless of etiology and confused with MIH. For example, Enamel hypoplasia (EH) is a quantitative defect associated with a reduced localized thickness of enamel, following disruption of the secretory phase of amelogenesis. MIH and EH can be difficult to differentiate when affected molars have PEB due to caries or masticatory trauma.
Hypomineralized Enamel Characteristics:
Hypomineralization is thought to follow deposition of the full thickness of enamel matrix. The transitional ameloblast is considered most vulnerable and when these cells do not undergo complete maturation, full-thickness hypomineralization occurs. Hypomineralization is thought to be due to disturbed resorptive potential of ameloblasts and proteolytic enzyme inhibition, leading to protein retention and interference w/ crystal growth and enamel maturation. Also, conditions affecting matrix pH during enamel maturation and impaired calcium metabolism may predispose MIH.
Factors Associated With MIH:
Putative factors associated w/ disrupted amelogenesis of PFMs include systemic conditions and environmental insults influencing natal and early development. Although a number of etiological factors may contribute to MIH, the threshold needed to cause enamel defects at sensitive stages of amelogenesis is unknown and 2 or more concurrent conditions may act synergistically to produce a defect. Conditions common in the first 3 years, such as upper respiratory diseases, asthma, otitis media, tonsillitis, chicken pox, measles, and rubella, appear to be associated w/ MIH. Antibiotic usage has also been implicated but due to the concurrence of the disease and antibiotic therapy, it is difficult to determine whether MIH is associated with the disease, the antibiotic, or both. Systemic conditions implicated to date include nutritional deficiencies, brain injury and neurological defects, cystic fibrosis, syndromes of epilepsy and dementia (Kohlschutter-Tonz syndrome), nephritic syndrome, atopia, lead poisoning, repaired cleft lip and palate, radiation treatment, rubella embryopathy, epidermolysis bullosa, ophthalmic conditions, celiac disease, and GI disorders.
Prevalence of MIH:
Prevalence data is limited due to several diagnostic classifications but range from 4-25%
Risk Identification, Remineralization, and Preventaive Management:
Children at risk for MIH should be identified prior to PFM eruption if possible based on history of etiological factors in the first 3 years and careful radiographic exam of unerupted first molar crowns. Thorough OH should be instituted including desensitizing toothpaste. Remineralization therapy should commence as soon as the defective surface is accessible, aimimg to produce a hypermineralized surface layer and to desensitize the tooth. This can be accomplished with casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) oral care products that enhance remineralization by creating a state of supersturation followed by deposition of calcium and phosphate ions at the enamel surface. OH strategies for sensitive, poorly mineralized affected molar should include brushing affected molars with fluoridated desensitizing toothpaste w/ a soft toothbrush, apply a CPP-ACP topical cream, and apply a low concentration fluoride treatment gel regularly. As remineralization and desensitization of the affect molars occurs, regular OH strategies can be instituted.
Restoring Hypomineralized First Permanent Molars:
Restoring affected PFMs is frequently complicated by difficulties in achieving anesthesia, managing the child’s behavior, determining how much affected enamel to remove, and selecting a suitable restorative material. The choice of material will depend on the defect severity and the age of the child. Restorative options include glass ionomer cements (GIC), resin-modified glass ionomer cements (RMGIC), polyacid modified resin composites (PMRC), resin composites (RC), amalgam, stainless steel crowns (SSCs), and indirect adhesive or cast onlays or crowns. Amalgam is the least durable due to poor retention in shallow cavity preps and inability to protect remaining tooth structure. Adhesive materials are usually chosen due to the atypical cavity outlines following removal of affected enamel. Removal of all defective enamel is recommended when bonding resin composite to hypomineralized PFMs due to the poor bond strength of resin adhesives to hypomineralized enamel.
Restoring Hypomineralized Permanenet Incisors:
Hypomineralized incisors commonly seen in MIH may present with esthetic concerns that can complicate treatment. A conservative approach includes etching lesion, bleach w/ 5% NaOCl, and re-etch the enamel prior to placing a sealant over the surface to occlude porosities and prevent re-staining. Little improvement was reported with acid/pumice micro-abrasion. Esthetic improvement was achieved when enamel reduction was combined with opaque resins then direct RC veneering.
Adhesion To Hypomineralized Enamel:
The limited literature on adhesion of dental materials to hypomineralized enamel has focused on case reports of Amelogenesis Imperfecta (AI). Bond strengths of RC to hypomineralized enamel of PFMs affected with MIH are significantly less than bond strengths to normal enamel for both single-bottle total etch and self-etching primer adhesives. After removing all discolored hypomineralized enamel, cavity margins should be placed on sound enamel and RC should be bonded w/ a self-etching primer adhesive.
Full Coronal Coverage Restorations:
When PFMs have moderate to severe PEB, SSCs are the treatment of choice. SSCs prevent further tooth deterioration, control tooth sensitivity, establish correct interproximal contacts and proper occlusal relationships, are not as technique sensitive or costly as cast restorations, and require little time to prepare and insert. If not adapted properly, however, SSCs may produce an open bite or gingivitis.
Extraction Of Severly Hypomineralized First Permanent Molars:
When PFMs are severely hypomineralized, restorations may be impossible and extraction must be considered. In such cases, early orthodontic assessment is recommended.
Summary of conclusions:
The prevalence of MIH appears to be increasing and managing affected children is now a common problem for pediatric dentists. Although the etiology is unclear and may be multifactorial, children born preterm and those w/ poor general health or systemic conditions in their first 3 years may develop MIH. The early identification of such children will allow monitoring of their PFMs so that remineralization and preventative measure can be instituted as soon as the affected surfaces are accessible.
Assessment of article:
Good review of MIH. More research needed. Because the prevalence of MIH is increasing it would helpful to know more info about the etiology and if in fact the condition is multifactorial.
Peripheral Ossifying Fibroma - A Clinical Evaluation of 134 Pediatric Cases.
Date: 22DEC10
Region: Providence
Article title: Peripheral Ossifying Fibroma - A Clinical Evaluation of 134 Pediatric Cases.
Author(s): Elvira S. Cuisia Zenaida
Journal: Pediatric Dentistry
Page #s: 245-248
Vol:No Date: 23:3 2001
Major topic: Peripheral ossifying fibroma
Minor topic(s): NA
Type of Article: Clinical Evaluation
Main Purpose: This study, the first devoted to children, investigated the clinical features of a large number of POF's and compared the findings to cases reported in the English language literature.

Key points in the article discussion:
I. General:
A. Solitary gingival enlargements common in children. Usually due to irritation.
B. Peripheral Ossifying Fibroma:
1. Gingival nodule, cellular fibroblastic connective-tissue stroma with dispersed calcified foci.
2. Localized, exophytic lesion with sessile or peduculated base.
3. Most studies on POF's concentrate on the entire category of "fibroma's". Also, there are NO studies on POF's in the pediatric population.
4. Reactive lesions like POF do have pediatric significance that require early recognition and treatment by a dentist.
5. Definative etiology unknown
6. DD: Pyogenic Granuloma, Fibroma, Peripheral giant cell granuloma, irritation fibroma, papilloma, peripheral odontogenic fibroma
II. Methods:
A. Clinical and historical information of 134 surgically-removed POF's in patients age 1-19.
B. Clinical Manifestations, histogenesis, treatment rationale, biological behavior were emphasized.
C. 657 POF's in the 43362 biopsies during the study period. Only 134 (20%) were pediatric patients.
III. Results
A. Females (60%)
B. Maxillary Gingiva (60%)
C. Incisor/cuspid region
D. Average age 14yo (6mo to 19yo)
E. 71% of cases were found in black pts. (MAY indicated increased incidence)
F. Color: pink to reddish
G. 63% of lesions were ulcerated.
H. Size: 0.3 - 3.0 cm
I. Only 2 (1%) associated with primary teeth.
J. Clinician RARELY included POF in DD.
K. Recurrence rate after excision 8% (vary from 7-46% depending on the study)
1. This 8% may be inaccurate due to the nature of this study. There was no attempt to determine the recurrence rate of patients who did not follow up.
VI. Conclusions
A. Must consider taking radiographs, even for soft tissue lesions such as POF in order to determine the extent of the lesion and eliminate the DD.
B. POF is a well-defined pathologic entity among reactive gingival lesions.
C. Peak incidence is in the 2nd decade. Incidence of POF in 1st decade is very uncommon.
D. POF most common in female.
E. POF found mostly in maxillary incisor region.
F. POF arising from PDL of primary tooth uncommon.
G. Proper treatment protocol is warranted with close follow-up.
Assessment of article: Informative. Large "n". The author attempts to tag this study as somewhat "ground-breaking" by mentioning it's the first PEDIATRIC study of it's kind. I suppose it's interesting, but I don't see it changing the way I treat patients. The conclusions were appropriate. Medium Likey.
Dentigerous Cysts in Primary Dentition: Report of 2 cases
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/Assessment: 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.
Sunday, January 2, 2011
Juvenile Oral Lichen Planus: A Report of 2 Cases
Meghan Sullivan Walsh January 2, 2011
Literature Review - St. Joseph/LMC Pediatric Dentistry
Juvenile Oral Lichen Planus: A Report of 2 Cases
Resident: Meghan Sullivan Walsh
Program: Lutheran Medical Center- Providence
Article Title: Juvenile Oral Lichen Planus: A Report of 2 Cases
Authors: Victoria L. Woo, DDS; Akanksha Manchanda-Gera, BA; Derek S. Park, BA, MA; Angela J. Yoon, DDS, MPH, MA; David J. Zegarelli, DDS
Journal: Pediatric Dentistry
Volume (number), Year, Page #’s; 29, NO 6, November/December 2007, pages 525-529.
Major Topic: Juvenile Lichen Planus
Overview of Method of Research: Lichen Planus or LP is an inflammatory disease which can present itself in a variety of formats and sites. Cutaneous LP is characterized as purple pruritic, polygonal papules with reticular striations found mostly on the extremities and lower back. Oral LP is divided into 6 subgroups; Papular, Reticular, Plaque-like, Ulcerative (erosive), Erythematous (atrophic) and Bullous. The two most common oral forms are Ulcerative and Reticular. Both forms present as bilateral, symmetric lesions with periods of quiescence and exacerbation. Of note is that LP is often found simultaneously with Lupus erythematosus, pemphigus, Sjogren’s syndrome, 10 autoimmune liver disease, rheumatoid arthritis and dermatomyositis. The purpose of this article was to report two children with documented cases of Juvenile Oral Lichen Planus and provide a literature review of this disease.
Findings: Two children presented to the Division of Oral Pathology, Columbia University College of Dental Medicine for evaluation of oral lesions. The first case was a 9 year old Caucasian female with bilateral tongue lesions which caused her discomfort with certain foods and liquids. Her medical history was negative. The lesions presented as ulcers on her right and left lateral ventral tongue surfaces with an adherent, white reticular and papular pattern. The histopathology report revealed lichenoid mucositis consistent with lichen planus. The patient was placed on beclomethasone dipropionate inhaler and dexamethosone elixir and advised to return every 6 months for future evaluation. Unfortunately this patient never returned for follow-up visits.
The second case was an 11 year old Caucasian female with bilateral, asymptomatic mucosal tongue lesions. The patient had a negative medical history but interestingly had received 3 hepatitis B vaccinations at 1 month, 2 months, and 6 months of age. The intra-oral examination showed classic white, lacy striations on the right and left posterior buccal mucosa. A biopsy confirmed lichen planus. Since the patient was asymptomatic no future treatment was given at this time. Follow-up of this patient in one year showed similar intra-oral lesions.
Key Points: Summary: Criteria for juvenile oral Lichen Planus include:
1: Patient is less than 20 years old
2: Clinical evidence of oral lichen planus
3: Oral biopsy confirmation of lichen planus, lichenoid lesion, or lichenoid mucositis
4: A clinical description of “reticular” or “reticulate,” “straie, or “straited,” and/or “lacy” oral lesions.
5: No evidence of mucosal contact with dental restorations, no exposure to medications known to induce oral lichenoid reactions and no history of graph verse host disease.
The literature review showed Juvenile OLP occurred more frequently in males, ages 11-15 with no ethnic predilection. The buccal mucosa was the most commonly affected site and most patients were affected by the reticular OLP. Important factors in the development of Juvenile OLP include previous Hep B vaccinations, liver disease and a genetic predisposition. Erosive OLP is extremely rare in the young population. Treatment of these patients is close monitoring of those asymptomatic and topical steroids for the symptomatic patients.
Assessment of the Article: Very well written article regarding Juvenile Oral Lichen Planus. Very thorough discussion of the disease, characteristics and treatment. Was surprised to hear about Juvenile OLP relationship with the Hepatitis B vaccination.
Tuesday, December 21, 2010
Dental Erosion in Children: A literature review
Meghan Sullivan Walsh December 21, 2010
Literature Review - St. Joseph/LMC Pediatric Dentistry
Dental Erosion in Children: A literature review
Resident: Meghan Sullivan Walsh
Program: Lutheran Medical Center- Providence
Article Title: Dental Erosion in Children: A literature review
Authors:Vivienne Linnett, BDSc, MDSc; W. Kim Seow, BDSc, DDSc, PhD, FRACDS
Journal: Pediatric Dentistry
Volume (number), Year, Page #’s; 23:1, 2001, pages 37-43
Major Topic: Review of Dental Erosion; diagnosis, causative factors, prevention and restorations.
Overview of Method of Research: Literature Review.
Findings: Studies have shown the prevalence of dental erosion in children to range from 2-57%. Dental erosion can cause tooth sensitivity, occlusal problems and even pulp exposures and abcesses in severe cases. The paper compiled literature regarding dental erosion to help establish the prevalence, clinical manifestation and etiology of pediatric dental erosion and to provide guidelines for patients and their restorative dentist.
Prevalence: Four studies were looked at with a wide range of prevalence on dental erosion in both primary and permanent dentition. All of these studies had a relatively small number of subjects which may have accounted for the wide range of numbers. In compiling the numbers, erosion in dentin showed prevalence of 30% in primary molars of 5 year olds and 2% in incisal surfaces of permanent incisors in 14 year olds. Children with CP showed a nigh prevalence of tooth erosion which was attributed to both parafunctional activity and GERD.
Clinical manifestation:
Appearance: Initially the tooth may show slight loss of surface luster when the enamel is clean and dry or show sensitivity or fracturing of thinned incisal edges. Once the erosion process has progressed the tooth will have a dished out, hard, smooth appearance where the dentin may be exposed. One scoring method for dental erosion in children with GERD scores the tooth from 0-3 where 0 is no erosion to 3 where dentin is exposed at the bottom of the holes on the occlusal surfaces.
Complications: Severe erosion can cause enamel fracture and compromise esthetics. Loss of tooth structure can also account for tooth shortening and loss of VDO. Dentin sensitivity, problems with eating, pulpal inflammation and pulpal exposures also account for a person with a more severe case of erosion.
Etiology: A source of intrinsic or extrinsic acid acting of the tooth structure as well as parafunctional habits all contribute to tooth wear.
Extrinsic sources: Workers in factories with toxic acidic fumes or aerosols, wine tasters or competitive swimmers all have shown tooth wear due to occupational exposure of acid. Dehydration following sports, followed by consumption of acidic drinks, chewable Vitamin C tablets and persons who chew Aspirin over long periods of time also have shown to have dental erosion.
Titratable acidity of foods and drinks: As the pH in the oral cavity falls below 5.5, or the critical pH, erosion will occur. The actual H+ concentration of acidic substances has been found to be more important than the actual pH of the food or drink.
Types of acidic foods and drinks associated with erosion: A study of acidic drinks reported that the first appearance of enamel wear occurred between the fourth and sixth weeks of use. Orange juice was found to cause less erosion than grapefruit juice or carbonated cola. Sports drinks are also found to be highly erosive.
Frequency: Those who consumed these acidic drinks more than twice a day or consumed at bedtime showed the highest signs of erosion.
Intrinsic sources: GERD is the most common source of intrinsic acids in the mouth. Findings have shown that clinical symptoms are not seen until gastric acid has acted on the teeth for a period of 1-2 years. Other conditions have shown erosion such as metabolic and endocrine disorders, medication side effects, drug abuse, and psychosomatic disorders such as stress induces vomiting, bulimia, anorexia, and rumination.
Factors modifying erosion: Swallowing habits, buffering capacity of saliva, chemical makeup of enamel, shape and contour of teeth, duration of contact.
Saliva: Saliva is known to have the most important properties in prevention of dental erosion, but the nature of the role is not completely understood.
Oral hygiene: Erosion is frequently seen in individuals with a high level of oral hygiene. Also, brushing immediately following consumption of acidic beverages is strongly discouraged.
Fluoride: Addition of fluoride to acid solutions decreases the erosion. Applying sodium fluoride solutions immediately before tooth brushing reduces abrasion.
GUIDELINES:
Diagnosis: Thorough medical and dietary history of several days to elicit causative factors. Referral to a gastroenterologist is desirable is GERD is suspected.
Monitoring: Determining if your diagnosis is correct and if the erosive process is ongoing or decreasing. The author suggests study models, clinical photographs and rubber indexes as well as 6 month recalls.
Dietary modification: Decreasing the total acid intake or allowing time for remineralization in between meals. In addition finishing meals with something neutral or alkaline has proven beneficial. Also patients should be told to avoid brushing immediately after consuming acidic foods.
Fluoride: Used to minimize tooth loss and diminish sensitivity.
Restorative Treatment: Primary teeth are often restored with SSCs and composites to improve esthetics, restore VDO, prevent sensitivity and early exfoliation.
Key Points: Summary: Dental erosion can be caused by acidic foods, drinks, environmental exposures or GERD. The manifestation of erosion can be sensitivity, loss of VDO and poor esthetics. Children should be evaluated to identify the source of the acid and appropriate referrals and restorative care should be made.
Assessment of the Article:
The was a great overview of dental erosion. They broke the process down into the many factors which cause erosion, what we as clinicians should look for and appropriate care for these patients. The article was titled as Erosion for Children, however, the paper was really written more as a general assessment on erosion.
Oral Pyogenic Granuloma: A Review





Resident: Swan
Article Title: Oral Pyogenic Granuloma: A review
Author: Jafarzadeh, et al.
Journal: Journal of Oral Science
Volume (Number): Vol 48, No. 4 pgs 167-175, 2006
Major Topic: A complete review of published information about pyogenic granulomas, including the most recent approaches for treatment
Key Points/Summary:
In General: Pyogenic granuloma is a type of inflammatory hyperplasia (made up of inflamed fibrous and granulation tissues histologically). It’s title is a misnomer because it doesn’t have pus and isn’t a granuloma. It is a common tumor-like growth that is non-neoplasitc, and is usually found on keratinized tissue in the mouth. It is especially common in pregnant women.
Etiology: PG is generally considered to be a reactive tumor-like lesion that arises in response to different stimuli like chronic low-grade irritation, trauma (1/3 of all PGs), hormonal factors, or certain drugs (Cyclosporine). Poor oral hygiene can be a precipitating factor for PGs. They have been reported as being a result of injury to a primary tooth, iatrogenic therapies (GTR), and after bone marrow transplantation. It may occur in all ages but is most common in females in their second decade (probably hormonally related). Gingival lesions account for 75% of all PGs, followed by the lips, tongue, and buccal musoca. Max>Mand, Ant>Post. Mostly found on marginal gingival
Clinical Features: PG is a smooth, lobulated, exophytic lesion. It manifests as small, red, usually pedunculated but sometimes sessile, with a base that is hemorrhagic and compressible. Size is anywhere from a few mm to several cm. Clinical development is slow, asymptomatic, and painless, although it can grow rapidly. Its surface is usually ulcerated and friable, and it may be covered by a yellow, fibrinous membrane. It’s color ranges from pink to red to purple. Younger lesions are more vascular and appear more reddish-purple; they will bleed a lot if traumatized. Older lesions are more collagenized and pink.
Pregnancy Correlation: Gingival PGs develop in about 5% of pregnancies (pregnancy tumor). They come about as a result of hormonal imbalances that promote pregnancy gingivitis. If the cases go uncontrolled, PGs may develop. The reasons behind the regression of PGs after childbirth are unclear.
Histology: PGs show a highly vascular make up that resembles granulation tissue. There are two types of PG—Lobular Capillary Hemangioma type (LCH) and non-LCH type.
Differential Diagnosis: Biopsy confirms PG, but the differential would include peripheral giant cell granuloma, peripheral ossifying fibroma, metastatic cancer, hemangioma, conventional granulation tissue, hyperplastic gingival inflammation, Kaposi’s sarcoma, angiosarcoma, and NH Lymphoma. PCCG is more bluish-purple compared to the typical bright red PG. Ossifying fibromas are generally much lighter in color (not much vasculature). Metastatic tumors to the mouth are rare, but the attached gingiva is the most common affected soft tissue (30%). These are usually diagnosed much later in life. PGs may be clinically indistinguishable from hemangiomas, so biopsy is the only definitive way to differentiate. However, hemangiomas typically occur on the tongue, are multinodular, and bluish red.
Treatment: Excisional biopsy is the treatment of choice, unless it would produce a large deformity. Excision should extend down to the periosteum. Recently, successful excision of PGs using a Nd:YAG laser has been described.The laser has superior coagulation ability and results in less chance of bleeding. Other successful techniques that have been described include cryogenesis and injection of ethanol or sodium tetradecyl sulfate into the lesion. After surgery, recurrence is about 16%.
Assessment of Article: Great comprehensive review of the literature on PGs. I especially liked how it went down the list of differential diagnoses and described how PGs are different from each of the listed lesions.
