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Oral Surgery

Authors : Dr. KNV Sudhakar, Dr. Rajesh Sabnis, Dr. Abdul Hameed

The pedicled buccal fat pad is a most reliable and versatile flap for the reconstruction of small to medium size of defects like OAF, palatal defects, buccal mucosal defects. It is durable, easy to harvest, and should be considered in settings where access to free flaps is limited and in cases other options have failed. The indications, anatomy and techniques of successful harvest are discussed here in this article.

Oral cavity is known to affect by various pathologic conditions leading to formation of defects of various size compromising function. The aim is not only to fill the defect but at the same time it should restore the function. Variuos factors are responsible for the selection of flap such as size, region, type, quality and quantity of tissue available. The buccal fat pad flap is an pedicle flap and may be used to fill small-to-medium sized soft tissue and bony defects in the palate, superior and inferior alveoli and buccal mucosa. It is often encountered as it bulges into the surgical field during surgery in the pterygomandibular region.1 The use of the buccal fat pad as a grafting source in the closure of intra-oral defects has gained popularity because of the ease of access and rich blood supply. The purpose of this article is to share the experience of buccal fat pad.

Anatomy 2, 5
The buccal fat pad is an anatomically rounded and biconvex structure.
  • The buccal fat pad is an encapsulated, rounded, biconvex, specialised fatty tissue which is distinct from subcutaneous fat which acts as gliding pads when masticatory muscles contract, and cushions important structures from the forces generated by muscle contraction.
  • The buccal fat pad is attached by 6 ligaments to the maxilla, posterior zygoma, and inner and outer rims of the infra-orbital fissure, temporalis tendon and buccinator membrane.
  • It has Four processes (buccal, pterygoid, superficial and deep temporal) extend from the body to surrounding tissue spaces
  • The parotid duct passes along the lateral surface of the buccal fat pad or penetrates the body of the fat pad before it opens on the buccinator muscle.
  • The body is divided into 3 lobes – anterior, intermediate and posterior, in accordance with the structure of the lobar envelopes, the ligaments and the source of the nutritional vessels.
  • The anterior lobe is located below the zygoma, extending to the front of the buccinator, maxilla and the deep space of the quadrate muscle of the upper lip and zygomaticus major muscle. The canine muscle originates from the infraorbital foramen and passes through the medial part of the anterior lobe. The parotid duct passes through the posterior part, and the anterior facial vein passes through the antero-inferior margin. The anterior lobe also envelops the infra-orbital vessels and nerve, and together enters the infra-orbital canal. The branches of the facial nerve lie on the outer surface of the capsule.
  • The intermediate lobe lies in and around the posterior lobe, lateral maxilla and anterior lobe. It is a membrane-like structure with thin fatty tissue in adults, but is a large mass in children.
  • The posterior lobe is situated in the masticatory and neighbouring spaces. It extends up to the infra-orbital fissure and surrounds the temporalis muscle, and extends down to the superior rim of the mandibular body, and back to the anterior rim of the temporalis tendon and ramus. In doing so, it forms the buccal, pterygopalatine and temporal processes.
Feeding vessels
It is an axial flap. The facial artery, transverse facial vessel and the internal maxillary artery as well as their anastomosing branches enter the fat tissue and form a lobar subcapsular vascular plexus by anastomosing with each other. When precisely dissected and mobilised, the buccal fat pad provides a 7x4x3 cm pedicled graft.1

Reconstruction of small to medium (<5 cm) acquired or congenital soft-tissue and bone defects in the oral cavity,
  • Oro-nasal and oro-antral communications following dental extraction;
  • Surgical defects following tumour excision and excision of leukoplakia and submucous fibrosis.
  • Primary and secondary palatal cleft.
  • Other medium defects of oral cavity.
  • In Tempromandibular joint reconstruction
Coverage of maxillary and mandibular bone grafts.Alternative or backup for other failed local flaps.
Technique of harvesting buccal fat pad. 3
  • Approach no 1:-An incision through vestibular mucosa in the molar region membrane 1 cm below opening of parotid duct. (Matarasso’s method). (Fig.3)
  • Approach no 2:- A vertical mucosal incision slightly lateral to the anterior margin of the ascending ramus . (Stuzin’s method) (Fig. 4)
  • Approach no 3:-Elevate mucoperiosteal flap in the molar region on the lateral aspect of the maxillary alveolar process and 24 incision of the periosteum at the level of buccal sulcus.
  • Easy to harvesting.
  • Simple.
  • Versatile.
  • Hardly any complications.
  • Can be done under local anaesthesia.
  • Fat pad located in the same surgical field as the defect
  • Minimal donor site morbidity.5
  • Complications are very rare (3 - 7%), and comprise postoperative infection, partial necrosis, bleeding, scarring and granulation, and sulcus obliteration
Fig-2: Case of Cleft palate: raw surface of palate after the palatal flap covered with buccal fat.
Fig -3: Post Surgical maxillary defect: closed with buccal fat pad
Fig-4: case Leukoplakia excision and defect closed with buccal fat pad.
The repair of oral defects is always a challenge for a surgeon because of anatomical constraints and the specialized nature of intra oral tissues. Various surgical techniques have been suggested for the closure of oral defects such as primary closure, buccal mucosal graft, split thickness skin graft, allogenic graft, Regional flaps, distant flaps have also been successfully used for intra-oral reconstruction but, they are generally preferred for defects of much larger dimensions. The use of buccal fat pad has gained popularity in the reconstruction of various defects because of the following reason,
  1. Easy to harvest.
  2. Local flap.
  3. Rich blood supply.
  4. Little postoperative morbidity,
  5. Good patient acceptance
Initially buccal fat pad was considered a surgical nuisance because of its accidental encounter during various operative procedures, but in 1977 Egyedi [4] reported the use of fat pad in reconstruction of maxillary defect. After it become popular among the surgeon for the reconstruction of minor to average oral defect. Size limitations of BFP must be understood in order to provide successful outcome. Defects of larger sizes and distant, the possibility of partial dehiscence of the flap is high due to the impaired vascularity because of stretching of flap 5.
It is important to preserve the thin capsule around the fat pad to avoid the damage to the blood vessel supplying it. The nature of healing of buccal fat pad 6

Reported complications associated with the buccal fat pad flap are haematoma, partial necrosis, scarring, infection and facial nerve injury 1, 7,8, 9. The use of buccal fat pad in patients with previously radiated, malar hyperplasia, thin cheek, facial microsomia or other local defects.

The buccal fat pad is a quick, simple, reliable flap for repair of small to medium sized oral defects. It has an excellent blood supply and causes minimal donor site morbidity. Furthermore it is closely located to the defect. In the light of these features, it is thought that the buccal fat pad will be used more often for the repair of various defects in the future.

  1. Rapidis AD, Alexandridis CA, Eleftheriadis E, et al. The use of the buccal fat pad for reconstruction of oral defects: Review of the literature and report of 15 cases. J Oral Maxillofac Surg 2000;58(2):158-163.
  2. Martin-Granizo R, Naval L, Costas A, Goizueta C, Rodriguez F, Monje F, et al. Use of buccal fat pad to repair intraoral defects: review of 30 cases. Br J Oral Maxillofac Surg 1997;35:81–4
  3. Liversedge RL, Wong K. Use of the buccal fat pad in maxillary and sinus grafting of the severely atrophic maxilla preparatory to implant reconstruction of the partially or completely edentulous patient: Technical note. Int J Oral Maxillofac Implants 2002;17:424-428.
  1. Egyedi P. Utilization of the buccal fat pad for closure of oro-antral and/or oro-nasal communications. J Craniomaxillofac Surg 1977; 5:241.
  2. Zhang H, Yan Y, Qi K, Wang J, Liu Z. Anatomical structures of the buccal fat pad and its clinical adaptation. Plast Reconstr Surg 2002; 109(7):2509-2518.
  3. Samman N, Cheung LK,Tideman H.The buccal fat pad in oral reconstruction. Int J Oral Maxillofac Surg 1993; 22:2–6.
  4. Dean A, Alamillos F, Garcia-Lopez A, Sanchez J, Penalba M. The buccal fat pad in oral reconstruction. Head Neck 2001;23(5):383-388.
  5. El-Hakim IE, El-Fakharany AM. The use of pedicled buccal fat pad and palatal rotating flaps in closure of oroantral communication and palatal defects. J Laryngol Otol 1999; 113:834–8.
  6. Seward GR, Harris M, McGowan DA. Killey and Kay’s Outline of oral surgery Part 1. 2nd ed pp 241- 247. Bristol: IOP Publishing Ltd, 1987.
Authors : Dr. Prajwalit Kende, Dr. Harsha Puri, Dr.Rahul Jagiasi

Intramuscular haemangioma are uncommon benign neoplasms arising most frequently in the masseter and trapezius muscle. Due to its location it is often mistaken for a parotid swelling and rarely is an accurate pre-operative diagnosis achieved clinically. The intra-masseteric location also poses special problem in terms of proximity to the facial nerve and the post-operative flattening following excision of the masseter muscle. Herein, the case is reported of a 35-year-old male who presented with a round, painless mass on the left cheek, which was interpreted as an intramuscular haemangiomaafter a magnetic resonance imaging scan.

Intramuscular haemangioma (IMH) in the head and neck region is rare and frequently involve the masseter muscle. It tends to be relatively well circumscribed, and insidiously infiltrate the muscle resulting in a mass with deceptive gross margins. The tumor has a tendency to recur following attempts at surgical extirpation. Inaccurate pre-operative diagnosis and treatment planning may lead to incomplete excision and unnecessary risk to facial nerve injury.

Case Report A 35 year old male reported to our department with the complaint of progressive, painless swelling of the left cheek. Swelling had been present since 3-year old and had gradually increased in size. Patient had H/O trauma 8 to 10 years back followed by similar swelling. That time patient had undergone a surgery. But swelling recurred to the present day size.
Figure 1: Extra-oral (Frontal View Figure 2: Extra-oral (Profile View)
Figure 3: Intra-oral View On Clenching Clenching Figure 4: Intra-oral View Open Mouth
Figure 5: Orthopantomograph Figure 6: Ultrasonographic Imaging Of The Tumor
Figure 7: MRI (Axial Slice) Figure 8: MRI (Coronal Slice)
Physical examination revealed a swelling (3x4 cm) over the left masseter region, soft in consistency with smooth surface [Fig.1, Fig.2]. It was mobile but fixed with the contraction of masseter. His facial movement was normal. There was nopalpable thrill and the overlying skin was normal. Intraoral examination was unremarkable [Fig.3, Fig.4]. Routine orthopantomograph (OPG) was taken which did not reveal any significant finding [Fig.5]. Ultrasonography (USG) of left parotid and masseter was performed which showed well defined expansive lesion of size 33x31x11 mm = 6cc [Fig.6]. USG guided fine needle aspiration cytology (FNAC) was performed which showed blood. Magnetic resonance imaging (MRI) revealed a well-circumscribed, brighter mass in the left masseter muscle [Fig.7, Fig.8]. Preoperative diagnosis was intramuscular haemangioma of the masseter muscle and surgery was performed.

Haemangioma usually occurs in the skin, subcutaneous tissue or muscle. Haemangioma of soft tissue can be divided into intramuscular and extramuscular. The most common sites for intramuscular haemangioma are the trunk and lower limbs. Only 10 to 20% of all intramuscular haemangiomas present in the head and neck, and 60% are in the masseter and trapezius 1. Other possible sites are periorbital muscle, sternomastoid, temporalis muscle, geniohyoid and medial pterygoid. Intramuscular haemangioma mostly present before the age of 30. It is believed to be benign, hamartomatous, congenital neoplasms that go undetected for long period of time until sudden growth gives rise to pain or cosmetic deformity. Traumatic and hormonal influences have been suggested and may contribute to the etiology or growth spurts 2.
Haemangioma presents as a slowly enlarging mass with generally normal overlying skin but may have a reddish blue discoloration or even hyperthermic. The swelling is normally diffuse in nature, compressible and characteristically deep within the muscle. However, softness and compressibility may be absent due to local fibrosis and overlying musculature or to the prominent cellularity of capillary type tumors. Pulsations, bruits or thrills are uncommon but when present, arteriography is indicated as to identify large vessel communications.
These neoplasms appear to grow as non-encapsulated masses characterizedby a multicentric proliferation of cords of endothelial cellsthat subsequently canalize. The characteristic of locally invasive tumor involves growth along planes of least resistance. It is confined to one muscle in 80% of cases 2.
Histologically, the lesions are classified as (1) capillary (vessels smaller than 140 micrometer in diameter), (2) cavernous (vessels larger than 140 micrometer in diameter) or (3) mixed. Capillary haemangioma usually presents with a short history. They are highly cellular, thus explain the firmness and lack of clinical signs to suggest vascular in nature 2. Cavernous haemangioma generally presents with longer history of symptoms, tends to be larger in size and painful. They are most common in lower extremity with only 19% occurring in the head and neck 3. Mixed type is histologically similar to cavernous type so does its clinical presentations. CT-scanning will reveal enhancing well circumscribed intramuscular mass but unable to define tissue planes and the vascularity of the lesion. MRI shows good tissue delineation. Intramuscular haemangiomas are characteristically much brighter on T2 than on T1 weighted images. Arteriography with pre-opembolization of the feeding vessels enhances hemostasis and can facilitate excision. Fine needle aspiration biopsy is non-diagnostic.
Management of intramuscular haemangiomas should be individualized according to the tumor location and extent, tumor growth rate, anatomical accessibility, patient age and cosmetic considerations. Some of the patients can be observed with the accuracy of MRI especially in young children 1. The optimal management is wide surgical excision 2 that includes gross muscle beyond the gross limits of the tumor. Cosmetic and functional disabilities after excision have been minimal even after significant removal of surrounding normal muscle 4. The indication for surgery include symptomatic but stable tumors in older children, sudden rapid acceleration of tumor growth, gross functional impairment, local skin necrosis, thrombocytopenia, cosmetic deformity and suspicious of malignancy 4. Local recurrences occur in approximately 18% due to incomplete surgical resection. Spontaneous regression does not occur 1. Regional and distant metastasis has not been reported.

Haemangiomas are benign vascular neoplasms characterized by an abnormal proliferation of blood vessels. They may occurin any vascularized tissue including skin, subcutaneous tissue muscle and bone. These tumors are common in infancy andchildhood and commonly involve subcutaneous or mucosal tissues. Intramuscular haemangiomas, a distinctive type of haemangiomaoccurring within skeletal muscle, account for less than 1% of all haemangiomas. They occur more often in trunk andextremity muscles, whereas involvement of the masseter muscle is rare. The clinician should be well aware of such lesions occurring in the head neck face region. These lesions should be diagnosed in a meticulous way so that an accurate treatment plan can be charted out and future complications may be avoided.

  1. Rossiter JL, Hendrix RA, Tom LWC, Potsic WP: intramuscular tumour of head and neck. Otolaryngology – Head and Neck Surgery 1993; 108: 18-26.
  2. Wolf GT, Daniel F, Arbor A, Krause CJ: Intramuscular haemangioma of the head and neck. Laryngoscope 1985; 95: 210-13
  3. Clemis JD, Briggs DR, Changeus GW : Intramuscular haemangioma in head and neck. Canadian Journal of Otolaryngology 1975; 4: 339-46.
  4. Kenali MS, Bridger PG: Intramuscular tumour of the medial pterygoid. Australian, New Zealand Journal of Surgery 2000; 70: 462-66.

Authors:-Dr. Arti

Ameloblastoma is a true neoplasm of odontogenic epithelial origin. It is the second most common odontogenic neoplasm. Its incidence combined with its clinical behavior, makes ameloblastoma the most significant odontogenic neoplasm. Unicystic ameloblastoma refers to those cystic lesions that show clinical, radiographic, or gross features of a mandibular cyst, but on histologic examination show a typical ameloblastomatous epithelium lining part of the cyst cavity.1 It accounts for 5-15% of all intraosseous ameloblastomas. This article report a case of 30-year-old female with unicystic ameloblastoma associated with right impacted mandibular molar.

Ameloblastoma develops from epithelial cellular elements and dental tissues in their various phases of development. It is a slow-growing, persistent, and locally aggressive neoplasm of epithelial origin. It is the second most common odontogenic neoplasm. The tumor is often asymptomatic presenting as slowly enlarging facial swelling. It is often associated with an unerupted third molar 2. It may be detected during the course of routine radiography. The vast majority of ameloblastomas arise in the mandible, and the majority of these are found in the angle and ramus region. There are three forms of ameloblastomas, namely multicystic, peripheral, and unicystic tumors3. Multicystic ameloblastoma is the most common variety and represents 86% of cases. Peripheral tumors are odontogenic tumors, with the histological characteristics of intraosseous ameloblastoma that occur solely in the soft tissues covering the tooth-bearing areas of the jaws. Unicystic tumors include those that have been variously referred to as mural ameloblastomas, luminal ameloblastomas, and ameloblastomas arising in dentigerous cysts 4. Various treatment methods for the lesion in relation to many factors, such as the tumour size and location, have been suggested. These include enucleation, marginal resection and aggressive resection. When a diagnosis of ameloblastoma is obtained, the treatment must be aggressive and radical. The goal of treatment of ameloblastoma is to achieve complete excision and appropriate reconstruction. We present a case of a large unicystic mandibular ameloblastoma in a 30 year old female.

Case Report
A 30 year old female came with a chief complaint of a slowly growing swelling on the right side of the face since one year (Figure1). Initially, the swelling was small in size but has gradually increased over a period of time to attain the present size. It was not associated with pain or difficulty in opening the mouth, chewing or articulating (Figure2). No abnormality was detected upon systemic examination. On inspection, a diffuse swelling measuring approximately 7x4 cms in size is present on the right side of face extending anteroposteriorly 2 cms from the symphisis mentii to the ramus of mandible and superoinferiorly from alatragal line to the inferior border of mandible. The surrounding oral mucosa was normal. On palpation, the inspection findings were confirmed. The swelling was non tender and hard in consistency. The lymph nodes were non palpable. An orthopantomogram (OPG) was done, which showed large cystic lesion in the right side of mandible. The patient was taken up for enucleation and marsupialisation (Figure3) and after that for surgery under general anaesthesia (Figure 4, 5). A segmental mandibulectomy was done (Figure 6) and reconstruction plate was put (Figure7). The resected specimen (Figure 11, 12) was sent for histopathological examination and it revealed features consistent with that of the unilocular ameloblastoma.

Fig 1: Preoperative picture-Swelling right side of face Fig 2: Intraoral view preoperatively Fig 3: Enucleation and Marsupialization done
Fig4:Intraoperatively under General anesthesia Fig5:Intraoperatively under General anesthesia Fig 6: Segmental mandibulectomy done
Fig 7: Reconstruction plate put Fig 8: Suturing done after placement of reconstruction plate intraoperatively Fig 9: Postoperative view of suturing
Fig 10: Postoperative OPG Fig 11:Resected specimen Fig12: Resected specimen

Unicystic ameloblastoma, a variant of ameloblastoma was first described by Robinson and Martinez 5 .Unilocular ameloblastoma is a rare type of ameloblastoma, accounting for about6% of ameloblastomas. It usually occurs in a younger age group, with about 50% of the cases occurring in the second decade of life. More than 90% are located in the mandible 6-8. Between 50 and 80% of cases are associated with tooth impaction, the mandibular third molar being most often involved. Patients most commonly present with swelling and facial asymmetry, pain being an occasional presenting symptom. Mucosal ulceration is rare, but may be caused by continued growth of the tumor. Small lesions are sometimes discovered more on routine radiographic screening examinations or as a result of local effects (like tooth mobility, occlusal alterations and failure of eruption of teeth) produced by the tumor 9. Histologically, the minimum criterion for diagnosing a lesion as Unilocular ameloblastoma  is the demonstration of a single cystic sac lined by odontogenic (ameloblastomatous) epithelium often seen only in focal areas. Unilocular ameloblastoma should be differentiated from odontogenic cysts because the former has a higher rate of recurrence than the latter 10 According to Reichart relative frequency has been reported as between 5% and 22% of all subtypes of ameloblastomas. No data is available concerning prevalence and incidence of unicystic ameloblastoma. There have been many debates regarding whether unicystic ameloblastoma develops or arises in an existing cyst 11. Leider et al,proposed three pathogenic mechanisms for the evolution of Unicystic ameloblastoma: reduced enamel epithelium, from dentigerous cyst and due to cystic degeneration of solid ameloblastoma. 11 .It often involves an impacted tooth and the focal area of the cystic tumor lining is often composed of a nonspecific, thin epithelium that mimics the dentigerous cyst lining. 13 In the present case the association with an impacted tooth and presence of non specific thin epithelium lining in focal areas of cystic tumor supporting the second hypothesis i.e. arising from preexisting dentigerous cyst. Based on the character and extent of tumor cell proliferation within the cyst wall, several histologic subtypes of unicystic ameloblastoma are recognized, which include simple cystic type, intraluminal and mural type. Gardner in 1984 has pointed out that there is a difference in biological behaviour between these lesions 14. Till now no recurrence has been seen and patient is still regularly being followed up. Perhaps the most important consideration regarding unicystic ameloblastoma is that of biologic behaviour. It has been widely stated that these lesions are less aggressive than their solid or multicystic counterparts and should be treated by enucleation or curettage. However, Gardner has pointed out that there is a difference in biological behaviour between those lesions that are simply cystic or show intraluminal proliferation and those in which the epithelium penetrated and breaches the fibrous wall, therefore having the capacity to invade the cancellous bone. It has been suggested that recurrence following conservative surgery is more likely to occur in the third group therefore these lesions should be treated in the same manner as solid ameloblastomas. 15 Whatever surgical approach the surgeon decides to take, long-term follow-up is mandatory, as recurrence of unicystic ameloblastoma may be long delayed .16

Unicystic ameloblastoma is a tumor with a strong propensity for recurrence, especially when the ameloblastic focus penetrates the adjacent tissue from the wall of the cyst. The ability to predict this potential occurrence prior to surgery would greatly enhance therapeutic strategies for reducing the incidence. Hence, the Pathologist should examine the tissue sections carefully in an attempt to determine whether ameloblastoma has penetrated the wall of the cyst or not so that the complications can be minimized


  1. Kalaskar R, Unawane AS, Kalaskar AR, and Pandilwar P. Conservative management of unicystic ameloblastoma in a young child: Report of two cases. Contemp Clin Dent. 2011 Oct-Dec; 2(4): 359–363.
  2. Gerzenshtein J, Zhang F, Caplan J, Anand V, Lineaweaver W. Immediate mandibular    reconstruction with microsurgical fibula flap transfer following wide resection for ameloblastoma. J Craniofac Surg. 2006;17(1):178–182.
  3. Philipsen HP, Reichart PA. Odontogenic tumors and allied lesions. Quintessence Pub. Co. Ltd; 2004. Classification of odontogenic tumors and allied lesions; pp. 21–3.
  4. Chana, Jagdeep S, Yang-Ming Chang, Wei, Fu-Chan, Shen, Yu-Fen, Chan Chiu-Po, Lin Hsiu-Na, Tsai Chi-Ying, Jeng Seng-Feng. Segmental mandibulectomy and immediate free fibula osteoseptocutaneous flap reconstruction with endosteal implants: An ideal treatment method for mandibular ameloblastoma. Plast Reconstr Surg. 2004;113(1):80–87.
  5. Robinson L, Martinez MG. Unicystic ameloblastoma: A prognostically distinct entity. Cancer 1977;40:2278-85
  6. Philipsen HP, Reichart PA. Odontogenic tumors and allied lesions. London: Quintessence Pub. Co. Ltd; 2004. Unicystic ameloblastoma; pp. 77–86.
  7. Pizer ME, Page DG, Svirsky JA. Thirteen-year follow-up of large recurrent unicystic ameloblastoma of the mandible in a 15-year-old boy. J Oral Maxillofac Surg. 2002;60:211–5.
  8. Navarro CM, Principi SM, Massucato EM, Sposto MR. Maxillary unicystic ameloblastoma. Dentomaxillofac Radiol. 2004;33:60–2.
  9. Roos RE, Raubenheimer EJ, van Heerden WF. Clinico-pathological study of 30 unicystic ameloblastomas. J Dent Assoc S Afr. 1994;49:559–62.
  10. Konouchi H, Asaumi J, Yanagi Y, Hisatomi M, Kawai N, Matsuzaki H, Kishi K. Usefulness of contrast enhanced-MRI in the diagnosis of unicystic ameloblastoma. Oral Oncol. 2006;42:481–6.
  11. Ackermann GL, Altini M, Shear M. The unicystic ameloblastoma: A clinicopathological study of 57 cases. J Oral Pathol 1988;17:541-6
  12. Leider AS, Eversole LR, Barkin ME. Cystic ameloblstoma. Oral Surg Oral Med Oral Pathol 1985;60:624-30.
  13. Li TJ, Wu YT, Yu SF, Yu GY. Unicystic ameloblastoma: A clinicopathologic study of 33 Chinese patients. Am J Surg Pathol 2000;24:1385-92
  14. Gardner DG. A pathologist's approach to the treatment of ameloblastoma. J Oral Maxillofac Surg 1984;42:161-6.
  15. Thankappan S, Thomas V, Kandamparambil S, Nair S. Unicystic ameloblastoma: 3 case reports and review of literature. J Indian Acad Oral Med Radiol 2008;20:65-70.
  16. Li TJ, Kitano M, Arimura K, Sugihara K. Recurrence of unicystic ameloblatoma: A case report and review of the literature. Arch Pathol Lab Med 1998;122:371-4.


Author : Dr. Gagan Sabharwal

Oro Facial Clefts (OFC) is one of the most commonly seen congenital anomaly after congenital cardiac anomalies. Various studies have been conducted and several factors have been attributed to the pathogenesis of OFC the commonly proposed etiological factors being genetics, drug abuse during pregnancy, stress and nutritional deficiencies during the gestational phase, consanguineous marriages. The role of folic acid in the prevention of clefts has been proven beyond doubt by various studies. The aim of this article is spread awareness about the effect of folic acid in the prevention of neural tube defects its mechanism of action in preventing OFC and its value as an important micronutrient in a balanced diet.

The face is an important source of information in interpersonal communication. It is the focus of attention in face-to-face interaction, and gives us information on which we form initial, automatic impression of other people. Cleft lip and palate forms a group of facial anomalies that have an additional disadvantage of being located in the nose mouth area and can have a significant physical and psychological impact on the patient. Oro Facial Clefts (OFC) is one of the most commonly seen congenital anomaly after congenital cardiac anomalies.1

In humans, a finely choreographed cascade of gene expression, cell migration, cell transformation and apoptosis between 14 and 60 days post conception creates the soft and hard tissues of the face from the originating oropharyngeal membrane. By 48 days the upper lip is continuous and by 60 days palatal shelf fusion completes facial embryogenesis. Disruption of any of the tightly regulated processes occurring in this time frame by environmental and/or genetic abnormalities may then predispose to cleft lip and/or palate.2 OFC include cleft lip with or without the palate (CLP) as well as palate only (CP). OFC occur in both isolated and non-isolated forms. Isolated or nonsyndromic forms involve no other major structural or developmental impairments and represent the majority of cases with CL. The non-isolated or syndromic forms with CLP occur due to more than 450 causes including chromosomal anomalies, single gene conditions, environmental exposures, and syndromes of unknown cause. OFC impose significant health, psychosocial, and economic burdens, both at them individual and family levels. 3

Various studies have been conducted and several factors have been attributed to the pathogenesis of OFC, the commonly proposed etiological factors being genetics, drug abuse during pregnancy, stress and nutritional deficiencies during the gestational phase, consanguineous marriages, etc .4-7

OFC deformities are completely correctable and provide the patient a chance to get back into normalcy with predictable quality of life. But, prevention of a condition when options are available is a much better option than the correction of the problem. The role of folic acid in the prevention of clefts has been proven beyond doubt by various studies.8-10

Incidence of Oro facial Clefts
There has been a lack of an established registry for craniofacial deformities in India, therefore the exact incidence is not available. The last dedicated multicenter study involving three cities in India and 94,906 births was conducted between 1994 and 1996.11 The present incidence of cleft deformities however is around 1 in 800 live births in India12 which translates to around 30,000 new patients every year. This is a large number and when added to the number of individuals, who have not been treated, gives us a huge figure as backlog.

The aim of this article is spread awareness about the effect of folic acid in the prevention of neural tube defects its mechanism of action in preventing OFC and its value as an important micronutrient in a balanced diet.

Role of Folic acid
The discovery of the role of folic acid as the single most important prophylactic supplement was around two decades back; the benefits of the discovery are yet to be realized. The incidence of OFC has remained the same and the associated benefits too have not been utilized solely due to the lack of awareness among the health care providers themselves. The use of folic acid as a prophylactic therapy to any woman of child-bearing age has been proven to decrease the incidence of orofacial cleft by as much as 85%, besides the other proven benefits of folic acid as a nutritional supplement.13-15
There is strong evidence from clinical trials for a large preventive effect of folic acid on both recurrence and occurrence of Neural tube defects (NTDs). The strongest evidence for a preventive effect of high dose folic acid supplementation on recurrence of NTDs comes from the Medical Research Council (MRC) double-blinded randomized study, where women with a previous child with NTD were randomly assigned to groups of 4 mg folic acid, vitamins other than folic acid, vitamins with 4 mg folic acid, and placebo, taken daily at preconception and throughout the first trimester of pregnancy. The study reported a significant reduction of about 72% in the rate of NTDs in the groups supplemented with folic acid compared to the other study groups. No significant decreases in NTD recurrence were observed in the group receiving vitamins without folic acid, indicating that preventive effects were due the folic acid component.16

Multivitamin supplementation with a 0.8 mg folic acid at preconception and through at least two months post conception was also shown to lower the risk of first occurrence of NTDs by up to 100% in a randomized clinical trial in Hungary using a sample of women with no history of NTDs among their children. This same study showed no decrease in the occurrence of OFC though the overall rate of congenital anomalies was reported to have decreased with the multivitamin supplementation.17

The NTD research provides a model for developing clinical trials aimed at assessing preventive effects of folic acid on recurrence and occurrence of OFC, which is of direct relevance for clinical practice. A connection between NTDs and OFC can be supported by their similar time of occurrence during embryogenesis, their status as defects involving the midline of the embryo, their near identical population genetic characteristics (variable by geographic origin but with near identical recurrence risks and very similar birth prevalence rates overall), evidence of similar gene and environment contributions and the failure to identify major genetic factors for either.18
Category of women Recommended doses
No history of a previous NTD 400ug
With history of previous NTD 4000ug
Other high risk patients 4000ug
Women with close relative with NTD
Type 1 DM
With seizure disorders
Public health program- supplementation/food fortification
NTD: Neural tube defects, DM: Diabetes mellitus

Table 1 :Folic acid dosage regimens for women of child-bearing age 18 Normal adults are prescribed a daily intake of 400 μg of folate. Administration of folic acid in excess of 1,000 μgm may mimic symptoms of Vitamin B12 deficiency, especially the changes in the nervous system in elderly people.18

Mechanism of action
Folic acid is an essential component in the development and maintenance of cells and tissues. It is necessary for homocysteine metabolism. Folic acid also plays a vital role in the synthesis of DNA and RNA, which are the building blocks of cells. They are essential for the synthesis of puridine, thymidylate and methionine.18

Other benefits of folic acid
  • Preventive role in neural tube defects apart from OFC
  • Helps in prevention of cardiovascular diseases, especially fetal coronary heart diseases
  • Helps in prevention of age-related hearing loss
  • Helps combat adverse effects of methotrexate in anti-cancer therapy
  • Important role in the prevention of psychological depression
  • Has been proven to have a role in the prevention of psoriasis19-21

Any factor that could prevent the facial processes from reaching each other by slowing down migration, multiplication or both of neural crest cells by stopping tissue growth and development for a time or by killing some cells that are already in that location, would cause a persistence of a cleft.22 There are several lines of evidence suggesting the folate-hemocysteine metabolism to be implicated in the risk of orofacial clefts. However the explanation for this association is unknown but recent information shows endothelial nitric oxide synthase (NOS3) genetic variants expressing NOS3 involvement in folate homocysteine metabolism which inhibits nitric oxide resulting in hypertension and fetal growth retardation in pregnant rats.23, 24 There is some suggestive evidence for a possible role of folic acid in prevention of OFC. However, several important questions remain unanswered including confirming whether folic acid prevents OFC, whether it prevents occurrence or recurrence or both, whether it prevents CLP, CP or both, and identifying whether low or high doses are effective for prevention. Studies to date have provided mixed results particularly in regards to whether low or high dose folic acid can prevent primary occurrence. Most case-control observational studies indicating a preventive effect are likely to have evaluated low to moderate doses of folic acid though the majority did not measure or report the dose.26 These findings suggest that daily periconceptional intake of 400 μg of folic acid (the dose most commonly contained in over-the-counter multivitamin preparations) reduces the risk of occurrent NTDs by approximately 60%. 25 It was noted that in women who took 400 μg of folic acid in the time between their pre-marital examination and their first trimester, there was a decreased incidence of neural tube defects by more than 85% in a region with a high risk and by 40% in regions with low risk.13
Although the importance of folic acid in the prevention of OFC was recognized and accepted worldwide, 13-15its practical implementation has eluded reality; the main reason for this is the extremely low degree or, in certain cases, lack of awareness among the medical population and health care providers who actually interact with people affected by OFC.It has been found that proper counseling of prospective mothers and their education is the best means of achieving the goal of prevention.18

  1. Wyszynski DF. Cleft lip and palate - from origin to treatment. Vol. 35. Oxford: Oxford University Press; 2002. p. 458-67.
  2. Geoffrey Sperber (2002 ): Wyszynski, DF., editor. Cleft Lip and Palate: From Origin to Treatment. Oxford University Press; 2002.p5-12
  3. Marazita, ML. Segregation analysis. In: Wyszynski, DF. editor. Cleft Lip and Palate: From Origin to Treatment. Oxford University Press; 2002. p. 222-233
  4. Beaty TH, Maestri NE, Hetmanski JB, Wyszynski DF, Vanderkolk CA, Simpson JC,et al. Testing for interaction between maternal smoking and TGFA genotype among oral cleft cases born in Maryland 1992-1996. Cleft Palate Craniofac J 1997;34:447-54.
  5. Kondo A, Kamihira O, Ozawa H. Neural tube defects; prevalence, etiology and prevention. Int J Urol 2009; 16:49-57.
  6. Murray JC. Gene/Environmental causes of cleft lip and/or palate. Clin Genet 2002;61:248-56.
  7. Zeiger JS, Beaty TH, Liang KY. Oral clefts, maternal smoking and TGFA: A meta-analysis of gene-environment interaction. Cleft Palate Craniofac J 2005;42:58-63.
  8. Folic acid for the prevention of neural tube defects. American Academy of Pediatrics. Committee on Genetics. Pediatrics 1999;104:325-7.
  9. Berry RJ, Li Z, Erickson JD, Li S, Moore CA, Wang H,et al. Prevention of neural tube defects with folic acid in China. N Engl J Med 1999;341:1485-90.
  10. Czeizel E, Timar L, Sarkozi A. Dose dependent effect of folic acid on the prevention of orofacial clefts. Pediatrics 1999;104:e66.
More References are available on request
Author : Dr. Prit Shah

Odontomas are the most common odontogenic tumor. They are considered to be hamartomas rather than neoplasms, and are composed of the tissues native to teeth: enamel, dentin, and cementum and pulp tissue. Odontomas are further sub-classified based upon their gross and radiographic features into compound (small tooth like structures) or complex (a conglomeration of dentin, enamel and cementum).

Case report -
A 14 year old male patient complained of slow growing enlargement of the buccal cortical plate with missing teeth. On radio graphical assessment revealed a presence of radio opaque masses resembling odontome. Surgically impacted teeth and masses excised, Histopathological report confirmed compound odontome. Patient reviewed after 1 month. 6 months. No history of recurrence and wound healing satisfactory.

Surgical management

Odontomas are the most common odontogenic tumor. They are considered to be hamartomas rather than neoplasms, and are composed of the tissues native to teeth: enamel, dentin, and cementum and pulp tissue.
It was in 1867 that Paul Broca first used the term “Odontoma.” Broca defined the term as “tumors formed by the overgrowth of transitory or complete dental tissues”.

According to W.H.O. classification, 1 Odontomas can be divided into three groups:
1. Complex odontome - when the calcified dental tissues are simply arranged in an irregular mass bearing no morphologic similarity to rudimentary teeth.
2. Compound odontome - composed of all odontogenic tissues in an orderly pattern that results in many teeth-like structures, but without morphologic resemblance to normal teeth.
3. Ameloblastic fibro-odontome - consists of varying amounts of calcified dental tissue and dental papilla like tissue, the later component resembling an ameloblastic fibroma. The ameloblastic fibro-odontome is considered as an immature precursor of complex odontome. According to Thoma and Goldman: 5
• Geminated composite odontomes - two or more, more-or-less well-developed teeth fused together.
• Compound composite odontomes - made up of more-or-less rudimentary teeth.
• Complex composite odontomes - calcified structure, which bears no great resemblance to the normal anatomical arrangement of dental tissues.
• Dilated odontomes - the crown or root part of tooth show marked enlargement.
• Cystic odontomes - an odontome that is normally en-capsulated by fibrous connective tissue in a cyst or in the wall of the cyst.

There are essentially two types of odontomes:
  1. Complex composite odontome;
  2. Compound composite odontome. A new type known as Hybrid odontome is also reported by some authors “Complex Composite Odontome”

Etiology and Indication for removal of the tumour
The etiology of odontoma is not known but environmental causes such as infection, trauma, family history and genetic mutation are hypothesized.
Although the Odontomas erupting in the oral cavity is controversial, the reason is attributed to the eruptive forces of the apparently impacted teeth and in cases of absence of teeth, the reasons could possibly be the resorption of alveolar ridge exposing the odontoma, sequestration of overlying bone, alveolar bone remodeling in young adults, reactive growth of the capsule surrounding odontoma in elderly patients. Odontomas have been associated with trauma during primary dentition as well as with inflammatory and infectious processes, hereditary anomalies (multiple Odontomas in Gardner syndrome, Hermann's syndrome), odontoblastic hyperactivity and alterations in the genetic components responsible for controlling dental development Association of this lesion with the unerupted tooth is high and three quarters of impacted teeth related to Odontomas can erupt after removal of the odontoma. Another reason for removing Odontomas is their association with cysts in a significant number of cases (27.6%).

Clinical features
The complex odontoma constitute 5-30% of all odontogenic tumors and are mostly found in the posterior mandible and compound odontoma in anterior maxilla. They are seen with unerupted teeth in 10-44% and about 17% of them are associated with impacted maxillary lateral incisors. Females are affected marginally more than male (1.5:1). Majority of cases (84%) are seen below 30 years but are seen in any age group with peak incidence in second decade. Less than 10% are found in patients above 40 years of age. and most lesions are detected on routine radiographs.
Odontomas are generally asymptomatic, often associated with delayed eruption or impaction of permanent teeth and retained primary teeth. In some occasional cases, pain, infection, regional adenopathies, alveolar bone expansion and tooth displacement may be present.
Odontomas can also manifest as part of syndromes, such as Gardner syndrome, basal cell nevus syndrome, familial colonic adenomatosis, Tangier disease or Hermann syndrome.
In the present case patient was asymptomatic few month back , but later complain of swelling on the left side which on radiographic diagnosis (OPG) ruled out to be multiple harmatomatous radio opaque body around the tooth in glomerulated aggregates.

Odontomas are circumscribed, encapsulated tumors that can be removed successfully by conservative surgery. Spontaneous eruption of the impacted tooth after removal of the obstruction like odontoma has been reported by many authors.
A less conservative approach is advocated by others with exposure of the unerupted tooth at the time of surgery and placement of bonded attachment and ligature/e-chain for orthodontic traction, to facilitate rapid eruption.
This approach, however, may result in poor gingival margin, inadequate gingival tissue attachment and a discrepancy of gingival level between the exposed tooth and its neighboring teeth.
Hence, in the present case, we advocated a more conservative approach of removal of odontoma and its fibrous capsule. Along with that, we removed bone unerupted canine , replaced the flap back in position.

Recurrence rate and association with tumors
A clinical case of CCOT associated with odontoma and a missing deciduous tooth in a 3-year-old female patient. Described by Gorlin et al. in 1962, the calcifying cystic odontogenic tumor (CCOT) may be associated with unerupted teeth, ameloblastomas, adenomatoid odontogenic tumors, and, in many cases, with odontomas.
Prognosis is very favourable because it has no to minimal recurrence.

  1. Hidalgo-Sánchez O, Leco-Berrocal MI, Martínez-González JM. Metaanalysis of the epidemiology and clinical manifestations of odontomas.Med Oral Patol Oral Cir Bucal.2008;13:E730–42.
  2. Shafer's text book of oral pathology.5th ed. Amsterdam: Elsever; 2006. Cysts and tumors of odontogenic origin.Disturbances of development and growth. Shafer, Hine, Levy; pp. 357–432.
  3. Batra P, Duggal R, Kharbanda OP, Parkash H. Orthodontic treatment of impacted anterior teeth due to odontomas: A report of two cases.J Clin Pediatr Dent.2004;28:289–94.
  4. Prætorius F, Piattelli A. Odontoma, Odontogenic tumors. In: Barnes L, Eveson JW, Reichart P, Sidransky D, editors.WHO Classification of tumors. Pathology and Genetics of Head and Neck Tumors.Lyon France: IARC Press; 2005. pp. 310–11.
  5. Yeung KH, Cheung RC, Tsang MM. Compound odontoma associated with an unerupted and dilacerated maxillary primary central incisor in a young patient.Int J Paediatr Dent.2003;13:208–12.
  6. Jafarzadeh H, Abbott PV. Dilaceration: Review of an endodontic challenge.J Endod.2007;33:1025–30