EFFECT OF PRE-EXISTING MEDICAL CONDITIONS ON ORTHODONTICS

CONTENTS

1. INTRODUCTION

2. INFECTIVE ENDOCARDITIS & CONGENITAL HEART DISEASES

3 . DIABETES MELLITUS

4. RESPIRATORY DISEASES

5. ALLERGY & HYPER SENSITIVITY

6.JUVENILE RHEUMATOID ARTHIRITIS

7. EPILEPSY

8. BLEEDING & CLOTTING DISORDERS

9. RENAL DISEASES

10 .ENDOCRINE DISORDERS 11. ORTHODONTIC TREATMENT FOR DISABLED CHILDREN

INTRODUCTION Orthodontic therapy is no longer reserved for only healthy patients. It is estimated that 10-15% of all children under the age of 16 are affected by chronic, long-term medical problems.(Burden et al, 2001). An even higher percentage of adult patients may be afflicted by a variety of medical problems that involve one or more of the tissue systems. Orthodontic therapy has been historically considered to be completely non invasive,specific orthodontic procedures may place some patients at risk for serious sequelae.so it becomes necessary to have a good knowledge of the existing medical conditions that may predispose a patient to the development of future medical complications.

INFECTIVE ENDOCARDITIS & CONGENITAL HEART DISEASES Endocarditis , is defined as an inflammation of the endocardium (lining membrane of the heart).It may involve only the membrane covering the heart valves (valvular) or the general lining of the heart (Mural).

Classification

Infective & Non InfectiveAcute & SubacuteShort & Long IncubationCulture + ve & -ve

EtiologyBacteria usually the source of endocarditis Microbial infection Bacterial Infection Rickettsia Infection Chylamydia & Fungus

Congenital AnomalyRheumatic Heart DiseaseCongenital Heart Disease

Microorganisms Responsible

Johnson & Rosenth et al showed that Alpha Hemolytic Strepto Cocci are the most prevalent bacteria. Dajani et al 1997 Strepto Cocci. Viridans is the most common cause of endocarditis following dental and oral prodedures

St. Viridians (st. Mitis & St. Sanguis) are commensals in the oral cavity and upper respiratory tract. They enter into the blood stream on chewing, teeth brushing and dental treatment procedure.St.Faecalis & St.Milleri ,St. Bovis enter the blood from bowel and urinary tract.

Staphylococcus aureus Cause for Acute endocarditis.Staphylococcus albus Post operative endocarditis.Rickettsia Q fever endocarditis.Fungi (Candida , Aspergillus)

PathophysiologyEndocarditis., occur at sites where the endothelium is damaged, this leads to deposition of platelets and fibrin,which are colonized by blood-borne organism creating vegetation.Large Vegetation Cause obstruction of blood flow Vegetation break away and form emboliComplicationsCongestive Heart Failure.Emboli StrokeGlomerulo nephiritisDamage to gastro intestinal organsAbscess in the heart

Siver and Martin stated that even while brushing ,transitory bacteremia is induced in humans with healthy gingiva

Zachirson & Zachirson showed that even with good cleaning most patients with fixed othodontics appliance exhibited hyperplastic gingiva and appliance act as a retention area for plaque.

Bloom & Brown concluded the placement of full orthodontic bands increases the mean population of oral bacteria.

Although most orthodontic treatment is minimally invasive ,the placement and the removal of orthodontic bands has been suggested to produce bacteremia.

Lucas et al (2002) obtained blood samples from children 30 sec after taking dental impressions, separator placement, band placement, and insertion of an adjusted archwire. Significant bacteremia was found only after separator placement. EJO 2002

Mclaughlin n et al studied the incidence of bacteremias after orthodontic banding in 30 helathy subjects.This study cohort were in excellent periodontal health,as having gingival / plaque index of less that one.Blood samples were collected before and 1 -2 min after band placement.Bacterial cultures revealed that the frequency of bacteremia following banding was 10 % compared to 3% in the pre treatment sample

Congenital Heart Disease

Ventricular Septal Defect 30 %Atrial Septal Defect 10 %PDA 10 %Pulmonary Stenosis - 7 %Aortic Stenosis 6 %

Cardiac conditions associated with endocarditis (Dajani et al.,1997)

High Risk1. Prosthetic cardiac valves, including bioprosthetic and homograft valves.2. Previous bacterial endocarditis.3. Complex cyanotic congenital heart disease ( tetrallogy of Fallot)4. Surgically-constructed systematic pulmonary shunts

Moderate Risk1. Acquired valvular dysfunction (e.g. rheumatic heart disease).2. Hypertrophic cardiomyopathy.3. Mitral valve prolapse with valvular regurgitation and/or thickened leaflets.

Negligible Risk1. Isolated secundum atrial septal defect.2. Surgical repair of atrial septal defect, ventricular septal defect or patent ductus arteriosus.3. Previous coronary artery bypass graft surgery.4. Mitral valve prolapse without valvular regurgitation.5. Physiological functional or innocent heart murmurs.6. Previous Kawasaki disease without valvular dysfunction.7. Previous rheumatic fever without valvular dysfunction.8. Cardiac pacemakers

BJO DEC 1999 The requirement for prophylactic antibiotics for orthodontic procedures in patients at high or moderate risk of infective endocarditis

Antibiotic prophylaxis recommended - Separator placement Cleaning and polishing prior to banding , Banding ,exposure of teeth.,mucosal trauma during archwire placement not recommended - Impression taking ,radiograph taking,placement and adjustement of removable appliance,placement of archwires with elastics or ligatures,

EJO JUN 2002 Which orthodontic procedures requires antibiotic prophylaxis? All the orthodontic procedures, Banding Debanding Separator placement Are potential source of odontogenic bacteremia. (Lucas et al 2002)

EJO2004 BSAC(British society for Anti Microbial Chemotheraphy) guidelines dont include ortho procedures,only recommend the use of antibiotic prophylaxis in at risk for dental extraction,scaling,surgery involving gingival tissue (Simmonds et al )

Dajani et al (1997)- latest American guidelines have been modified to include the recommendation of antibiotic prophylaxis should be used for initial banding, but not when removing bands.

STANDARD REGIMENS Adults Not allergic to penicillin Oral -2.0 g Amoxicillin 1 hr before Non oral-2.0 g Ampicillin IM or IV 30 min before

Penicillin allergic Oral- 600 mg Clindamycin 1hr before or 2.0 g Cephalexin 1 hr before Non-oral-600 mg Clindamycin IV 30 min before

Children Not allergic to penicillin Oral- 50mg/kg Amoxicillin 1 hr before Non oral- 50mg/kg Ampicillin IM or IV 30 min before Penicillin allergic Oral- 20 mg/kg Clindamycin 1 hr before (or) 50 mg/kg Cephalexin 1 hr before Non-oral -25 mg/kg IM or IV Cefazolin 30 min before

If a patient forget to take his pre medication ,American Heart Association suggests that anti biotic given at the time of the treatment are up to 2 hours from the treatment .Antimicrobial rinses such as Chlorhexidine gluconate ,may be of value in temporarily reducing the oral bacterial count before the placement or the removal of bands.(Seminars in Orthodontics 2004).

DIABETES MELLITUS

Diabetes Mellitus is a metabolic disease , characterized by dysregulation of carbohydrate,protein and lipid metabolism.Due to Absolute or relative deficiency of insulin.Characterized by hyperglycemia.Clinically : Polyuria, Polydypsia, Polyphagia

ClassificationPrimary DM.Type I IDDM / Juvenile 10%.Type II NIDDM /Adult onset 80%.MODY 5% maturity onset - young - GeneticSecondary DM islet destruction.Infectious congenital rubella, CMV.Pancreatitis/tumors/Hemochromatosis.Endocrinopathy, gestational DM, downs.Drugs Corticosteroids.

Pathogenesis of Type I DMEnvironment ?Viral infe..??Genetic HLA-DR3/DR4Severe Insulin deficiency cell DestructionType I DMAutoimmune Insulitis

Pathogenesis of Type II DMEnvironmentObesity ??? cell defectGenetic cell exhaustionType II DMInsulin resistance Relative Insulin Def.IDDMAbnormal Secretion

Complications:

Short term Complications: (metabolic)

HypoglycemiaDiabetic KetoacidosisNon Ketotic hyperosmolar diabetic comaLactic acidosis

Long term Complications:(microangiopathy)

Angiopathy, Retinopathy, Nephropathy, Neurophathy

AngiopathyAtherosclerosisHyaline arteriolosclerosisDiabetic microangiopathyNephropathyNodular glomerulosclerosisRetinopathyNon Proliferative & ProliferativeNeuropathyPeripheral axonal neuropathy

Laboratory Diagnosis:

Urine glucose - dip-stick ScreeningRandom or fasting blood glucose ( 7mmol, Random >11mmolIf Fasting level is between 7-11 then OGTTHbA1c - for follow-up, not for diagnosisFructosamine - for long term maintenance.HbA1c is extremely useful for assessing glycemic control over a 6-to-12week period in patients with either type 1 or type 2 DM. An HbA1c of less than 7.5% or more than 9% indicates,Respectively, good or poor control of DM.

TYPE I DM Clinical ManagementRequire insulin replacementNeed regular blood glucose measurementMultiple insulin injections dailyVariable with daily activity and dietary intakeHigher risk of getting hypoglycaemics and ketoacidosisTYPE II DM Clinical ManagementDiet, weight reduction, exerciseOral hypoglycaemic MedicationsControl Blood Pressure and cholesterolAspirin and other medicationsMay require insulin at later stageOnce daily glucose measurementRegular follow-up

ORAL MANIFESTATIONS OF DM

Approximately half of the people with DM are undiagnosed, and a dental examination might give the first indication of thedisease.Important clues are drymucous membranes (xerostomia), oral candidiasis, burning mouth or tongue (glossopyrosis), impaired wound healing, recurrent oral infections, and acetone breath. Erythematousgingival enlargement is, frequently found in subjects with uncontrolled diabetes.

ORTHODONTIC CONSIDERATIONOrthodontic treatment should not be performed in a patient with uncontrolled diabetes. If the patient is not in good metabolic control (HbA1c -9%), every effort should be made to improve blood glucose control.

It is important to stress good oral hygiene, especially when fixed appliances are used. These appliances might give rise to increased plaque retention, which could more easily cause tooth decay and periodontal breakdown in these patients. Daily rinses with a fluoride-rich mouthrinse can provide further preventive benefits. Candida infections can occur, and then blood glucose levels should be monitored to rule out deterioration of the DM control. Diabetes-related microangiopathy can occasionally occur in the periapical vascular supply, resulting in unexplained odontalgia, percussion sensitivity, pulpitis,or even loss of vitality in sound teeth.

It is advisable to apply light forces and not to overload the teeth.

Holtgrave and Donath studied periodontal reactions to orthodontic forces. They found retarded osseous regeneration, weakening of the periodontal ligament, and microangiopathies in the gingival area. They concluded that the specific diabetic changes in the periodontium are more pronounced after orthodontic tooth movement. Because DM patients, and especially those who are uncontrolled or poorly controlled, have a higher tendency for periodontal breakdown.

During orthodontic treatment, the orthodontist should monitor the periodontal condition and control inflammation. As with all orthodontic patients, maintaining strict oral hygiene is very important. If plaque control is difficult to achieve with mechanical aids such as toothbrush and interdental brush, then using a disinfectant mouthrinse of the chlorhexidine type as an adjuvant chemical plaque control can be considered

HYPOGLYCEMIC REACTION

Patients who require large doses of insulin can have periods of extreme hyperglycemia and hypoglycemia (brittle diabetes), even with the best medical management. They are more prone to developing a so-called hypoglycemic reaction.

When a hypoglycemic reaction occurs in the dental office, the dentist should recognize the symptoms and act appropriately. If patients fail to eat normally but continue to take their regular insulin dosage, a hypoglycemic reaction can occur because of excess insulin, resulting in insulin shock. These patients might appear weak, nervous, and confused. Their skin is moist and pale, and they have an excessive flow of saliva. Respiration is normal, the pulse is full and pounding, and blood pressure is usually normal.

The cooperative and conscious patient who demonstrates clinical symptoms of hypoglycemia should be given a high-carbohydrate beverage, such as orange juice or cola. patient will respond almost immediately or very shortly and should remain under observation until all signs and symptoms have disappeared. If a state of hypoglycemia continues, the patient will soon become unconscious unless 50% dextrose solution (50 ml) is administered intravenously. Another drug that can be administered is glucagon (1 mg intramuscularly); this is preferable if the patient is conscious but uncooperative.Management of the unconscious patient also includes airway maintenance, oxygen administration, and monitoring of vital signs

RESPIRATORY DISEASES: STRUCTURE OF UPPER AIRWAY The structures forming the upper airway are the nose and the pharynx with its 3 divisions (ie, nasopharynx, oropharynx, hypopharynx). Changes in the dimensions of the respiratory tract i.e. constriction will decrease the airflow(Solow and Greieve`79)Nose: The internal nasal valve, the septum, and the choana Nasopharynx: The adenoids are commonly hypertrophied, producing obstruction. Hypertrophied adenoids are the most common cause of OSA in children. Oropharynx: The soft palate, tonsils, palatoglossal and palatopharyngeal arches, and the tongue are structures of concern. In addition, the cross-sectional diameter of the pharynx can be smaller in many patients, playing an important role in the pathogenesis of OSA. Hypopharynx: The base of the tongue is the most influential structure in this area.

UPPER-AIRWAY INFECTIONSViral Upper Respiratory InfectionsAllergic Rhinitis and ConjunctivitisOtitis MediaSinusitisLaryngitis and LaryngotracheobronchitisPharyngitis and Tonsillitis

DISORDERS CAUSING UPPER AIRWAY OBSTRUCTION: AnatomicNasal - Septal deviation Nasal polyposis Nasal massesNasopharyngeal Choanal stenosis or atresia Adenoid hypertrophy

OropharyngealTonsillar hypertrophyMacroglossiaRetrognathiaMicrognathiaCraniofacial SyndromesApertCrouzonDownTreacher CollinsNeuromuscularCerebral palsyVocal cord paralysis Miscellaneous Allergic rhinitis,ObesityCongenital myxedema ,Storage disease

TREATMENT OPTIONS FOR UPPER AIRWAY OBSTRUCTIONMedications (steroid,acetazolamide,protriptyline)Intervention : bypass of obstructionNasopharyngeal airwayTracheotomySurgery : removal of obstructionAdenoidectomy,TonsillectomyAdenotonsillectomyUvulopalatopharyngoplastySeptoplasty Nasal polypectomyTongue reductionSurgery : positional manipulation of airwayHyoidplasty Orthognathic surgeryCraniofacial surgery

Sinusitis

Sinusitis is defined as an inflammation of the epithelial lining of the paranasal sinuses. The inflammation of these tissues causes mucosal edema and an increase in mucosal secretions.The most common trigger is an acute upper respiratory infection although other causes (such as exacerbations of allergic rhinitis, dental infections or manipulations, and direct trauma) can be implicated

Chronic sinus infections are often accompanied by mouth breathing. This condition is associated with oral dryness and (in longtime sufferers) increased susceptibility to oral conditions such as gingivitis.

Pharyngitis and Tonsillitis

Inflammation of the tonsils and pharynx is almost always associated with infection, either viral or bacterial.More than 90% of cases of sore throat are related to viral infections.

The major viral etiologies are Epstein-Barr virus, coxsackievirus A, adenovirus, Rhinovirus, and measles virus.The most common bacterial cause of acute tonsillopharyngitis is group A beta-hemolytic Streptococcus (GABHS) infection,specifically Streptococcus pyogenes infection.

ORAL HEALTH CONSIDERATIONS

The association between GABHS infection and the development of severe complications, such as rheumatic fever and its associated heart condition, is well known.

One study found a significant association between the persistence of GABHS on toothbrushes and removable orthodontic appliances and the recovery of GABHS in the oropharynx of symptomatic patients after 10 days of treatment with penicillin. Interestingly, when toothbrushes were rinsed with sterile water, organisms could not be cultured beyond 3 days whereas nonrinsed toothbrushes harbored GABHS for up to 15 days. Thus, patients with GABHS infections should be instructed to thoroughly clean their toothbrushes and removable acrylic appliances daily. It is also advisable to change to a new toothbrush after the acute stage of any oropharyngeal infections.

ADENOID HYPERTROPHY

Nasal obstruction can be due to the hypertrophy of adenoid tissues. This obstruction affects the breathing pattern and could result in mouth breathing. Linder-Aronson, Ricketts, and Subtelny have termed the appearance of craniofacial structures affected by nasal obstruction as respiratory obstruction syndrome, long face syndrome or vertical maxillary excess. The evident characteristics of this structure are narrow nostrils, together with a flat nose, maxillary constriction, posterior rotation of the mandible, and excessive vertical dimension of the lower face. These investigators claim that there is some recovery in these structures following the elimination of the nasal obstruction.WJO-2002

LONG FACE SYNDROME

In 1872, C.V. Tomes coined the term Adenoid Facies or Long Face Syndrome to describe the dentofacial changes associated with chronic nasal airway obstruction. In reality, any condition that causes nasal obstruction like deviated nasal septum, hypertrophic turbinates or external nasal deformity, could lead to this typical facial morphology.

This syndrome is characterized by an increased LAFH,increased dentoalveolar height,gummy smile,high arched palate ,steep mandibular plane,excess incisal show,anterior marginal gingivitis and long-standing nasal obstruction may lead to "disuse atrophy" of the lower lateral cartilages, resulting in as slit-like external nose with a narrow nasal vault.

The "long face syndrome" is often associated with crossbite, tension nose, and a Class-II (mandibular retrognathic) occlusion. Another group of children develop Class-III occlusion (mandibular prognathic) occlusion which may be due to anterior displacement of the tongue due to tonsillar hypertrophy. This creates a pressure affects on the lingual aspect of the lower dental arch, causing a prognathic mandible and undererupted lower teeth. Children who have hypertrophied adenoids, tonsils and inferior turbinates develop long face syndrome 30 percent of the time. In contrast, children with normal respiratory airways develop long face syndrome 2 percent of the time

TONSILLECTOMY AND ADENOIDECTOMY

Over 75% of tonsil/adenoid operations are performed on children less than 15 years of age, and 60% on children under 6 years of age. The model age of children undergoing of this type of surgery is five years.

INDICATIONS FOR SURGERY Tonsillectomy and adenoidectomy, either in combination or separately, are most frequently performed to correct Recurrent or chronic throat infectionHypertrophyRecurrent attacks of otitis media or chronic otitis media with effusion.Hypertrophy of the tonsils and adenoids is more common in boys under 6yrs of age than in girls, but hypertrophy of the tonsils is twice as common in adult females as in adult males.

TONSILLECTOMY INDICATIONSRecurrent tonsillitis defined by a history of atleast 7 episodes in the preceding year, or 5 episodes in each of the last 2 years, or 3 episodes in each of the last 3 years.Chronic tonsillitis persisting for atleast 6 months despite intensive antibiotic therapy.

ADENOIDECTOMYPersistent obstruction due to enlarged adenoidsRecurrent otitis medial with effusionAdenoidectomy with or without tonsillectomy is by far the most common treatment for nasal obstruction in children.

RAPID MAXILLARY EXPANSION

Brown, a rhinologist, was a vigorous supporter of midpalatal suture opening for the purpose of overcoming nasal stenosis. Although Brown indicated that RME ''provided relief of hypertrophied conditions of the nasal mucous membranes, thus increasing nasal permeability," he did not indicate the etiology of nasal mucous membrane hypertrophy. Rapid maxillary expansion (RME) broadens the maxillary arch which also serves to widen the nasal vault and improve nasal patency.

Maxillary expansion pattern

RME and nasal airflow. Anatomically, there is an increase in the width of the nasal cavity immediately following expansion, particularly at the floor of the nose adjacent to the midpalatal suture. As the maxillae separate, the outer walls of the nasal cavity move laterally. The total effect is an increase in the intranasal capacity. The nasal cavity width gain averages 1.9 mm, but can widen as much as 8 to 10 mm at the level of the inferior turbinates, while the more superior areas might move medially. AJO 1987 Bishara and Staley

ASTHMA

Chronic inflammatory disorder of the airways Inflammation associated with Airways hyperresponsivenessAirflow limitation (at least partially reversible)Respiratory symptoms (wheeze, cough, tight chest) Airway inflammation can be present even in mild disease

ASTHMATIC AIRWAY OBSTRUCTIONNORMAL ASTHMA

PATHOLOGYEARLY RESPONSES rapid release of preformed inflammatory mediators by mast cells,synthesis of Eicosanoids,Bronchoconstriction.LATE RESPONSES second round of bronchoconstriction Acute attack can be fatal,acute asphyxiation,marked constriction and occlusion of the bronchi.

INTRINSIC ASTHMA

Non atopic,originally thought to be non-IgE mediated,may be due to local production of IgE with in airways. Trigger unknown but may develop from seasonal allergy,may be due to imbalance of physiological control of smooth muscle tone

FACTORS PREDISPOSING TO DEVELOPMENT OF EXTRINSIC ASTHMA

1. Heredity 2. PRENATAL EFFECTS - high cord blood IgE levels, prenatal exposure to allergens 3. HIGH POSTNATAL IgE serum level 4. EARLY DIET - early exposure to eggs, wheat, bovine products 5.LOW SERUM IgA LEVELS at 3 months of age 6. LOW LEVELS OF T LYMPHOCYTES at 3 months of age 7 EXPOSURE TO animals,molds,tobacco

PATHOPHYSIOLOGY OF ASTHMA

ORAL HEALTH CONSIDERATIONS

1. Fluoride supplements should be instituted for all asthmatic, particular those taking 2-agonists. 2. The patient should be instructed to rinse his or her mouth with water after using inhalers. 3. Oral hygiene should be reinforced to reduce the incidence of gingivitis , periodontitis. 4. Antifungal medications should be administered as needed, particularly in patients who are taking inhaled corticosteroids.

ORTHODONTIC CONSIDERATIONS

External apical root resorption is an undesirable sequela of orthodontic treatment resulting in loss of tooth structure from the root apex. It has been proposed that factors, such as the inflammatory mediators produced in asthma, may enter the periodontal ligament and act synergistically to enhance root resorption. Eosinophils are bone-marrow-derived granulocytes that are involved in both allergic and nonallergic inflammation.Eosinophils release preformed cytotoxic granule proteins and produce superoxide and cytokines. Each of these functional capabilities is linked to the production of tissue damage and physiologic derangements that are characteristic of human diseases associated with eosinophil-dominated inflammation, such as asthma

Using a cellular biology approach, Davidovitch et al questioned whether mediators generated outside of the PDL influenced cellular interactions involved in root resorption, by attracting and/or activating cementoclast (osteoclast) progenitors. Conditions that were implicated in contributing to the production of such mediators were gingivitis, asthma, and alcoholism.. In the aged population, resorption of the mandibular canal wall is more prevalent in subjects with asthma, and these patients are in the high-risk group for severe resorption of the residual mandibular ridge after tooth loss.

Davidovitch et al induced allergic asthma in guinea pigs and applied an orthodontic force against the maxillary molars. Although root resorption was not observed on these cementum-free and continuously erupting teeth, the number of alveolar bone osteoclasts in areas of compressed PDL increased over the controls, suggesting that chemical mediators produced in the asthmatic state may influence cell populations and subsequently the resorption process .

The increased incidence of EARR for the upper first molars in asthmatics may result from local sinus inflammation, which itself is the result of a systemic inflammatory condition.

Asthmatic children are reported to have a higher incidence of dental decay and a poorer periodontal status; the degree of periodontal inflammation is said to be higher in adult asthmatics compared with nonasthmatics AJO1999 Avoid dental materials that may precipitate an attack. Acrylic appliances should be cured prior to insertion. Dental materials without methyl methacrylate should be considered.

Schedule these patients appointments for late morning or later in the day, to minimize the risk of an asthmatic attack.

There are no contraindications to the use of local anesthetics containing epinephrine, but preservatives such as sodium metabisulfite may contribute to asthma exacerbation in susceptible patients

Care should be used in the positioning of suction tips as they may elicit a cough reflex.

Up to 10% of adult asthmatic patients have an allergy to aspirin and other nonsteroidal anti-inflammatory Agents A careful history concerning the use of these type of drugs need to be elicited. Although the use of acetaminophen has been proposed as an alternative to the use of aspirin, recent data suggest caution because these type of drugs have also been associated with more severe asthma.

Guidelines for emergency

During an acute asthmatic attack, discontinue the dentalprocedure, remove all intraoral devices, place the patient in a comfortable position, make is opened, and administer a 2-agonist and oxygen. If no improvement is noted, administer epinephrine (1:1,000 concentration, 0.01 mg/kg body weight, up to a maximum of 0.3 mg) and alert emergency medical assistance.

ALLERGY AND HYPERSENSITIVITY

TYPE I ALLERGIC RESPONSES immediate hyper sensitivity, mediated by IgE and causes the release of hisatamine,leukotrines and prostaglandins from mast cells and basophils

IgE binds to mast cells Antigen cross bridging Histamine releease(Mast cell degranulation)

MEDIATORS OF ALLERGY

IgE antibody produced by B cells,sensitizes mast cells for mediator release,usually in very low amounts in serumHISTAMINE - secreted by Mast cells,causes vasodilation,increase vascular permeability of venules.H1 receptors responsible most allergic responsesPLATELET ACTIVATING FACTOR - secreted by basophils,neutrophils,monocytes,macrophages.constricts bronchial airways PROSTAGLANDINS derived from arachidonic acid PGD2 consticts bronchial airways PGE2 causes vasodilation,potentiates effects of histamine and leukotrines.LEUKOTRIENES derived from arachidonic acid ,induce bronchoconstriction,slow reacting substances of anaphylaxis. LTC4-increase vascular permability,broncho constriction

COMMON ALLERGENS IN DENTAL PRACTICE

METALS-Nickel, Cobalt, Chromium. ACRYLIC Methyl MethaAcrylate LATEX GLOVES,LATEX ELASTICS.

CLINICAL RESPONSES TO ALLERGY Adverse hyper sensitivity are manifested most often as allergic contact dermatitis of the face and neck,but mucosal and gingival reactions,as well as general dermal and systemic reactions occur in some cases. Kerosuo and Kanerva identified systemic dermatitis caused by nickel from a stainless steel appliance. Kanerva et al have shown for acrylics that type 4 allergic reaction occurs. AJO MAY2004

NICKEL AND CHROMIUM ALLERGY AJO FEB 93

The predominant systemic effects in human beings from exposure to nickel or chromium compounds are allergy, dermatitis, and asthma.

The incidence for nickel allergy was reported to be 1% in male subjects and 10% in female subjects. On the other hand, the incidence for chromium allergy is estimated at 10% in male subjects and 3% in female subjects

Most causes for nickel and chromium allergies have been attributed to dermatologic exposures to these metals or to compounds containing these metals.The manifestations of nickel allergy, dermatitis, and urticaria can be found distant from the nickel source, and is one of the reasons why nickel hypersensitivity has been of growing concern among dentists.

Bishara in AJO 1993 conducted a study to determine whether orthodontic patients accumulate measurable concentrations of nickel in their blood during their initial course of orthodontic therapy. Results showed that patients with fully banded and bonded orthodontic appliances neither had a significant nor consistent increase in nickel blood levels during the first 4 to 5 months of orthodontic therapy. Orthodontic therapy using appliances made of alloys containing nickel-titanium did not result in a significant or consistent increase in the blood levels of nickel. The results obtained indicated that orthodontic appliances used, in their "as-received" condition, corrode in the oral environment releasing both nickel and chromium, in amounts significantly below the average dietary intake.

AJO 93 The purpose of this investigation was to analyze different types of alloys used in orthodontics, and to study whether nickel and chromium will be released from these alloys when stored in physiologic saline. Face-bows, brackets, molar bands, and arch wires were analyzed. Most of the different parts in the face-bows, brackets, and molar bands were similar to conventional 18/8 stainless steel. Except the wires, most appliances included a variable amount of silver solder, the greatest in face-bows. After 14 days in 0.9% sodium chloride (NaCI), the largest amount of nickel and chromium were leached out from the face-bows and the least amount from the arch wires. Soldered stainless steel face-bows seemed to be very susceptible to corrosion. The release of nickel seemed to be related to both the composition and the method of manufacture of the appliances, but the release was not proportional to the nickel content

AJO 1996 FEB

Metallic orthodontic appliances are usually made of 18/8 stainless steel (18% chromium and 8% nickel). Some arch wires with elastic properties (shape memory alloys) can contain more than 50% nickel. Release of nickel from metallic orthodontic appliances has been observed in several in vitro studies. Nickel release in vivo in the oral cavity has been more difficult to demonstrate, although corrosion has clearly been evident in the orthodontic appliances after treatment.There has been concern about hypersensitivity reactions of nickel allergic subjects in association with metallic orthodontic appliances. Adverse responses have been reported occasionally. In general, nickel sensitive patients have not been found to be at any greater risk of developing discomfort in the oral cavity during orthodontic treatment compared with nonsensitive patients. appliances has also been a concern, although evidence is scarce

Kocadereli et al in ANGLE 2000 studied on the alterations in salivary chromium and nickel in patients during orthodontic treatment. They found that fixed appliances do not significantly affect the nickel and chromium concentrations of saliva during treatment. They concluded that minor amounts of nickel and chromium dissolved from appliances could be important in cases of hypersensitivity

Tulin et al in ANGLE 2001 evaluated the concentration of nickel and chromium ions in salivary and serum samples from pts treated with fixed appliances. They found that fixed orthodontic appliances release measurable amount of nickel and Cr when placed in the mouth, but this increase doesnt reach toxic levels for nickel and chromium in saliva and are similar to values found in healthy individuals

AJO JULY 2004

Menezes n Campos et al, studied the incidence of hypersensitivity to orthodontic metals,patch tests were carried out before and 2 months after the placement of orthodontic appliance in 38 pt,tested metals are cobalt, copper,chromium,iron,manganese,molybdenum, Ni,Ti.

8 strips containing the test substances were positioned on the patients back.they were removed after 48 hrs and assessed by dermatologist.significant positive reactions were observed for nickel sulfate,potassium dichromate,manganese chloride. No differences were observed between the reactions before and after placement of the ortho appliance.this indicates that they didnt sensitize the patient.

Staerklaer and Menne reported no allergic reactions of the adjacent oral mucosa from orthodontic appliances in Nickel sensitive patients.Bass et al conculed that the Nickel containing appliances had no allergic effects on the oral tissues, although the applainces may play a role in inducing Nickel sensitivity.Despite the research evidence to suggest otherwise, there have several case reports of localized allergic responses credited to nickel-containing orthodontic applainces. Jacobsen and Hensten Patterson reported Nickel allergic reactions in two categories Dermal Reactions Redness, Irritation, Itching eczema, soreness, fissuring and desquamation attributed to headgear facebow. Intraoral Reactions Redness,swelling,soreness of the lips and oral mucosa and inflammation of the gingival

Nickel allergy alternatives Kim et al in ANGLE 1999 found that titanium wires were the most inert and can be used intraorally in a corrosive environment. It contains no nickel and is an excellent alternative for orthodontic patients with nickel allergy. If nickel titanium wires have to be used, then epoxy coating of the wire is recommended. This would reduce the corrosive potential and the subsequent release of nickel. If the epoxy coatings can be maintained during orthodontic procedures, corrosion of the wire and the subsequent release of metal ions into the oral environment are minimized. According to Hamula et al in JCO 1996, the problems of nickel sensitivity, corrosion, and inadequate retention of SS brackets has been solved with the introduction of new, pure titanium bracket (Rematitan). Its one-piece construction requires no brazing layer, and thus it is solder- and nickel-free. A computer-aided laser (CAL) cutting process generates micro- and macro-undercuts, making it possible to design an ideal adhesive pattern for each tooth.

Sernetz et al in 1997 evaluated the qualities and advantages of titanium brackets. The biocompatibility of these brackets is maintained by preserving the integrated base made of a single piece of pure titanium. Lesser stiffness of titanium compared to stainless steel allows torque to be fully expressed without deforming the bracket wings. Latex Based Allergic ReactionsSourceLatex based glovesLatex elasticsTwo types of Allergic reaction may occurType I Hyper sensitivity immediate Antibody - mediated allergic response to multiple protein on the latex product. Delayed Type reactions Type IV hyper sensitivity is usually an allaergic reaction to one or more of the compounding chemicals added to liquid natural rubber latex during the manufacturing process.The typical response is the development of a circumoral erythema,which usually represents a type IV reation

Clinical FeaturesDiffuse or patchy eczema on the contact area.ItchingRednessVesicle formationDry skin and fissures Studies relate the allergic reactions to the use of latex gloves and the development of stomatitis with acute swellings and erythematous buccal lesions to the use of orthodontic elastics. . Reactions to latex carry with them a wide range of risk, including dermatologic reactions, respiratory reactions, and systemic reactionsin the extreme, anaphylactic shock. Mucosal or parenteral contactas with the use of orthodontic elasticsis more likely to induce a rapid systemic reaction such as anaphylactic shock.

Among health care workers, the risk of becoming sensitive to latex protein is increased by prolonged and repeated exposure to the allergen.Inital signs of allergic reaction is erythema on the back of the hands and between the fingers.

Reasons for Latex Allergy

During the processing of untreated natural latex,ammonia and other chemicals such as thiurams, carbamates and mercaptobenzothiazoles are added as accelerators or antioxidants during the manufacture of latex-based products.These compounds are thought to function as possible allergens in the final product.

Alternative method: Russell et al in AJO 2001 suggested that as the incidence of latex allergic reactions increases, the use of non-latex products is increasing within the orthodontic specialty. The use of non-latex orthodontic elastics is required in patients with known latex sensitivities Natural latex gloves should be substituted with alternative one made of other components such as nitrile,neoprene,vinyl,polyurethane, and styrene based rubbers or blends of these synthetic materials.In addition,the use of powder-free gloves will diminish the amount of aerosolized allergens.

Management of Latex Allergy Administration of pre treatment antihistamines. In severe type I reaction administration of epinephrine.

AUTO IMMUNE DISEASE JUVENILE RHEUMATOID ARTHIRITIS JRA is an auto immune disease and systemic joint disease marked by inflammation,degeneration,or metabolic derangement of connective tissue.its etiology is unknown and the onset occurs in children and adolescents less than 16 yrs of age. ClassificationPauciathiritis/Oligoarthiritis when 4 or less joints are involvedPolyarthiritis-5 or more joint is involved

Large joints knee,wrist,ankle are involved,in the craniofacial complex TM joint is involved.Treatment includes suppressing the articular inflammation and pain,preserving the joint mobility,preventing deformationInitial diagnostic criteria for JRA are persistent morning stiffness, pain and limitation on motion, tenderness, joint warmth, swelling, and effusion in one or more joints for at least 6 to 12 weeks.

Cepalometric findings in JRA patients BJO MAR 2001

Retrognathic mandibleIncreased mandibular posterior rotationIncreased vertical growth in anterior part of face.Aberrant facial morphology has been associated with condylar destruction. Walton et al suggested that the restricted growth of the mandible resulting in severe class II discrepancy occurs in 10 to 30 % of subjects with JRA.Classic signs of rheumatoid destruction of TMJ include condylar flattening and large joint space.

Anterior open bite is a JRA consequence, usually treated by selective prosthetic rehabilitation. Sometimes, a stabilization splint is indicated to prevent activity during sleep and physical therapy. Such treatment provides temporomandibular joint (TMJ) stability and more comfortable mandibular dynamics during the day.

Functional orthopedics is an excellent option for relieving pain and stiffness and enhancing morphofunctional considerations in properly chosen patients. It is a proper early treatment alternative for reducing open bite, eliminating compensatory tongue and perioral habits, improving chewing performance, and achieving a satisfactory esthetic appearance. Functional appliances, particularly the bioelastic type, can be an indispensable tool in the therapeutic armamentaria.After functional orthopedic treatment, geneoplasty may satisfy a patient's esthetic demands without the need for orthognathic surgical mandibular advancement. WJO2001

Orthodontic Considerations EJO 2001If the wrist joints are affected these patients can have difficulty with tooth brushing. Use of electric toothbrush should be considered.

Some authors have suggested that orthodontics procedure that places stress on the TMJs,such are functional appliances and heavy class II elastics, should be avoided if there is rheumatoid involvement of the TMJs (Proffit,1991).Instead, consideration should be given to using headgear to treat children with rheumatoid arthritis who have moderate mandibular deficiency. However, others feel that functional appliance may unload the affected condyle and act as a joint-protector (kjellberg et all., 1995).

It has been suggested that in cases of severe mandibular deficiency mandibular surgery should be avoided, and be more conservative approach using maxillary surgery and genioplasty should be considered (van Venrooy and Proffit, 1985).

EPILEPSYA seizure is a sudden, involuntary, time-limited alteration in neurologic function resulting from abnormal electrical discharge of cerebral neurons.Epilepsies are a group of disorders of the CNS, charcterised by paroxysmal cerebral dysrhythmia, manifesting as brief episodes (seizures) of loss or disturbance of consciousness, with or without characteristic body movements (convulsions). ETIOLOGY:Primary Epilepsy Idiopathic Secondary Epilepsy

In child : Congential abnormalities ,Birth-related Complication,Trauma Meningitis Encephalitis Malignancy

In Adult : Brain Tumors Cerebral Vascualr disease Head Trauma

EPILEPSYPartial SeizuresSimple Partial SeizuresComplex Partial SeizureSimple Partial / Complex Partial Seizures4. Secondarily generalised

Generalised SeizuresGeneralised Tonic clonic SeizuresAbscence SeizuresAtonic SeizuresMyoclonic Siezures

TRIGGERING FACTORS Flashing lightsanxiety/stressillnesshyperventilationmissed medication/non prescribtion medicationsalcholvitamin/mineral deficiency MEDICAL AND SURGICAL MANAGEMT Anti epileptic drugs (AED)Surgical procedure-remove/ disconnect epileptogenic areas of the brain include focal excision,resection of a brain lobe,multiple subpial transactions,stearotactic ablations with gamma knife radio surgeryImplanted nerve stimulation device- vagus nerve stimulator (VNS)

ANTI EPILEPTIC DRUGS Barbiturates, Phenytoin, Carbamazepine, Ethosuximide, Sodium valproate, Benzodiazepines, Gabapentin, Vigabatrinan.SIDE EFFECTS AND AED RELATED ORAL FINDINGSGingival hyperplasiaRecurrent apthous like ulcerationsGingival bleedingHypercementosisRoot shorteningDelayed eruptionDento facial trauma occurring during seizures has been reported to include injuries to the tongue, buccal mucosa,facial fractures, avulsion, luxation,or fractures of teeth, and subluxation of the tempero mandibular joint.

ORTHODONTIC TREATMENT PLANNINGAdverse side effects of AEDs and past dental trauma should be consideredMechanical challenges such as closing inter dental spaces in the presence of gingival hypertrophy should be considered.Metal in fixed appliance may distort images obtained by MRI.so arch wires and removable components should be removed before the scan,some others will require the removal of the entire orthodontic appliance.

MANAGEMENT OF SEIZURES Do not try to restrain the patient, if possible help the patient to lie down on his/her side Remove all dangerous objects from the area Note the seizure time,if seizure lasts more than 5 min,if the seizure is accompanied by apnea or other cardiopulmonary symptoms they require further medical care.

GINGIVALHYPERPLASIA AND ORTHODONTIC TREATMENT

Classification of gingival enlargement Inflammatory enlargement Fibrotic enlargementCombined enlargementEnlargement associated with systemic conditions/disease Drug induced gingival hyperplasia Anti epileptic drugs Phenytoin, Sodium valproate,Ethosuximide Immuno suppressants Cyclosporine Calcium channel blockers Nifedipine

Gingival overgrowth occurs in about 50 per cent of persons taking phenytoin. The hyperplasia involves the gingival margin with extension to the inter-dental papilla.The lesion may involve the inter-proximal spaces, and become so extensive that the teeth are displaced and their crowns covered. Gingival overgrowth related with a syndrome Rutherfurd Syndrome, Cross Syndrome, Ramon Syndrome, Laband Syndrome BJO MAR 2003

Melsen et al. (1976) studied the effect of phenytoin on bone biopsies from the iliac crest in adult epileptic patients. They found an increase in parameters expressing new bone formation such as an increase in osteoid bone relative to trabecular bone and an increase in bone formation surfaces. They suggested that such changes within the alveolar bone, possibly in addition to a hindrance caused by hyperplastic gingiva could prolong orthodontic tooth movement.

Lau et al. (1994), phenytoin was shown to stimulate proliferation, differentiation and mature osteoblastic activity in normal human bone cells and to increase in vivo serum osteocalcin levels in epileptic patients.

Dahllf et al. (1993) compared the periodontal condition in adult epileptic patients on long-term therapy with phenytoin to patients receiving other anticonvulsants and observed that patients medicating phenytoin did not exhibit increased marginal bone loss, despite an increase in gingival pocket depth, compared to patients medicating other anticonvulsants. BJO AUG 1997

The influence of the anticonvulsive drug phenytoin on the periodontal tissues during orthodontic tooth movement in the rat was studied. The experimental and the control group each consisted of 10 SpragueDawley rats. The test group was injected daily with phenytoin during the experimental period of 6 weeks. A fixed appliance for expansion was applied on the first molars in both groups after 2 weeks (day 15). At the end of the experiment (day 42), radiographic measurements revealed less tooth movement in the phenytoin-treated rats. Compared to the control group, significant histologic changes in the periodontal tissues such as increased density of fibroblasts, decreased number of osteoclasts in contact with alveolar bone wall of the pressure side and deeper layer of non-mineralized osteoid on the tension side were observed in the phenytoin group. BJO AUG 1997

Half of patients medicating phenytoin develop gingival hyperplasia implying increased pocket depth (Angelopoulos and Goaz, 1972). It has been suggested that phenytoin may contribute to periodontal disease (Lundstrm et al., 1982). If this was true, then in combination with other factors that need to be considered in adult orthodontics such as marginal bone loss, reduced mineralization, and increased fenestratin in the lamina dura with age, it would seem reasonable to fear that the adult epileptic patient about to undergo orthodontic treatment, is going to risk increased breakdown of periodontal tissues (Williams et al., 1982)

Seymour et al. (1985), however, published contradicting results of less marginal bone loss in adult epileptic patients treated with phenytoin for 4 years compared to other anticonvulsants

BLEEDING AND CLOTTING DISORDERS CLASSIFICATION OF BLEEDINGDISORDERSVessel Wall DisordersPlatelet DisordersCoagulation DisordersFibrinolytic Disorders

Vessel wall disordersBleeding is usually mild and confined to the skin,mucosa, and gingiva.Vascular purpura can result from damage to capillary endothelium, from abnormalities in the vascular subendothelial matrix or extravascular connective tissue bed, or from abnormal vessel formation.

Scurvy, resulting from dietary deficiency of water-soluble vitamin C, Many of the hemorrhagic features of scurvy result from defects in collagen synthesis.Vitamin C is necessary for the synthesis of hydroxyproline, an essential constituent of collagen. Hemorrhage can occur in the muscles, joints, nail beds,and gingival tissues. Gingival involvement may include swelling, friability, bleeding, secondary infection, and loosening of teeth. Scurvy results when dietary vitamin C falls below 10 mg/d. Implementation of a diet rich in vitamin C and administration of 1 g/d of vitamin C supplements provides rapid resolution.

Cushings syndrome, resulting from excessive exogenous or endogenous corticosteroid intake or production, leads to general protein wasting and atrophy of supporting connective tissue around blood vessels. Patients may show skin bleeding or easy bruising.

Ehlers-Danlos syndrome is an inherited disorder of connective-tissue matrix, generally resulting in fragile skin blood vessels and easy bruising. It is characterized by hyperelasticity of the skin and hypermobile joints. Type VIII has skin findings similar to those in type I, with easy bruising following minor trauma, and is characterized by early-onset periodontal disease with loss of permanent dentition.22 Children with type VII syndrome may present with microdontia and collagen-related dentinal structural defects in primary teeth, in addition to bleeding after tooth brushing.23 Other oral findings include fragility of the oral mucosa, gingiva, and teeth, as well as hypermobility of the temporomandibular joint, and stunted teeth and pulp stones on dental radiographs.

Platelet Disorders:

Congenital

Thrombocytopenic quantitative platelet deficiencyWiskott-Aldrich syndromeNeonatal alloimmune thrombocytopenia

Nonthrombocytopenic qualitative or functional platelet defectGlanzmanns thrombastheniaPlatelet-type von Willebrands diseaseBernard-Soulier syndrome

Acquired Thrombocytopenic quantitative platelet deficiency

Autoimmune or idiopathic thrombocytopenia purpuraThrombotic thrombocytopenia purpuraCytotoxic chemotherapyDrug-induced (eg, quinine, quinidine, gold salts, trimethoprim/sulfamethoxazole, rifampin)LeukemiaAplastic anemiaMyelodysplasiaSystemic lupus erythematosusAssociated with infection: HIV, mononucleosis, malariaDisseminated intravascular coagulation

Nonthrombocytopenic qualitative or functional platelet defect

Drug-induced (eg, by aspirin, NSAIDs, penicillin, cephalosporins)UremiaAlcohol dependencyLiver diseaseMyeloma, myeloproliferative disorders, macroglobulinemiaAcquired platelet-type von Willebrands disease

Normal platelet counts are 150,000 to 450,000/mm3. Spontaneous clinical hemorrhage is usually not observed with platelet counts above 10,000 to 20,000/mm3. Surgical or traumatic hemorrhage is more likely with platelet counts below 50,000/mm3.Spontaneous gingival bleeding is associated with platelet counts of 20,000 cells/mm or less.

CONGENITAL CLOTTING DISORDERSVon Willebrand diseaseIncidence c. 0.6-2% of populationHemophiliaIncidence 20/100,000 males85% Hemophilia A15% Hemophilia BMost serious bleeding disorder HEMOPHILIA Clinical Severity - Correlates with Factor LevelMild > 5% factor level Bleeding only with significant trauma or surgery; only occasional hemarthroses, with traumaModerate 15% factor level Bleeding with mild trauma; hemarthroses with trauma; occasionally spontaneous hemarthrosesSevere < 1% factor level Spontaneous hemarthroses and soft tissue bleeding

CLOTTING DISORDERS AcquiredVitamin K deficiencyLiver diseaseCoumadin therapyHeparin therapyDisseminated Intravascular Coagulation

Viral infection risk Factor concentrates are derived from human blood donations, continued use of concentrates, despite careful donor selection still carries a small risk of transimitting serious transfusion derived viral infection Hepatitis and HIV (Grundy et al 1993)

Orthodontic Consideration EJO 2001For patience with bleeding disorder, the biggest orthodontic associated risk is associated with extractions. Amircar (aminocaproic acid) and tranexamic acid are anti-fibrinolytic agents that prevent the breakdown of the clot in the extraction site, allowing for better organization and thereby decreasing the likelihood of postoperative bleeding.To minimize the risk and cost, all planned extractions at a single visit. Where possible non extraction procedure should be adapted.Chronic irritation from an orthodontic appliance may cause bleeding Care should be used in the placement and removal of orthodontics hardware to minimize the risk of mucosal injury. it has been suggested that elastomeric modules are preferential to ligature wire.The duration of an orthodontic treatment for any patient with bleeding disorder should be given careful consideration. The longer the duration of treatment the greater the potential complications. (Van Venrroy and Profitt 1985).

RENAL DISEASES ClassificationOnset Acute and chronicLocation Pre renal, renal or instrinsic, and postrenal failure.

Chronic renal failure is a slow, irreversible, and progressive process that occurs over a period of years whereas acute renal failure develops over a period of days or weeks. Acute disease isusually reversible if managed appropriately whereas chronic renalfailure is a progressive and irreversible process that leads to deathin the absence of medical intervention.

NEPHROTIC SYNDROME

Nephrotic syndrome (NS) is a condition that is often caused by any of a group of diseases that damage the kidneys filtering system, the glomeruli. Nephrotic syndrome is a condition often characterized by the following: very high levels of protein in the urine low levels of protein in the blood swelling, especially around the eyes, feet, and hands high cholesterol.

CAUSES Generally, nephrotic syndrome results from damage to the kidneys' glomeruli - the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine. However, in some cases, the cause remains unknown.

Nephrotic syndrome may occur with many diseases, including the kidney diseases caused by type 2 diabetes. Prevention of nephrotic syndrome relies on controlling these diseases

Less than 1yr old - Congenital nephrosis

Less than 15 years old -Min change FSGS

Calcium and Skeletal Disorders (Renal Osteodystrophy)

Renal osteodystrophy refers to the skeletal changes that result from chronic renal disease and that are caused by disorders in calcium and phosphorus metabolism, abnormal vitamin D metabolism, and increased parathyroid activity. In early renal failure, intestinal absorption of calcium is reduced because the kidneys are unable to convert vitamin D into its active form. Upon exposure to sunlight, 7-dehydroxycholesterol in the skin is converted to cholecalciferol (vitamin D3) and is subsequently metabolized in the liver to a more biologically active form, 25-hydroxycholecalciferol (25-HCC). Further conversion to either 1,25-dihydroxycholecalciferol (1,25- DHCC) or 21,25- dihydroxycholecalciferol (21,25-DHCC) then occurs in the kidney parenchyma. When the serum calcium level is high, 25-HCC is metabolized to 21,25-DHCC; conversely, a hypocalcemic state initiates the conversion of 25-HCC to 1,25-DHCC.

This hypocalcemia is associated with a compensatory hyperactivity of the parathyroid glands (parathyroid hormone production) that increases the urinary excretion of phosphates,decreases urinary calcium excretion, and augments the release of calcium from bone. Oral manifestationsEnlarged (asymptomatic) salivary glands,Decreased salivary flow,Odor of urea on breath Metallic taste,Increased calculus formation,Enamel hypoplasia,Dark brown stains on crownsExtrinsic (secondary to liquid ferrous sulfate therapy)Intrinsic (secondary to tetracycline staining)Pale mucosa with diminished color demarcation between attached gingiva and alveolar mucosa Petechiae and ecchymosis, Bleeding from gingiva Prolonged bleedingCandidal infections Burning and tenderness of mucosaErosive glossitis,Tooth erosion (secondary to regurgitation associated with dialysis)

Radiographic manifestations

Demineralization of bone,Loss of bony trabeculation,Ground-glass appearance

Loss of lamina dura,Giant cell lesions, brown tumors,Socket sclerosis

Pulpal narrowing and calcification,Tooth mobility

ORTHODONTIC CONSIDERATION

Prior to commencing orthodontic treatment all renal transplant patients should be examined to assess the extent of drug induced gingival overgrowth.Orthodontic treatment should not commence until the oral hygiene is very good and the use of 0.2 per cent chlorhexidine mouthwash is advisable.If gingival overgrowth is present orthodontic treatment should be delayed until the excessive gingival tissue has been surgically removed.As far as possible, the treatment time with fixed appliances should be kept to a minimum duration.

ENDOCRINE DISORDERSDENTOFACIAL INFLUENCE OF ENDOCRINES depends on stage of development of the teeth.tooth size is not altered as a rule by the endocrine disturbances.Fetal stage + Early post natal Bone&Tooth development under the action of thyroid After 3-4 years - pituitary regulates growthCalcification depends on ParathyroidsEruption of teeth influenced by thyroid.Hypopituitary Dwarfism marked dwarfing,but no physical disproportion. Epiphyseal closure is retarted.Dental considerations - Tooth eruption is retarded - Pulpal walls are wide and parallel and apical closure is delayed

AcromegalyAdenoma of the pituitary gland starts in the adult.Great increase in the length of the ramus of the mandible as a result of the type of ossification of the condyle.Over eruption of the teeth followed by an apposition of bone at the alveolar crest which increases height of mandibular bodyTongue enlargement, spacing in mandibular dentition, hypercementosis.

Hypo thyroidismCongenital retardation in the normal rate of deposition of calcium in the bones., delay in development of toothbuds in the fetusChildhood- delay in ossification of the toth buds is more significant in these casea than retarded eruption

Charactersitic feature Retardation in the normal rate of deposition of calcium in the bones and in tooth buds,disharmonies in the eruption of the teeth, prolonged retention of deciduous teeth, it may be found coexistent with permanent teeth as lateas the 3 rd decade of life., permanent teeth are slow to erupt,abnormal dental calcification and root resorption Becks and cowden stated that hypothyroidism associated with root resorption even in the absence of orthodontic load.Hyperthyrodism Increase rate of maturation, increase in metabolic rate, exopthalmic goiter.Characteristic feature Pre mature eruption, disturbed resorption of the roots of the deciduous teeth, association early eruption of teeth, bones are fragile, increased salivation, teeth may show a bluish white coloring Melsen thyroid hormones, in excess conditions, increase bone turn over have found to be reduce root resorption

Hypoparathyroidism Delay in tooth eruption, affect the morphology of teeth, teeth have a white appearance, but later turn brown through staining. They are brittle, pitted, show opaque areas, fractured easily because of poor calcification Hyperparathyrodism Increase in blood calcium which is with drawn from bone.demineralisation of bone, diaphysis of bone involved, early distortion of trabecular pattern, demineralization and disappearance of laminadura.formation of osteodentin.Teeth may become loose as a result of loss of cortical bone resorption of the alveolar process in parathyroid tumour patients.Goldie and king- in secondary hyper parathyroidism, there is an increased bone resorption with decreased root resorption.

Adrenals Adrenogenital syndrome-teeth show acceleration of development and eruption.tumours of the adrenals at the time of tooth development may produce premature eruption of permanent teeth. Adrenal insufficiency -Most commonly seen in persons who have received steroid theraphy, patients with a history of addisons disease,adrenal suppression occurs as a result adrenocortical atrophy. Management The clinical manifestation of adrenal insufficiency usually occurs when a patient on gluococorticoids is being withdrawn from glucocorticoid therapy or when a patient with a previous history of glucocorticoid therapy is challenged by a stressful event. Stress may occur in the form of an invasive surgical procedure, the onset of infection, an exacerbation of an underlying disease, or a serious life event. During stress in normal individuals, plasma cortisol levels may double, suggesting an inherent ability of the adrenal glands to increase cortisol production by 100%.

In the patient with adrenal insufficiency, adrenal function is inadequate to produce adequate cortisol in the face of stress, and the patient may experience severe hypotension, nausea, cardiovascular events, stroke, coma, and death.

The premedication of the patient with 100 mg of hydrocortisone acetate intramuscularly 30 minutes before an invasive procedure. Patients with a history of adrenal insufficiency are often aware of the risk of stress and may self-medicate and increase or double their chronic dose of oral glucocorticoids before a procedure.

To summarize,

ROOT RESORPTION

Hypothyrodism Hypoparathyroidism HyperpituitarismDELAYED ERUPTION

Hypothyroidism Hypopituitarism Thymic hyper trophy Adrenal insufficiency

ORTHODONTIC TREATMENT FOR DISABLED CHILDRENSpecial needs individuals are children or adults who are prevented by a physical or mental condition from full participation in the normal range of activities of their age groups. Gullikson (1969) reported that malocclusion occurs more frequently in children with physical or mental disability than in healthy children.Commonly encountered problems General behaviour is often problematic because of reduced understanding and increased apphrehension, short attention span, and limited tolerance.Uncontrolled limb and head movementsLevel of cooperation during treatment is significantly impairedExaggerated gag reflexIncreased salivation

AUTISM Autism is a distinct brain damage disorder that produces a characteristic range of behavioural abnormalities.

symptoms Disturbances in the rate of appearance of physical, social and language skills. Abnormal responses to sensations. Any one or a combination of senses or responses are affected: sight, hearing, touch, pain, balance, smell, taste, and the way a child holds his body. Speech and language are absent or delayed while specific thinking capabilities might be present. Abnormal ways of relating to people, objects and events.

EtiologyMERCURY poisoning in a genetically predisposed child Autism can occur or be closely simulated in children with known organic brain damage

CLASSIC AUTISM (INFANTILE ONSET) Measles virus vaccine-induced (classic infantile autism, age of onset 12-15 monthsRubella virus vaccine-induced (often within 4 days of birth, due to maternal immunization while in hospital)OTHER TYPES OF AUTISMPERVASIVE DEVELOPMENTAL DISORDER (PDD) due to (a) Clostridia toxins (b) Salmonella toxins (c) AspergillosisDELAYED DEVELOPMENTAL DISORDER (DDD) Usually due to effects of one or more toxic heavy metals on brain and thyroidATTENTION DEFICIT DISORDER (ADD) LANDAU-KLEFFNER SYNDROME (AUTISM-EPILEPSY SYNDROME)ASPERGER'S SYNDROME

Downs syndrome Down syndrome is a frequent form of mental retardation associated with characteristic morphologic features (mongolism) and many somatic abnormalities due to a number of chromosomal aberrations CLINICAL FEATURESMental retardation - Mild to severe, intelligence quotient (IQ) of 25-50, constant featureCharacteristic head appearance - Small head (brachycephaly), flat facies with increased interocular distance (hypertelorism), depressed nasal bridge, flat occiput, and broad short neckOcular anomalies - Narrow and upward and outward slating of the rima palpebrarum (80%), white Brushfield spots arranged in concentric rings on the periphery of the iris (60%), medial epicanthal folds, keratoconus, strabismus, cataracta (2%), and retinal detachmentOral features - Small mouth (relatively) with protrusion of the tongue (macroglossia) and,, hypoplasia of the maxilla, delayed tooth eruption, hypodontia, juvenile periodontitis, and cleft lip or palate (rare)

Skeletal anomalies - Short stature (below normal height); broad, short hands, feet, and digits; short curved fifth finger (dysplasia of the mid phalanx), clinodactyly of the fifth finger; dysplasia of the pelvis (shallow acetabular angle with small iliac wings); joint laxity; a wide gap between the first and second toes; and atlantooccipital instabilityMuscle hypotonia in newborns with decreased response to normal stimuliCutaneous manifestations Soft and velvety skin in early childhood Dry skin in late childhood - Xerosis (70%), atopic dermatitis (50%), palmoplantar hyperkeratosis (40-75%), and seborrheic dermatitis (31%) Premature wrinkling of the skin, cutis marmorata, and acrocyanosis Bacteria infections, fungal infections (tinea), and ectoparasitism (scabies)

Causes: A free trisomy 21 results from nondisjunction during meiosis in one of the parents. This occurrence is correlated with advanced maternal and paternal age Translocation may occur de novo or be transmitted by one of the parents. Translocations are usually of the centric fusion type. They frequently involve chromosome 14 (14/21 translocation), 21 (21/21 translocation), or 22 (22/21 translocation).Mosaicism is considered a postzygotic event (following fertilization). Two cell lines are found; one with a free trisomy, and the other with a normal karyotype. This finding leads to patients with a great phenotypic variability, ranging from near normal to the classic trisomy 21 phenotype

XXX syndrome: Trisomy X Clinical features Frequently no distinguishing phenotype, especially in 1st year of life. slight neuromotor developmental delay, followed by slight delay in speech and language. Lack of co-ordination and Tall. Normal sexual development. Frequent psychiatric disturbance, Karyotype-47,XXX, but many mosaics, e.g. 45,X/47,XXXKlinefelters syndrome: 47,XXY Clinical features Infertility: abnormal seminiferous tubules; Leydig cell hyperplasia; small testes, tall (long legs, short body), gynaecomastia in adolescence (female risk of breast cancer), increased incidence of intellectual retardation,karyotype -47,XXY. mosaics: 46,XY/47,XXY

Binder syndrome AJO 1989 FEB Maxillonasal dysplasia is characterized by retrusion of the midface with aplasia or hypoplasia of the anterior nasal spine. Characteristic features Facial appearance of the patient is typical with a frontonasal angle of almost 180 degrees, a short columella, a convex upper lip, and underdevelopment of the anterior part of the maxilla. The anterior part of the hard palate is dysplastic and the maxillary dental arch is flattened. -By vestibular palpation the absence or reduction of the bony crest at the base of the nostrils can be established Radiographically the absence or hypoplasia of the anterior nasal spine and a downward inclination of the nasal bonescommon malocclusions anterior cross-bite relationship is common .proclination of the upper incisors, mandibular prognathism (pseudo-prognathism), open bite, and crowding.

McWilliam and Linder-Aronson examined 31 children between 8 and 18 years of age with maxillonasal dysplasia. They found some significant criteria for example, a short anterior cranial base, a small cranial base angle, reduced sagittal development of the nose, a straight profile, a retrognathic maxilla, a short maxilla, reduced sagittal depth of the nasopharynx, and reduced vertical growth of the maxilla.Delaire has suggested that the treatment should be performed with face mask. Orthodontic therapy should be conducted as early as possible and include, principally, an advancement of the maxilla by heavy extra-oral postero-anterior traction on an orthodontic mask.Surgical advancement of the maxilla at a later stage may thereby be avoided and surgical intervention may be limited to correction of the nose.

Treatment delivery often requires different behavior management approaches, starting from simple behaviour modification techniques through concious and deep sedation to general anesthesia.Behavior management techniques, such as Tell,Show, Do, positive and negative reinforcement. Concious sedation is a pharmacologically induced state of relaxation. It may be elicited by administration of drugs through Inhalation nitrous oxide and oxygen Transmucosally Midazolam Oral chloral hydrate, Diazepam I.v p ropofolEJO FEB 2002 Intra venous deep sedation is an alternative to GA and have found successful in many cases, most suitable agent is propofol, induction and recovery are rapid, a safe level of sedation is easily achieved, with few side effects, the risk of aspiration and other medical emergencies is less.

GuidelinesRealistic treatment goals-Jackson (1967) felt that children with learning disability should not be discounted merely because an idealorthodontic result was not possible. For these patients, the aims of orthodontic treatment may need to be modified from ideal but orthodontic treatment may offer an aesthetic improvement and hence enhanced social acceptance.Simplifying treatment- problems encountered with removable appliances are less severe than fixed appliances and adjustement of removable appliances is made extraorally and doesnot disturb the children. Hausdorff (1980) recommended that orthodontic treatment of the mentally retarded should be on a selective basis and that, to be successful, appliance therapy must be adapted to the needs of the specific patient. The use of a multiband appliance with light wires was found to be the most effective appliance and the use of removable appliances was not recommended.

Becker and shapira found excellent acceptance and rapid results with the full time wearing of removable, enbloc, integral extraoral splintfor the treatment of severe class 2 malocclusion.Adapting treatment to sedation /G.A.In cerebral palsy and muscular dystrophy patients, the cough reflex is impaired and there is an increased danger of aspiration. Chaushu and Becker have recommended the use of a rubber dam as a useful aid and an effective safe guard in bracket bonding during G.A EJO JUNE2000An oropharyngeal pack is mandatory while impression taking, band fitting, or palatal and lingual arch placement. Indirect bonding is faster, reduces sedation time, and minimizes the possibility of aspiration.

CONCLUSION

Living with some kind of medical problems has now become a part of life. The number of medically compromised patients seeking orthodontic care is increasing. Prevention is the most important aspect of risk management for these people. A proper medical history, communication with the patients physician and some modifications from the normal treatment decisions are key factor for successful orthodontic treatment in medically compromised patients