DRUGS IN ORTHODONTICS

CONTENTS

Introduction Analgesics

Fluorides

Bisphosphonates

Echistatin and RGD peptides

Hormonal drugs

Corticosteroids

Chemotherapeutic drugs

Antiepileptic drugs

Alcohol abuse

Antiasthamatic drugs

Drugs used for Temporomandibular disorders

Immunosuppressant drugs

Immunomodulatory drugs

Antibiotics

Conclusion

References

INTRODUCTION

During orthodontic treatment ,often drugs are prescribed to manage pain from force application to biological tissues , manage TMJ problems and tackle some infections throughout course of treatment. Apart from these drugs patients who consume vitamins , minerals, hormonal supplements and other compounds for the prevention or treatment of various diseases, can also found in every orthodontic practice.

Some of these drugs may have profound effects on the short and long term outcomes of orthodontic practice. Hence it is necessary to review the mechanism of action and effects of commonly used drugs on tissue remodeling and orthodontic tooth movement.

DRUG- It is the single active chemical entity present in a medicine that is used for diagnosis , prevention, treatment /cure of a disease.

According to WHO(1966) - Drug is any substance or product that is used to modify or explore physiological systems or pathological states for the benefit of the recipient.

ProstaglandinsProstaglandins(PGs) and leucotrienes released from paradental cells in sites of compression and tension have significant stimulatory effects on bone remodeling.

Yamasaki et al. found an increased number of osteoclasts in rats alveolar bone after local injection of PGE1 A similar regimen in human subjects increased significantly the rate of canine and premolar movement

PGs act by increasing no. of osteoclasts, and by promoting the formation of ruffled borders, thereby stimulating bone resorption.

PGE2 stimulated osteoblastic cell differentiation and new bone formation along with bone resorption in vitro

ANALGESICSAnalgesic is a drug that selectively relieves pain by acting on the CNS or peripheral pain mechanisms, without significantly altering consciousness.

TYPES OF ANALGESICS

1.Opiod /narcotic/morphine like analgesics2.Non-opiod /non-narcotics /NSAID’S

CLASSIFICATION OF NSAIDS

1. NON SELECTIVE COX-2 INHIBITORS

Salicylates Aspirin

Propionic acid derivatives Ibuprofen,Naproxen,Ketoprofen,Flurbiprofen.

Anthranilic acid derivatives Mephenamic acid

Aryl-acetic acid derivatives Diclofenac

Oxicam derivatives Piroxicam,Tenoxicam

Pyrrolo-pyrrole derivatives Keterolac

Indole derivative Indomethacin

Pyrazolan derivatives Phenylbutazone,Oxyfenbutazone

2.PREFERENTIAL COX-2 INHIBTORS.1.Nimesulide,2.Meloxicam,3.Nabumetone.

3.SELECTIVE COX-2 INHIBITORS1.Celicoxib,2.Roficoxib,3.Valdicoxib,4.Etoricoxib

4.ANALGESIC-ANTIPYRETIC WITH POOR ANTI-INFLAMMATORY ACTION.1.Para-aminophenol derivative – paracetamol (Acetaminophen)2.Pyrazolone derivatives-Metamizole (Dipyrone), Propiphenazone.3.Benzoxacaine derivative -Nefopam

Analgesic property

NSAID’s do not affect the tenderness induced by direct application of PG’s, but block the pain sensitizing mechanism induced by bradykinins, TNF’s,IL’s .etc. therefore they are more effective against inflammation associated pain. Antipyretic Action

NSAID’s reduce body temperature in fever,but do not cause hypothermia in normothermic individuals.NSAID’s block the pyrogenic actions of IL’s,TNF’s,IF’s which induce PG production in hypothalamus. SALICYLATES

Aspirin

Aspirin is acetylsalicylic acid, which is rapidly converted in body to salicylic acid.

Mechanism of action

The analgesic action is mainly due to obtunding of peripheral pain receptors and prevention of PG mediated sensitization of nerve endings.

Aspirin resets the hypothalamic thermostat and rapidly reduces fever by promoting heat loss by sweating,cutaneous vasodilation.

Actions -

Analgesic, antipyretic and anti-inflammatory

Irreversibly inhibits TXA2 synthesis by the platelets.Thus interfere with the platelet aggregation and prolongs Bleeding Time.

Contraindications

Pregnant women

Bleeding disorders

G-6-PD deficiency

Uses

Analgesic for head ache, toothache, orofacial pains, myalgia, joint pain,neuralgias. Dose; 0.3-0.6g,6-8hourly

Antipyretic

Osteoarthritis.(OA)

Rheumatoid arthritis(RA) Dose; 3-5g/day.

Acute rheumatic fever

Postmyocardial infraction and post-stroke patients.

Aspirin, acetaminophen, and ibuprofen: Their effects on orthodontic tooth movement

Oscar R. Arias and Maria C. Marquez-Oro Am J Orthod Dentofacial Orthop 2006;130:364-70

NSAIDS such as aspirin and ibuprofen diminish the no. of osteoclasts, probably by inhibiting the secretion of prostaglandins, thereby reducing orthodontic tooth movement.

Acetaminophen did not significantly reduce no. of resorption lacunae and osteoclasts because it acts at the central nervous system level and does not affect the peripheral secretion of PGs.(like aspirin and ibuprofen)

Acetaminophen -the analgesic of choice for treating pain associated with orthodontic treatment.

PROPIONIC ACID DERIVATIVE

Ibuprofen

Acts by inhibition of PG synthesis at the site of injury.Its anti-inflammatory actions similar to aspirin.

A/E –better tolerated than aspirin.Side effects are milde like gastric discomfort,nausea and vomiting, Headache, dizziness, blurring of vision, tinnitus and depression.

Dose- 400-600mg TDS.

Ketoprofen ;50-100mg BID, Naproxen; 250mg BID

Uses

Analgesic and anti-pyretic.

Rheumatoid arthritis, osteoarthritis.

Musculo-skeletal disorders.

Soft tissue injuries.

Extractions and fractures-to reduce post-operative swelling and inflammation.

Effects of analgesics on orthodontic pain

Shreena Patel,Susan P.McGorray et al Am J Orthod Dentofacial Orthop 2011;139:e53-e58

Ibuprofen administered 1 hour before separator placement, and 3 and 7 hours after placement, reduced post separator placement pain compared with a placebo.

Acetaminophen and naproxen sodium did not show significant differences compared with the placebo.

The analgesic effects diminished by day 2, resulting in peak pain levels and decreased chewing efficiency at this time. Additional drugs might be necessary to maintain pain relief.

Pain reduction after initial archwire placement in orthodontic patients: A randomized clinical trial

Fahimeh Farzanegan et al Am J Orthod Dentofacial Orthop 2012;141:169-73

Findings suggest that viscoelastic bite wafers can be good substitutes for NSAIDs in orthodontic pain reduction.

Chewing gum can also be recommended for orthodontic patients to reduce pain during chewing.

ANTHRANILIC ACID DERIVATIVE

Mephenamic acid (Fenamate)

It is an analgesic, Antipyretic and Anti-inflammatory drug. It inhibits COX as well as antagonises certain actions of PG’s. it has peripheral and central analgesic actions.Oral absorption is slow but almost complete

A/E : Diarrhoea, epigastric distress,rashes, rarely haemolytic anaemia.

Uses -as a analgesic in muscle, joint and soft tissue pain where strong anti-inflammatory action is not required.

Dose: 250-500mg TDS

ARYL –ACETIC ACID DERIVATIVE

Diclofenac sodium

It is an analgesic, antipyretic & anti-inflammatory drug. It inhibit PG synthesis. Because of its good tissue penetrability ,concentration in synovial fluid is maintained for longer period of therapeutic effect.

A/E - nausea, headache, rashes

Uses: Post-traumatic and post-operative conditions, tooth ache, osteoarthritis, rheumatoid arthritis

Dose :100mg BID, 50mg TID

OXICAM DERIVATIVE

Piroxicam. tenoxicam

It is long –acting NSAID with potent anti-inflammatory, good analgesic, anti-pyretic actions. It is reversible inhibitor of COX,It lowers PG concentration of synovial fluid and inhibits platelet aggregation prolongs the bleeding time. It is absorbed rapidly and completely by oral route

A/E : Heart burns,nausea,rashes.

Uses - dentistry, RA,OA,Ankylozing spondylitis,musculo-skeletal injuries.

Dose: 20mg BD for two days, followed by 20mg daily OD

Tenoxicam controls pain without altering orthodontic movement of maxillary canines

Arantes GM et al Orthod craniofacial res 2009 Feb;12(1):14-9

Tenoxicam did not influence orthodontic movement of the upper canines. It was effective for pain control and did not present any preemptive analgesic effect.

PYRROLO-PYRROLE DERIVATIVE

Ketorolac

It is NSAID with potent analgesic and anti-inflammatory activity.it is most effective in postoperative pain. It acts by inhibition of PG synthesis and relieves pain by peripheral mechanism.It is rapidly absorbed after oral and i.m. route.

A/E: Nausea, abdominal pain, ulceration,head ache dizziness.

uses - in postoperative, dental and musculoskeletal pain, pain due to bony metastasis.

Dose :10-20mg 6hourly oral route. 15-30mg i.m.

INDOLE DERIVATIVE

Indomethacin

It is a potent anti-inflammatory drug with prompt antipyretic action.It is a highly potent inhibitor of PG synthesis and suppress the neutrophil motility.it is well absorbed orally

A/E - High incidence of GIT&CNS side effects-anorexia, nausea,gastric irritation,gastric bleeding,frontal head ache,dizziness,mental confusion, hallucination, depression and psychosis, leukopenia, rashes & hypersensitivity.

Contraindications : In machinery operators, drivers, psychiatric patients, renal disease, bleeding disorders,children, pregnancy.

Dose - 25-50mg BD

Uses : Ankylosing spondylitis,psoriatic arthritis, Closure of PDA, acute gout, Malignancy associated fever

PREFERENTIAL COX-2 INHIBITORS

Nimesulide:

NSAID is a relatively weak inhibitor of PG synthesis and anti-inflammatory action may be exerted by reduced generation of superoxide by neutrophils, inhibition of PAF synthesis and TNF release, free radical scavenging. It completely absorbed from oral route

A/E: epigastric pain,heart burn, nausea, skin rashes.

Uses - short lasting painful inflammatory conditions like sinusitis, dental surgery, osteoarthritis and fever

Contraindications: In children below 4 years, known to cause hematuria, fulminant hepatic failure.

Dose: 100mg BD.

Nabumetone

It is a prodrug which generates an active metabolite(6-MNA).it is relatively more potent COX-2 than COX-1 inhibitor.it has analgesic ,antipyretic and anti-inflammatory actions.

Uses –Rheumatoid Arthritis,Osteoarthritis and soft tissue injuries.

A/E -Lower incidence of gastric erosions, bleeding because active COX inhibitor produced in tissues after absorption.

Dose: 500mg tab. OD

Villa PA, Oberti G et al reported that nabumetone reduces the amount of root resorption along with control of pain from intrusive orthodontic forces, without affecting the pace of tooth movement.

SELECTIVE COX-2 INHIBITORS

Incidence of gastric mucosal damage and peptic ulcer with selective COX-2 inhibitors lower than other NSAID’s.

They do not depress TXA2 production by the platelets(cox 1 dependent),don’t inhibit platelet aggregation or prolonged BT.

Celecoxib

It has anti-inflammatory,analgesic and antipyretic actions. It is slowly absorbed

A/E- diarrhoea, dyspepsia

Uses - osteoarthritis and rheumatoid arthritis

Dose: 100-200mg BD.

Valdecoxib

It has similar actions ,efficiency & tolerability like Celecoxib.

Dose :10mg OD in osteoarthritis and rheumatoid cases. 20mg BD in Dental or postoperative pain.

Etoricoxib

It has highest COX-2 selectivity

Uses- acute dental surgery pain, osteoarthritis and rheumatoid arthritis

Rofecoxib

It is highly selective COX2 inhibitor commonly used for, dental, post-operative osteoarthritis, rheumatoid arthritis and musculoskeletal pain.

Comparison of some effects of acetylsalicylic acid and rofecoxib during orthodontic tooth movement

Emel Sarı, Huseyin Olmez, and A. Umit Gurton Am J Orthod Dentofacial Orthop 2004;125:310-5

Rofecoxib was not found to affect PGE2 levels (increases the number of osteoclasts in the periodontal membrane) significantly during the experimental period, but aspirin inhibited PGE2 synthesis significantly more than rofecoxib

These results suggest that rofecoxib can be used during orthodontic treatment.

Orthodontic tooth movement after inhibition of cyclooxygenase-2

Felix de Carlos et al Am J Orthod Dentofacial Orthop 2006;129:402-6

No statistically significant differences were found between the effects of rofecoxib and diclofenac on OTM at 50 and 100 g forces,only diclofenac completely eliminated movement.

Accordingly, acetaminophen is still the analgesic of choice for treating the discomfort of tooth movement, because no advantages are derived from the use of the new anti-inflammatory COX-2 inhibiting drugs.

PARA-AMINO PHENOL DERIVATIVE

Phenacetin

Introduced in 1887 was extensively used as analgesic-antipyretic.It was banned because it was implicated in analgesic abuse nephropathy.

Paracetamol(Acetaminophen)

It is a de-ethylated active metabolite of phenacetin, The central action of paracetamol is by raising pain threshold with weak peripheral anti-inflammatory actions. Negligible anti inflammatory action- poor inhibitor of PG synthesis in peripheral tissues,but more active on COX in brain. It is well absorbed from oral route

A/E: Anti-pyretic doses of paracetamol is safe and well tolerated.Nausea,rashes occurs rarely, anlagesic nephropathy(long term use).

Acute paracetamol poisoning -seen in small children having low hepatic glucuronide conjugating ability. Larger dose-extensive liver damage-liver failure

Treatment of paracetamol poisoning: Induce vomiting or gastric lavage. Activated charcoal given to prevent further absorption.

Antidote; N-acetylcysteine 150mg/kg i.v. infusion over 15 min. it replenishes hepatic glutathione and prevents binding of toxic metabolite to other cellular constituents.

Large dose of paracetamol causes saturation of

glucoronidation capacity

More of minor metabolite is formed which depletes

hepatic glutathione

It starts binding to protein of liver cells causing

necrosis

Dose -500mg-1g TDS In children -1-3 years 80-160mg TDS; 4-8 years 240-320mg TDS; 9-12years 300-600mg TDS

Uses- headache, musculoskeletal pain, OA, fever

Effect of NSAID’s on tooth movement

Kyrkanides S et al in 2000-the molecular mechanisms behind the inhibition of tooth movement by NSAIDs.

The levels of matrix metalloproteinases (MMPs)-9 and -2 were found to be increased, along with elevated collagenase activity, followed by a reduction in pro-collagen synthesis, which are considered essential as far as bone and periodontal ligament remodeling is considered.

The whole process is thought to be the result of inhibition of COX activity, leading to altered vascular and extracellular matrix remodeling, causing a reduction in the pace of tooth moveme

FLUORIDES

Fluoride is a one the trace element that affect hard tissue metabolism.

Actions - Fluoride increases bone mass, mineral density and because of these skeletal actions ,it has been used in treatment of metabolic bone diseases and osteoporosis. in dentistry it is used to prevent caries

Effect of fluoride on orthodontically induced root resorption with light and heavy orthodontic forces for 4 weeks: A microcomputed tomography study

Ersan et al (Am J Orthod Dentofacial Orthop 2011;140:e199-e210)

Fluoride suppresses orthodontic root resorption under a heavy force.

Fluoride reduces the average volume of root resorption craters and decreases the number of resorption lacunae

Sodium fluoride was found to induce osteoclast-like cell apoptosis and osteoprotegerin synthesis.Even a very active caries treatment with sodium fluoride during orthodontic treatment maydelay orthodontic tooth movement and increase the time of orthodontic treatment.

BISPHOSPHONATES

Bisphosphonates(BPNs) have high affinity for calcified tissues and are potent blockers of bone resorption. They have commonly used in treatment of hypercalcemia, osteoporosis and metabolic bone diseases that causes bone resorption.it increases osteoblastic differentiations and inhibit osteoclast recruitment and activity.

Classification of bisphosphonates

1st generation; Alkyl side chain.

- Etidronate.

2nd generation-Amino-bisphosphonate

- Aledronate.

-Pamidronate.

3rd generation-Cyclic-side chains.

-Resedronate.

Mechanism of Action

BPNs have strong chemical affinity for calcium phosphate. When calcium is released from bone surface BPNs get internalized into osteoclasts and 1)Accelerate apoptosis of osteoclasts2)Disrupt cytoskeleton &ruffled border of osteoclasts

Effects BPN’s on bone and tooth movement

Studies have shown that BPN’s can inhibit orthodontic tooth movement and delay the orthodontic treatment.Topical application of BPN’s could be helpful anchoring and retaining teeth under orthodontic treatment. A significant potential side-effect of BPN’s is the development of osteo- necrosis in the mandible or maxilla, particularly related to i.v.therapy or high dose, longterm, oral usage. This adverse effect due to death of osteoclasts along with bone related capillary inhibition, decreasing microcirculation to the maxilla or mandible.

Optimizing orthodontic treatment in patients taking bisphosphonates for osteoporosis

James J. Zahrowski Am J Orthod Dentofacial Orthop 2009;135:361-74

Use of BPN -decreased tooth movement, impaired bone healing, and osteonecrosis in the mandible and the maxilla.

Tooth movement, tooth mobility, and radiographic changes of the lamina dura and the PDL spaces need to be evaluated and monitored in patients taking oral BPN.

Effects of clodronate on early alveolar bone remodeling and root resorption related to orthodontic forces: A histomorphometric analysis, Josefina Choi et al Am J Orthod Dentofacial Orthop 2010;138:548.e1-548.e8

Clodronate(1st generation BPN) might decrease root resorption related to orthodontic tooth movement, patients should be informed about the possible decrease in the amount of tooth movement and the longer period of orthodontic treatment.

Orthodontic tooth movement and root resorption in ovariectomized rats treated by systemic administration of zoledronic acid

Irin Sirisoontorn et al Am J Orthod Dentofacial Orthop 2012;141:563-73

Zoledronic acid inhibits excessive orthodontic tooth movement and also reduces the risk of severe orthodontically induced root resorption in ovariectomized rats.

Bisphosphonates as a risk factor for adverse orthodontic outcomes: A retrospective cohort study

Raj B. Lotwala et alAm J Orthod Dentofacial Orthop 2012;142:625-34

For patients having extractions, treatment times were longer for those taking bisphosphonates.

Among patients with extractions or initial spacing, there are higher odds of poor space closure and poor root parallelism at the end of treatment in those who took bisphosphonates.

ECHISTATIN AND RGD PEPTIDES

Local injection of echistatin and RGD(Arginine-glycine-aspartic acid) peptides on rats have shown to prevent tooth movement, there by enhancing anchorage.

Dolce et al. made the first attempt this aspect,reported that ELVAX-40 a non-biodegradable,non-inflammatory, sustained release polymer used to deliver integrin inhibitors like echistatin and RGD peptide agents, to reduce tooth movement at a local level.

Recent research has demonstrated decrease in root resorption following orthodontic force application after adminstration of echistatin.

HORMONAL DRUGS

Vitamin-D

Vitamin D is collective name given to anti-rachitic substances synthesized in the body and found in dietary sources ,activated by UV radiation

Uses - prophylaxis(400 IU/day) & treatment of rickets (3000-4000 IU/day) , osteoporosis and hypoparathyroidism

Actions

Vitamin D and its active metabolite, 1,25 2(OH) D3, together with Parathyroid hormone and calcitonin, regulates the amount of calcium and phosphorus levels.It promotes intestinal calcium and phosphorus absorption and promotes calcium release from the skeletal system to blood circulation. Increases bone mass and thus reduces fractures in osteoporotic patients.

Effects of vitamin-D on bone and tooth movement

Some author consider vitamin D3 to be a bone resorption-promoting agent because stimulatory effects on osteoclasts. Vitamin D receptors are present in osteoblasts and osteoclasts.

In 1976 study by Bran and colleagues, treated rats with vitamin-D showed increased bone formation on pressure side of the PDL after application of orthodontic forces.

In 1988, Collins and Sinclair demonstrated that intraligamentary injections of vitamin-D metabolite,1,25-dihydroxy cholecalciferol caused in increase in the no. of osteoclasts and amount tooth movement during canine retraction with light forces.

Stimulatory action of vitamin-D on osteoblasts can help stabilize orthodontic tooth movement.

In 2004 Kale and colleagues ,observed that the local application of vitamin D enhanced the rate of tooth movements in rats due to well balanced bone turnover induced by vitamin-D.

Kawakami M et al 2005- local application of 1,25(OH)2D3 enhances the reestablishment of supporting tissue, especially alveolar bone of teeth, after orthodontic treatment.

Medication effects on the rate of orthodontic tooth movement: A systematic literature review

Theodosia BartzelaAm J Orthod Dentofacial Orthop 2009;135:16-26

Physiologic doses of 1,25(OH)2D3 do not stimulate bone resorption; conversely, low supplemental administration does, possibly by up regulation of RANKL (receptor activator for nuclear factor B ligand) expression in osteoblasts, leading ultimately to osteoclast differentiation through the RANK/RANKL system.

ESTROGENS

Estrogens is considered to be most important hormone to affect bone metabolism in women. It controls bone remodeling during reproductive life,and maintenance of maximum bone mass after

menarche. Estrogens on bone tissue results in decrease the rate of bone resorption.It increases expression of bone matrix proteins like osteonectin, osteocalcin and alkaline phosphatase.

Estrogen inhibit the production of various cytokines, mainly interleukin-1(IL-1),(TNF-a)&(IL-6),which are involved in bone resorption.

Accelerates apoptosis of osteoclasts

Effect of estrogens on tooth movement

Yamashiro T et al 2001- the effect of ovariectomy on buccal movement of rat molars. A significant increase in the rate of OTM was established.

Haruyama N, Igarashi K et al 2002- the rate of buccal movement of molars during the normal estrous cycle in rats. It was found that the rate of OTM was inversely related to the estrogen serum level.

Arslan SG, et al 2007 -Estrogen deficiency increased orthodontic tooth movement.

Tooth movement and root resorption; The effect of ovariectomy on orthodontic force application in rats

Irin Sirisoontorna et al Angle Orthod. 2011;81:570–577

Ovariectomy affected not only tooth movement but also OIRR. Tooth movement in the ovariectomized (OVX) group was more rapid than the control group. Furthermore, the amount of OIRR in the OVX group was more severe than the control group.

THYROID HORMONES

Thyroid hormones are recommended for the treatment of hypothyroidism and used afterthyroidectomy in substitutive therapy.

Thyroxin administration leads to interleukin-1(IL-1B) production causing increased bone remodelling ,increased bone resorptive activity, and reduced bone density.

Because of the skeletal actions of thyroid hormones, it seems possible that speed of orthodontic tooth movement (OTM) can be increased in patients undergoing such medication.

Loberg EL, Engstrom C.et al 1994-The main hormone prescribed to reduce root resorption is L-thyroxine, which increases the resistance of cementum and dentin to clastic activity.

Shirazi et al.1999 - confirmed through the administration of increased doses of L-thyroxine to rats, which resulted in the reduction of the extent of root resorption

luis et al 2002- low doses of thyroid hormone play a protective role on tooth surface during OTM and in those patients who present with spontaneous root resorptive lesions

RELAXIN.

Relaxin has been known for decades as a pregnancy hormone,it is released just before child birth

to loosen the pubic symphysis ,so that the relaxed suture will allow widening of the birth canal

for parturition. It has also been shown to have effects on a multitude of other physiological

processes ,including the regulation of vasotonus, plasma osmolarity, angiogenesis , collagen

turnover , and renal function,Relaxin influence on soft tissue remodelling and several mediators

that stimulate osteoclasts formation

Effects of Relaxin on bone and tooth movement.

In 2005 ,Liu and colleagues showed that the adminstation of relaxin might accelerate the early

stages of orthodontic tooth movements in rats. Stewart and collegues used gingival injections of

relaxin in dogs to relieve rotational memory in the connective tissues of maxillary lateral

incisors that had been orthodontically rotated.

In 2000,Nicozis and colleagues suggested that relaxin might be used as an adjutant to

orthodontic therapy, during or after tooth movement for promotion of stability; for rapid

remodeling of gingival tissue, during extraction space closure; for orthopedic expansion in

non-growing patients, by reducing the tension of the stretched soft tissue envelope,

particularly the expanded palatal mucosa, after orthognathic surgery.

CALCITONIN

Calcitonin is a peptide hormone secreted by thyroid .Synthesis and secretion of calcitonin is regulated by plasma calcium concentration; rise in plasma calcium increases,while fall in plasma calcium decreases calcitonin release.

Calcitonin is used in the treatment of hypercalcemia, osteoporosis and paget’s disease of bone.

Effects of calcitonin on bone and tooth movement.

Calcitonin inhibits bone resorption by direct action on osteoclasts-decreasing their ruffled surface which forms contact with resorptive pit . It also stimulates the activity of osteoblasts.

Calcitonin inhibits proximal tubular calcium and phosphate reabsorption by direct action on kidney.

Because of its physiological role, it is considered to inhibit the tooth movement, consequently delay in orthodontic treatment can be expected.

PARATHYROID HORMONE(PTH)

Parathyroid hormone produced by parathyroid glands to regulate serum calcium concentration.In bone-increases resorption of calcium from bone. In low doses leads to bone formation.In kidneys,PTH increases renal calcium reabsorption and stimulates the excretion of urinary phosphate.

Its effects on osteoclasts occur through the production of RANK-L, a protein plays a crucial role in osteoclast formation and activity.

Effects of PTH on tooth movement

In 1970s ,animal studies demonstrated that PTH could induce an increase in bone turnover that would accelerate orthodontic tooth movement.

More recently ,observed an increased rate of tooth movements in rats treated with PTH,whether adminstered sytemically or locally.

These results indicate that orthodontists should take note of patients being treated with PTH-for example,in cases of severe osteoporosis.

Effect of teriparatide on induced tooth displacement in ovariectomized rats: a histomorphometric analysis.

Salazar M, Hernandes et alAm J Orthod Dentofacial Orthop 2011 ;139(4):e337-44

The treatment of osteoporosis with teriparatide is a good alternative for patients undergoing orthodontic treatment.

CORTICOSTEROIDS

Used in treatment of arthritis,allergic,blood,renal,collagen neoplastic diseases, recurrent oral ulcers, Oral lesions like pemphigus,errosive lichen planus.

Intra-articular hyrocortisone injections in TMJ to relieve refractory pain.

Prophylatic supplementary corticoid to cover dental procedure-in patients who have been on long term corticosteroid therapy

Effects of corticosteroids on bone and tooth movement

The main effect of corticosteroid on bone tissue is direct inhibition of osteoblastic function and thus decreases total bone formation.

Corticosteroids increases the rate of tooth movement, and since new bone formation can be difficult in treated patients, they decrease the stability of tooth movement and stability of orthodontic treatment in general. A more extensive retention may be required.

Studies on acute and chronic corticosteroid treatment revealed that the tooth movement rate increased in the chronic group. orthodontic force level should be reduced and controlled more frequently in patients on chronic steroid treatment

CYTOTOXIC DRUGS(CHEMOTHERAPY)

These are used for the treatment of childhood cancers, threre are every chances of observing

disturbences in dental as well as general body growth and development ,due to adverse effects

of chemotherapeutic agents and radiotherapy. It is clearly stated that patients who had been on

chemotherapy with Busulfan /cyclophosphamide, belongs to risk group, for orthodontic

treatment.These drugs are known to produce damage to precursor cells involved in bone

remodelling process there by complicating tooth movement.

ANTICOVULSANTS.

Seizure disorders ,the most common serious chronic neurological conditions, are characterized

by sudden involuntary time limited alteration in neurological function result from abnormal

electrical discharge of cerebral neurons.

Commonly used drugs for treatment these conditions are

Valproric acid (sodium valporate) - Absence seizures,myoclonic seizures.

Phenytoin –Tonic clonic seizures,status epilepticus,Trigiminal neuralgia.

Gabapentin- Diabetic neuropathy,post-herpatic neuralgia.

Valporic acid-

It has a potential to induce gingival bleeding even with minor trauma, making orthodontic

maneuvers difficult.Fetal abnormalities are more common.

Phenytoin-

It induces gingival hyperplasia due overgrowth of gingival collagen fibers,which involves the

interdental papilla,making application of orthodontic mechanics and difficulty in maintaining

oral hygiene.Used during pregnancy-can produce fetal hydontion syndrome characterized by

hyppoplastic phalanges, cleft palate, hare lip and microcephaly. Osteomalacia and

megaloblastic anaemia.

Gabapentin;

Gabapentin produces xerostomia,making oral hygiene maintenance difficult during orthodontic

treatment.In these cases, clinician should be aware of possible difficulties encounter during

treatment period , and discuss it with the patients and/or parents and educate them so that

adequate measures to maintain oral hygiene are followed.

ALCOHOL ABUSE.

Chronic ingestion of large amounts on daily basis may have devastating effects on a number of

tissue systems ,including skeletal system .Alcoholism may lead to severe complications ,such as

liver cirrhosis, neuropathies, osteoporosis, and spontaneous bone fractures.Circulating ethanol

inhibits the hydroxylation of vitamin D3in liver , thus impending calcium homeostasis.In such

cases the synthesis of PTH is increased ,tipping the balance of cellular function towards the

enhanced resoption of mineralized tissues ,including root resorption in order to maintain

normal levels of calcium in blood. Davidovitch et al. have found that chronic alcoholics

receiving orthodontic treatment are high risk of developing severe root resorption during course

of orthodontic treatment.

ANTIASTHMATIC DRUGS

Chronic use of inhalers with steroids results in oral candidiasis and xerostomia. topical antifungal agents and salivary substitutes have to be performed before and during the orthodontic treatment period.

Aggressive oral hygiene measures and topical fluoride application is required.

Patients with a history of asthma seem to be at a high risk for developing excessive root resorption during the course of orthodontic treatment. This emphasizes the prescription of low forces for these patients, just enough to produce tooth movement without any adverse effects like root resorption.

DRUGS FOR TMJ DISORDERS

Prescription of muscle relaxants like cyclobenzaprin, tricyclic antidepressants like amitryptilin and benzodiazepins like diazepam. The main side effect associated with all these drugs is xerostomia, a significant condition in patients under orthodontic care

In these individuals, xerostomia can negatively affect proper maintenance of oral hygiene, increasing the risk for caries and periodontitis. Xerostomia might particularly increase the incidence of root surface caries, as well as gingival hyperplasia and hypertrophy.

IMMUNOSUPPRESSANT DRUGS

Patients with chronic renal failure or kidney transplants. Drug consumed for prevention of graft rejection (cyclosporin A) produce severe gingival hyperplasia, making orthodontic treatment,and maintenance of oral hygiene difficult.

Treatment should be started or resumed once good oral hygiene and after surgical removal of excessive gingival tissues.

Whenever possible,fixed appliances should be kept to a minimum period with brackets,and avoiding the use of cemented bands. Removable appliances in these cases not recommended, due to improper fit.

IMMUNOMODULATORY DRUGSMost of these drugs used for treatment Rheumatoid arthritis includes - Immunomodulatory agents- Leflunomide.

-TNF antagonists- Etanercept, Infliximab, Adalimumbab.

- Interleukin antagonists- Anakinra.

Immunomodulatory drugs – modulates nuclear factor kappa-B,tyrosine kinases in signaling pathway, interleukin-6.MMPs,and PGE2, all of which are essential for the bone remodeling process.

TNF alpha antagonists - block TNF alpha in inflammatory cytokines ,which are essential for inflammatory responses following force application.

Interleukin antagonists - inhibits IL-1, which are important for the inflammatory response and IL-6 and COX-2.

These drugs will influence the inflammatory response following force application reducing the pace of tooth movement and bone remodeling.

Effects of interferon-gamma on bone remodeling during experimental tooth movement.

Bengi et al Angle Orthod 2007 Jan;77(1):135-41.

Increases in trabecular bone volume and trabeculae bone number and decreases in trabecular separation revealed the antiosteoclastic activity of IFN-gamma.

IFN-gamma administration may be useful clinically for anchorage control.

Inhibitory effect of interferon-γ on experimental tooth movement in mice. Kohara et al

J interferon cytokine res2012 Sep;32(9):426-31

IFN-γ was induced in experimental tooth movement, and could inhibit mechanical force-loaded osteoclastogenesis and tooth movement.IFN-γ might be useful in controlling orthodontic tooth movement

ANTIBIOTICS:

Chemotherapy :

It is the treatment of systemic infection / malignancy with specific drugs that have selective

toxicity for the infecting organism / malignant cell with no / minimal effects on the host cells.

Antibiotic agent :

Chemical substances produced by microorganisms,which selectively suppress the growth of or

kill other micro-organisms in dilute solutions, to produce antimicrobial action.

Antimicrobial agent :

Substances that will suppress the growth /multiplication of microorganisms. antimicrobial agents

may be antibacterial, antiviral / antifungal.

CLASSIFICATION OF ANTIMICROBIAL DRUGS

A. Mechanism of action :

i. Inhibit cell wall synthesis

-Penicillins.

-Cephalosporins.

-Vancomycin.

-Bacitracin.

ii. Cause leakage from cell membranes

-Polypeptides – Polymyxins, colistin, Bacitracin.

-Polyenes – Amphotericin B, Nystatin.

iii. Inhibit protein synthesis

-Tetracyclines

-Chloramphenicol

- Erythromycin,

- Clindamycin

- Linezolid

iv. Cause misreading of m-RNA code and affect permeability

-minoglycosides.

-Streptomycin.

-Gentamicin.

v. Inhibit DNA gyrase

-Fluoroquinolones – Ciprofloxacin.

vi. Interfere with DNA function.

-Rifampin

-Metronidozole

vii. Interfere with DNA synthesis .

-Idoxuridine

-Acyclovir

-Zidovudine

viii. Interfere with intermediary metabolism.

-Sulfonamides

-PAS

-Sulfones

Ethambutol

PENICILLINS.

Most important antibiotics first extracted from the mould Penicillium notatum. First used in

1941 clinically and was a miracle drug with a least toxic effect.

Classication of penicillins.

1.Natural penicillins.

-Penicillin G (benzyl penicillin, PnG).

-Procaine penicillin G.

-Benzathine penicillin G.

2.Acid resistant penicillins.

-Phenoxymethyl penicillin (pencillin V)

-Phenoxyethylpenicillin (phenethecillin)

3.Penicillianse – resistant penicillins.

-Acid labile – methecillin, nafcillin, cloxacillin, dicloxacillin.

4. Extended spectrum penicillins.

a) Amino penicillins; - Ampicillin ,

-Amoxicillin,

- Becampicillin.

b) Carboxypenicillins: - Carbenicillin,

- Ticarcillin.

c) Ureidopenicillins: - Piperacillin,

- Mezlocillin.

5.Betalactamase inhibitors; -Clavulanic acid,

-Sulbactam

Mechanism of action of penicillins.

Bactericidal drug effective mainly against multiplying organisms.As the cell wall synthesis

occurs during the growth phase the antibiotic is more effective against actively multiplying

organisms. Penicillins bind to these proteins and inactivate them, thereby preventing the

synthesis and cross linkage. This weakens bacterial cell wall and makes organism vulnerable to

damage. Penicillin binding to this proteins are bacterial enzymes on the cell wall are responsible

for synthesis and cross linkage of peptidoglycans in the cell wall.

Preparation and dose :

-PnG inj 0.5-5 MU i.m or i.v 6-12 hours

-Procaine pencillin inj 0.5, 1 MU dry powder in vial

-Penidure 0.6, 1.2, 2.4 MU as dry powder in vial

-Fortifide PP inj 3+1 lac U vial

Adverse reactions

Nausea and vomiting on oral PnG ,Intolerance Prolonged IV administration may cause

thrombophlebitis. Accidental IV administration of procaine PP cause anxiety, mental

disturbances paraesthesia and convulsions Major problem with PnG includes idiosyncratic,

anaphylactic and allergic reactions Sterile inflammatory reaction at the site of IM inj.

Uses of penicillins.

-Periapical abcess, Periodontal abcess,Pericocoronitis,Acute supporative pulpitis

-Acute necrotising ulcerative gingivitis , Cellulitis, Diptheria, Prophylaxis against endocarditis.

Potassium phenoxymethyl penicillin (penicillin V)

Similar antibacterial spectrum like benzylpenicillin.More active against resistant staphylococci.

Less inactivated by the gastric acid.Plasma levels achieved is 2 to 5 times higher than

benzylpenicillin.50-70% is bond to plasma proteins.25% of drug is eliminated in

urineAdministered in the dose of 250 –500 mg at 4-8 hours intervals, atleast 30 min before food.

Uses; Streptococcal pharyngitis,sinusitis,otitis media,prophylaxis.

Pencillinase resistant penicillins :

Methicillin ;

Effective in staphylococcal infections.It is given IM or IV (slow) in the dose of 1 gm every 4-6

hours. Haematuria, albuminuria and reversible interstitial nephritis are the special adverse

effects of methicillin.

Cloxacillin;

Weaker antibacterial activity.Incompletely but dependably absorbed from oral route.Distributed

through out the body, but highest concentration in kidney and liver.30% excreted in urine. dose;

0.25-0.5g orally every 6hrs.

Ampicillin – amino penicillin.

Partly excreted in bile and partly by kidney. Drug is effective against H.influenzae

strep.viridans, N.gonorrhea, Salmonella, shigellae, Klebsilla and enterococci.

Dose : 0.5-2 gm oral/IM or IV depending on severity of infection every 6 hours. - 250, 500 mg

caps. Children : 25-50 mg/kg/day

Uses :

Septicaemias,Prophylaxis against endocarditis,Respiratory tract infections,Aerobic and anaerobic

infections. Gonorrhoea Typhoid fever.

Adverse effects :

Diarrhoea is frequent Patient with history of hypersensitivity to PnG should not be given

ampicillin.Unabsorbed drug irritates lower interstines Skin rashes is more common

Amoxycillin

This is a semisynthetic penicillin .(amino-p-hydroxy benzylpencillin) Antibacterial spectrum is

similar to ampicillin but less effective.Oral absorption is better; food does not interfere; higher

and more sustained blood levels are produced.It is less protein bound and urinary excretion is

higher than that of ampicillin.Incidence of diarrhea is less.

Dose : 0.25-1 g TDS oral; 250, 500 mg cap, 125 mg/5ml dry syr, 500 mg/vial inj.

Uses;

Prophylaxis against local wound infection.

Prophylaxis against SBE.

Periapical abcess,osteomylitis

Extractions and minor surgical procedures

Carbenicillin

It is a carboxypenicillin,actively against pseudomonas aeurginosa an proteus which are not

inhibited by penicillin-G and aminopenicillins.Carbenicillin is neither penicillin resistant nor

acid resistant. it is inactive orally and rapidly excreted in urine.

Adverse effects;

Fluid retention, CCF in patients with renal and cardiac dysfunctions, bleeding tendencies due

disturbs in platelet functions.

Uses

Infection caused by pseudomonas,burns,septicaemia,Oro-dental infections.

Dose: it is used with a sodium salt in a dose of1-2g i.m. or 1.5g i.v every 4-6 hrs.

BETA LACTAMASE INHIBITORS

Clavulanic acid

Obtained from Streptomyces clavuligerus.It has betalactam ring – no antibacterial activity,it

inhibits betalctamase produced by both gram positive and gram negative bacteria .It permeates

the outer layers of cell wall of gram-ve bacteria and inhibits periplsamically located beta

lactamase.

Adverse effects; gastric intolerence, hepato-toxicity..

Uses :Amoxicillin+clavulanic acid (augmentin) -dental infections

Sulbactam

Semisnythetic betalactamase inhibitor.Related chemically in activity to clavulanic acid.

Progressive inhibitor ,highly active against betalactamase.

2-3 times < potent.Oral absorption-inconsistent,preferablyim/iv.

Sulbactam+ ampicillin= Dicapen.

Adverse effects :Pain-thrombophebitis,Rashes and diarrhoea

Uses :Mixed aerobic-anaerobic infections,Gonorrhoea ,Skin/soft tissue infections.

CEPHALOSPORINS.

Cephalosporium acremonium was the first source.They contain 7 amino cephalosporonic acid

nucleus. Structurally they contain betalactam and didhydro thiazine rings.

Mechanism of action :

Act by inhibiting bacterial cell wall synthesis and are bactericidal.

Classification

GENERATION EXAMPLES

First generation parenteral-cefazolin

Oral – cephalexin, cephradine, cefadroxil

Second generation Parenteral –cefuroxime

Oral –cefaclor ,cefuroxime axetil

Third generation Parenteral –cefotaxime , ceftriaxone

Oral – cefixime , ceftibuten

Fourth generation Parenteral –cefepime .cefpirome

Cephalexin

Orally effective 1 st generation

Used in dentistry as alternative to amoxicillin

DOSE- 0.25g 8hourly

Cefadroxil

Good tissue penetration including in alveolar bone

Frequently selected for dental infections

Cefuroxime axetil

Orally effective 2nd generation

Highly active against anaerobes so used in dental infections

DOSE- 250-500 mg BD

A/E- Local reactions – cause pain (IM) and cause thrombophlebitis (IV),Diarrhoea, rashes,super infection, nephrotoxicity, Bleeding, cross reactivity with penicillin

USES-

Orally active 1st and 2ng generation are used for dental infections

Mixed aerobic and anaerobic infections

Prophylactic treatment in neutropenic patiens

Fourth generation cephalosporins :

Developed in 1990 similar to that of 3rd generation.Highly resistant to b-lactamases. Active

against many bacteria resistant to earlier drugs. It has high potency and extended spectrum.

Effective in many serious infections.

Parenteral

CEFEPINE, CEFPIROME

USES :

1. Serious and resistant hospital acquired infections.

2. Septicaemia,

3. Lower respiratory tract infection.

Dose : 1-2g IM / IV 12 hrly.

CEFROM, CEFORTH – 1g inj.

Adverse reactions.

1. Local reactions – cause pain (IM) and cause thrombophlebitis (IV) .

2. Allergy – skin rashes .

3. Super infection.

4. Nephrotoxicity, CNS toxicity, Blood toxicity .

5. Cross reactivity with penicillin.

Uses

1. Alternatives to penicillins.

2. Penicillinase producing staph infection.

3. Septicaemias.

4. Surgical prophylaxis

5. Mixed aerobic and anaerobic infections

6. Infection by odd organism or hospital infections

7. Prophylactic treatment in neutropenic patients.

MACROLIDES

They are called macrolides because they contain a many membered lactone ring to which are

attached one or more deoxy sugars.Clarithromycin differs from erythromycin only by

methylation of the hydroxyl group at the 6 position, and Azithromycin by the addition of a

methyl substituted nitrogen atom into the lactone ring.

Erythromycin.

Erythromycin was isolated from Streptomyces erythreus and widely employed mainly an

alternative to penicillin

Mechanism of action:

Erythromycin acts by inhibiting bacterial protein synthesis.It combines with 50s ribosome sub

unit and interferes with ‘translocation’ .

Antibacerial action

Baceriostatic in low concentration and bactericidal at high concentration. Effective against gram

positive bacteria.It is more active in alkaline medium due to non-ionised form of the drug is

favoured at higher pH.

Adverse effects :

1. GIT – epigastric pain

2. On high doses – hearing impairment.

3. Hypersensitivity reactions – rare

Uses :

1. Aerobic and anaerobic infectios of dental origin.

2. Peridontal/peiapical abcess, ANUG,pericoronitis ,cellulitis.

3. Post-extraction infections .

4. Prophylaxis to cover dental procedures.

5. Penicillin resistant infections

Roxithromycin

Semisynthetic – it is a long acting stable macrolide. Its antibacterial spectrum similar to

erythromycin.it has better enteral absorption and tissue penetration and better gastic

tolerability.It is mainly used for oro-dental infections.

Dose - 150-300mg BD

Children - 2.5-5mg/kg BD, 50mg kid tab,150 mg tab

AZITHROMYCIN

This differs chemically from other macrolide group in that lactone ring contains nitrogen atom. It

is new azilide congener of erythromycin has an expanded spectrum . Less active against gram

+ve organisms

Uses

1. Prophylaxis against SBE.

2. Alternative to erythromycin.

3. Respiratory infections.

4. Strep and Staph skin and soft tissue infections

Dose : 500mg once daily for 3days , 100,250,500mg tab, are available.

CLINDAMYCIN

It is lincosamide antibiotic having similar action (macrolide 50s). Semisynthetic derivative of

Lincomycin Bacteriostatic at low concentration. Bacteriocidal at high concentration

Most active against gram+ve cocci, C.diphtheriae, Actinomyces

Highly active against anaerobes (B fragilis)

Adverse effects :

1. Rashes

2. Urticaria

3. Abdominal pain

4. Superinfection

5. Enterocolitis

Uses :

Anaerobic and mixed infections

Doses : 150-300 mg caps QID orally.

200-600mg I.v. 8 hourly

TETRACYCLINES

Tetracyclines are napthacene derivatives.Obtained from Actinomycetes.All tetracyclines are

bitter solids which are weakly water soluble,but their hydrochlorides are more soluble.‘Broad

spectrum antibiotic’- affecting wide range of micro-organisms.The napthacene nucleus is made

up by fusion of 4 partially unsaturated cyclohexane radicals and hence the name tetracyclines.

Incompletely absorbed from GIT,better absorption with empty stomach,

Mechanism of action

Tetracyclines to inhibit bacterial protein synthesis by binding to the 30 S bacterial ribosome and

preventing the access of aminoacyl tRNA to the acceptor (A) sites on the mRNA- ribosome

complex.

Tetracyclines have chelating property, calcium tetracyline chelate gets deposited in

developing teeth and bone .When given from mid-pregnancy to 5 months of extra-uterine life,the

deciduous teeth are affected; brown discolouration ,illformed teeth ,more susceptible to

caries.Tetracyline given between 3months and 6 years of age affect the crowns of anterior

teeth.Prolonged use of tetracycline during late pregnancy or childhood can cause temporary

supression of bone growth.

Dose :

Tetracycline-250 mg ,qid.

Mino-cycline 100mg ,bid.

Doxy-cycline 100mg, od.

Local drug delivary systems in peridontal pockets.

Actisite- tetracycline fiberes (25% of tetracycline).

Periocline-2% minocycline.

Atridox- 10% doxycycline.

PRECAUTIONS

1. Not to be used in pregnancy, lactation and in children.

2. Avoided in patients on diuretics.

3. Do not mix injectable Tc with Pn- inactivation occurs.

4. Beyond expiry date should not be used.

5. Used cautiously in renal and hepatic insufficiency.

Uses of tetracyclines.

1. Chronic periodontitis.

2. Refractory periodontitis.

3. Juvenile periodontitis.

4. Mixed infections.

In periodontal diseases tetracyclines suppress the activity of collagenase enzymes derived from neutrophils,fibroblasts that contribute to the gingival inflammation and scavanging free radicals.

QUINOLONES

Synthetic antimicrobials having a quinolone structure that are active primarily against gram –ve

bacteria.

Mechanism of action :

The FQs inhibit the enzyme bacterial DNA gyrase, which nicks The DNA gyrase consists of

two A and two B subunits; A subunit double stranded DNA. carries out nicking of DNA, B

subunit introduces –ve super coils and then a subunit reseals the strands.

Ciprofloxacin •

1st generation FQ active against broad range micro-organisms,especially aerobic gram -

negative bacilli.Rapid bactericidal activity and high potency.Relatively long post antibiotic effect

on enterobacteriaceae pseudomonas staphalococus.Low frequency of mutational

resistance.Active against many lactam and amino glycoside resistant bacteria.Less active at

acidic pH.

Dose; 250, 500,750 mg tab, 200mg/100 ml IV infusion..

Adverse reactions

GIT – Nausea, vomiting, bad taste, anorexia, diarrhoea is infrequent.

CNS- Dizziness, headache, restlessness, anxiety, insomnia and seizures.

Skin/hypersensitivity – rashes, pruritis, urticaria.Tendonitis and tendon rupture

Uses.

Gram -ve septicaemias

Typhoid.

Bone and soft tissue infections.

Periapical abscess. Bacterial gastroenteritis

METRONIDAZOLE

It is the prototype nitroimidazole and found to be highly active amoebicide.Broad spectrum

cidal activity against protozoa and anaerobic bacteria's .Metronidazole is selectively toxic to

anaerobic microorganisms. Metronidazole has been found to inhibit cell mediated immunity and

cause radiosensitization.Effective against many anaerobic periodontal pathogens like

Fusobacterium, Bact.fragalis,Prevotella ,Veillionella, Bact.melanogenicus,Campylobacter, etc.

Mechanism of action

After entering cell by diffusion,its nitro group is reduced by certain redox proteins of anaerobs

to highly reactive nitro radical which interfere with the DNA function,

Uses - Amoebiasis anaerobic bacterial infections,.Extensively used in oro-dental anaerobic

infections like periodontis,acute apical infections.Drug of choice in cases of Acute necrotising

ulcerative gingivitis (ANUG).

Dose METROGYL 200, 400 mg tab , Metronidazole gel- for local application.

Antibiotic prophylatic regime against infective endocarditis

Situation Antibiotic Regimen

Standard

prophylaxis

Amoxicillin Adult – 2gm children 50mg/kg PO, 1 hr before.

Cannot use

oral medication

Ampicillin Adult – 2gm, children 50 mg/kg IM/IV. 30 min

before.

Allergic to

pencillin

Clindamycin Adult – 600mg ,children 20 mg/kg PO, 1 hr before

Cephalexin /

cefadroxil

Adult – 2gm ,children 50 mg/kg PO, 1 hr before

Azithromycin or

clarithromycin

Adult – 500mg children 15 mg/kg PO, 1 hr before

Allergic Pn,

cannot use oral

Clindamycin Adult – 600mg children 15 mg/kg IV 1 hr before

Cefazolin Adult 1 gm, children 25 mg/kg IM / IV30 min

before

Dental procedures which requires prophylaxis against SBE:

1. Dental Extractions.

2. Pridontal procedures,flap surgery,curretage,scaling,root planing, Probing and recall

maintainance.

3. Dental implant placement and reimplatation of avulsed teeth.

4. Endodontic procedures & Apesectomy.

5. Sub-gingival placement of anti-biotic fibers & gingival retraction cords.

6. Initial placement of orthodontic bands but not brackets.

7. Prophylaxis cleaning of implants/teeth where bleeding is anticipated.

CONCLUSION

Orthodontists have long observed that teeth move at different rates ,and individuals have

differing responses to treatment. Some of the differences are caused by change in bone

remodeling induced by drugs and systemic factors.All the drugs reviewed have the therapeutic

effects, as well as side effects that influences the cells targeted by orthodontic forces.

There fore it is imperative that the orthodontist need to pay attention to drug consumption ,

history of each every patient, before and during course of orthodontic treatment .So the best

treatment strategy-including force control and appointment intervals-can be selected for each

case.

Acetaminophen , which does not have significant influence on the rate of tooth movement, can

be recommended for controlling pain during orthodontic treatment.

REFERENCES

Essentials of medical pharmacology K.D Tripathi- 6th edition

Aspirin, acetaminophen, and ibuprofen: Their effects on orthodontic tooth movement Am J Orthod Dentofacial Orthop 2006;130:364-70

Effects of analgesics on orthodontic pain Am J Orthod Dentofacial Orthop 2011;139:e53-8

Pain reduction after initial archwire placement in orthodontic patients: A randomized clinical trial Am J Orthod Dentofacial Orthop 2012;141:169-73

Tenoxicam controls pain without altering orthodontic movement of maxillary canines Orthod Craniofacial Res 2009 Feb;12(1):14-9

Comparison of some effects of acetylsalicylic acid and rofecoxib during orthodontic tooth movement Am J Orthod Dentofacial Orthop 2004;125:310-16

Orthodontic tooth movement after inhibition of cyclooxygenase-2 Am J Orthod Dentofacial Orthop 2006:129:402-6

Effect of fluoride on orthodontically induced root resorption with light and heavy orthodontic forces for 4 weeks: A microcomputed tomography study Am J Orthod Dentofacial Orthop 2011;140:e199-210

Optimizing orthodontic treatment in patients taking bisphosphonates for osteoporosis Am J Orthod Dentofacial Orthop 2009;135:361-74

Effects of clodronate on early alveolar bone remodeling and root resorption related to orthodontic forces: A histomorphometric analysis Am J Orthod Dentofacial Orthop 2010;138:548.e1-548.e8,Orthodontic tooth movement and root resorption in ovariectomized rats treated by systemic administration of zoledronic acid Am J Orthod Dentofacial Orthop 2012 141:563-73

Bisphosphonates as a risk factor for adverse orthodontic outcomes: A retrospective cohort study Am J Orthod Dentofacial Orthop 2012;142:625-34

Medication effects on the rate of orthodontic tooth movement: A systematic literature review Am J Orthod Dentofacial Orthop 2009;135:16-26

Tooth movement and root resorption; The effect of ovariectomy on orthodontic force application in rats Angle Orthod 2011;81:570-77

Effect of teriparatide on induced tooth displacement in ovariectomized rats: a histomorphometric analysis. Am J Orthod Dentofacial Orthop 2011;139(4):e337-44

The effect of drugs on orthodontic tooth movement Orthod Craniofacial Res 9, 2006/163–171

Orthodontically induced root and alveolar bone resorption: inhibitory effect of systemic doxycycline administration in rats European Journal of Orthodontics 27 (2005) 215–225

Effect of diabetes on orthodontic tooth movement in a mouse model. Eur j oral sci 2011 Feb;119(1):7-14

Effects of interferon-gamma on bone remodeling during experimental tooth movement Angle Orthod 2007 Jan;77(1):135-41

Inhibitory effect of interferon-γ on experimental tooth movement in mice. J interferon cytokine res 2012 Sep;32(9):426-31