This document discusses growth spurts in babies. It explains that growth spurts typically last 1-2 days in young babies and up to a week in older babies, and may occur around 2 weeks, 3 weeks, 6 weeks, 3 months, and 6 months of age. During a growth spurt, a baby may feed more often, sleep more or less, and can become fussy or clingy as they devote extra energy to growing. The document provides tips for responding to a baby's needs during a growth spurt and distinguishes growth spurts from other causes of changes in a baby's behavior.

1. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
Growth spurt
What happensduringagrowth spurt?
Duringa growthspurtyour babywill putonweight,lengthandheadcircumference more quicklythan
usual.She mayalso hita developmentalmilestone,ormastera skill she’sbeenworkingonfora
while. Manymumsfindthatthe mostnoticeable signof agrowthspurt istheirbabyfeedingmore,so
lookout fortimeswhenyourlittle one seemsparticularlyhungry. If yourbabyis breastfed,feedsmay
take longerthanusual.If she’s formula-fed,she mayseemasif she’sstill hungryatthe endof a
feed. Some babiessail throughgrowthspurtswithoutshowinganyobvioussigns.Youmaytake your
babyto be weighedandsee thatherweight’sjumpedtoahigherpercentile,ornotice thathernew
onesie issuddenlytightatthe toes! Whenyourbaby’shavinga growthspurt,she may needmore or less
sleepthanusual.There'ssome researchtoshow thatbabiesgoingthroughgrowthspurtsbecome
clingy,fussyandunsettled,andthiscandisruptnaptimesandnight-times.
Whendo growthspurtshappen,andhow long dotheylast?
Growth spurtscan happenat anytime.In youngbabies,theyusuallylastforone dayor two days.In
olderbabies,theycanlastup to a week.
Some expertsbelieve thatgrowthspurtsare more likelyatcertainpointsin yourbaby’sfirstyear.These
are:
 at two weeks
 at three weeks
 at six weeks
 at three months
 at six months
Each baby’sgrowthpatternis different,sotrynot to worryif your babydoesn’tseemtobe having
growthspurtsat these times.If she’sfeedinghappilyandgainingweight,youcanbe sure that she’s
growingwell.
Are growthspurts the same as feedingspurts?
No,but theyare related.Feedingspurtsare timeswhenyourbabyseems hungrierthanusual.Theymay
or may not be linkedtoa growthspurt. During a feedingspurt,yourbabymayfeedforlonger.If she’s
breastfed,she maybe fussy atthe breast,andif she’sformula-fed,she mayseemhungryafter
feeds. Youmayalso hearor read about“frequencydays”,whichare dayswhen breastfedbabiesfeed
more often,upto 18 timesin24 hours. Surprisingly,thereisn’talotof researchlinkingfeedingspurtsto

2. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
increasedgrowth.Butitmakessense thatwhenyourbaby’stakinginmore calories,she’ll grow more
quickly. Because of this, some people use the terms“growthspurt”and“feedingspurt”tomeanthe
same thing.
Apart fromfeedingmore,whatare the othersignsof a growthspurt?
Sleep
Justbefore andduringa growthspurt, yourbaby mayseemsleepierthanusual.Wakingupless atnight,
havinga lie-in,ortakingmore napsmaybe signsthat she’schannellingherenergyintogrowing.One
small studysuggestedthatduringagrowthspurt, babiesmaysleepuptofourand half hoursmore than
usual overone or two days. It’snot clearexactlywhythishappens,buta proteincalledhumangrowth
hormone (HGH) is producedinthe brainduringsleep.HGHiscrucial forgrowth,so sleepmayprovide
the fuel thatyour baby needstogrow.
Some babiesseemtoneedlesssleepduringgrowthspurts,soyoumay alsonotice yourbaby wakingup
more frequentlyatnight,ortakingshorternaps. You may findthese changesinyourbaby’sroutine
tiringor confusing.If you’re feelingoverwhelmed,remindyourself thatagrowth spurtonlylastsfor a
fewdays.Before toolong,yourbaby’sroutine will be backtonormal.
Behaviour
Duringa growthspurt,yourbaby may be more restlessand clingy thanusual. Youmay findthat she
wantsto be heldall the time,andcrieswhenyoutry to put herdown.Or you maynotice that she’s
unsettledandweepyattimeswhenshe’susuallylaid-backandcalm. It’snotknownexactlywhatcauses
these changesinbehaviour.Theymaybe downtoyour babyfeelingtiredoroverwhelmedasshe
devotesherenergytofeedingandgrowing. There'salsoatheorythat behavioural changesmaybe a
signthat a developmentalleapiscoming.Thismayhappenalongside agrowthspurt,or at a different
time.Soif your babyseemsfussyorcranky,she maybe gettingreadytounveil anew skill,such
as rollingoverorcrawling!
What shouldIdo duringa growthspurt?
Respond toyour baby’scuesand try togive herwhat she needs,whetherit’sextrafeeds,amorning
nap,or quiettime andcuddles. Breastfedbabiescanseemasif they’re not gettingenoughmilk duringa
growthspurt.Don’t worry,yourbreastswill produce plentyof milkforyourbaby’sneeds. However,if
she ishungrierthanusual,it maytake a day or twofor yourbodyto catch up,so a growth spurtcan feel
a little overwhelmingatfirst. Helpyourmilkproductionalongbylettingyourbabyfeedasoftenandfor
as longas she wants,whichiseasiersaidthandone!Take care of yourself by eatingregularmeals,
drinkinglotsof fluids,andlettingfamilyandfriendshelpoutwithchores. If yourbabyis formula-fed,

3. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
she may seemhungryaftera feed.It’sfine togive heranextrabottle if she wantsone.There’susually
no needtoswitchto “hungry”milk,butif you’re consideringit,talktoyourhealthvisitorfirst.
Is ita growthspurt,or is somethingwrong?
Growth spurtscan make babiessleepyandout-of-sorts,buttheydon’tcause fevers,extreme irritability,
or listlessness.These canbe signsthatyour babyisunwell.ContactyourGP if yourbaby showsanyof
these symptoms. If youbreastfeedandyou’re worriedthatyourbabyisnot gettingenoughmilk,ask
your doctoror healthvisitorforadvice andextrasupport. Growthspurts aren’tthe onlyexplanationfor
a cranky, hungrybaby.Holidays, teething,changesinroutineand minorillnessescanalsoaffectyour
baby’sfeeding,sleepandbehaviour.
If your baby’sroutine haschangedandshe'sfeelingunsettled,she mayfindfeedingcomforting.Soif
she seemsmore hungrythanusual,she mayjust wantthe reassurance of contact withyou.
If your baby’sbehaviour,feeding,orsleepinghabitschange suddenlyandyou‘re concerned,ask
your GP or healthvisitorforadvice.
Osteogenesis:
Some of the mostobviousstructuresderivedfromthe paraxial mesodermare bones.We canonlybegin
to outline the mechanismsof bone formationhere;studentswishingfurtherdetailsare invitedto
consulthistologytextbooksthatdevote entirechapterstothistopic.
There are three distinctlineagesthatgeneratethe skeleton.The somitesgenerate the axialskeleton,
the lateral plate mesodermgeneratesthe limbskeleton,andthe cranial neural crestgivesrise tothe
branchial arch and craniofacial bonesandcartilage.*
There are twomajormodesof bone formation,
or osteogenesis,andbothinvolvethe transformationof apreexistingmesenchymal tissue intobone
tissue.The directconversionof mesenchymal tissueintobone iscalled intramembranousossification.
Thisprocessoccurs primarilyinthe bonesof the skull.Inothercases,the mesenchymal cells
differentiateintocartilage,andthiscartilage islaterreplacedbybone.The processbywhicha cartilage
intermediate isformedandreplacedbybone cellsiscalled endochondral ossification.
Mechanismof bone growth
We obviouslyhave alotof growingtodo afterwe're born.Not onlydoour bonesneedtogetlongerand
thickeras we grow,but an adultskeletonisverydifferentfromafetal orinfantskeleton.A fetal
skeletonhasabout275 bonesanda fairlyhighpercentof cartilage (thishelpsthe skeletontobe
somewhatflexible).Comparethattoan adultskeleton,whichhas206 bonesand a much smaller
percentage of cartilage.We fuse several bonestogetheraswe age,whichaccountsfor the decrease in
bone number.

4. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
There are twomainprocessesthatoccur duringfetal developmentthatcontribute toourbone
formation.These are intramembranousossification andendochondral ossification.The term
'ossification'referstothe processof formingbone.There are a couple of thingsthatdistinguishthese
twoprocessesfromone another.
Intramembranous ossification
Intramembranousossificationisthe characteristicwayinwhichthe flatbonesof the skull andthe turtle
shell are formed.Duringintramembranousossificationinthe skull,neuralcrest-derivedmesenchymal
cellsproliferate andcondense intocompactnodules.(Thus,intramembranousossificationisnot
occurringfrom sclerotome-derivedcells.)Some of these cellsdevelopintocapillaries;otherschange
theirshape to become osteoblasts,committedbone precursorcells.The osteoblastssecrete acollagen-
proteoglycanmatrix thatisable to bindcalciumsalts.Throughthisbinding,the prebone (osteoid) matrix
becomescalcified.Inmostcases,osteoblastsare separatedfromthe regionof calcificationbyalayerof
the osteoidmatrix theysecrete.Occasionally,though,osteoblastsbecome trappedinthe calcified
matrix and become osteocytes—bonecells.Ascalcificationproceeds,bonyspiculesradiateoutfromthe
regionwhere ossificationbegan.Furthermore,the entire regionof calcifiedspiculesbecomes
surroundedbycompactmesenchymal cellsthatformthe periosteum(amembrane thatsurroundsthe
bone).The cellsonthe innersurface of the periosteumalsobecomeosteoblastsanddepositosteoid
matrix parallel tothatof the existingspicules.Inthismanner,manylayersof bone are formed.
Schematicdiagramof intramembranousossification.(A)Mesenchymal cellscondense toproduce
osteoblasts,whichdepositosteoidmatrix.Theseosteoblastsbecome arrayedalongthe calcifiedregion
of the matrix.Osteoblaststhatare trappedwithinthe
The mechanismof intramembranousossificationinvolvesbone morphogeneticproteinsandthe
activationof a transcriptionfactor calledCBFA1.Bone morphogeneticproteins(probablyBMP2,BMP4,
and BMP7) fromthe headepidermisare thoughttoinstructthe neural crest-derivedmesenchymal cells
to become bone cellsdirectly.The BMPsactivate the Cbfa1gene inthe mesenchymal cells.Justasthe
myogenicbHLHfamilyof transcriptionfactorsiscompetenttotransformprimitivemesenchyme cells(or
justabout anyothercell) intomuscle-formingmyoblasts,the CBFA1transcriptionfactorappearstobe
able to transformmesenchymecellsinto osteoblasts. Ducyandhercolleagues. foundthatthe mRNA for
mouse CBFA1is severelyrestrictedtothe mesenchymalcondensationsthatformbone,andislimitedto

5. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
the osteoblastlineage.The proteinappearstoactivate the genesforosteocalcin,osteopontin,andother
bone-specificextracellularmatrix proteins.
Confirmationandextensionof thisconclusionwasobtainedfromgene targetingexperimentswherein
the mouse Cbfa1gene wasknockedout .Mice homozygousforthisdeletiondiedshortlyafterbirth
withouttakingabreath,and theirskeletonscompletelylackedbone.The mutantshadonlythe
cartilaginousskeletal model .Inthese mice,bothendochondral andintramembranousossificationhad
beeneliminated.The osteoblastswereinanarrestedstate of development,expressingneither
osteocalcinnorosteopontin.
Gene targetingof Cbfa1inmice causeslack of bone formation.Newbornmice (wild-typeand
homozygotesforCbfa1) were stainedwithalcianblue(forcartilage)andalizarinred(forbone).Cartilage
developmentinbothmice wasnormal.(A) Wild-typelittermate.
Mice that were heterozygousfor Cbfa1showedskeletal defectssimilartothose of a humansyndrome
calledcleidocranial dysplasia(CCD).Inthissyndrome,the skullsuturesfailtoclose (adultsretainthe
fontanel associatedwithyounginfants),growthisstunted,andthe clavicle (collarbone) isoftenabsent
or deformed.†
WhenDNA frompatientswithCCDwas analyzed,eachpatienthadeitherdeletionsor
pointmutationsinthe CBFA1gene.Control individualsdidnothave suchmutations.Therefore,it
appearsthat cleidocranial dysplasiaiscausedbyheterozygosityof the CBFA1gene.
Endochondral ossification
Endochondral ossificationinvolvesthe formationof cartilage tissue fromaggregatedmesenchymal cells,
and the subsequentreplacementof cartilage tissue bybone .The processof endochondral ossification
can be dividedintofive stages.First,the mesenchymal cellsare commitedtobecome cartilage cells.
Thiscommittmentiscausedbyparacrine factorsthat induce the nearbymesodermal cellstoexpress
twotranscriptionfactors,Pax1and Scleraxis.These transcriptionfactorsare thoughtto activate
cartilage-specificgenes .Thus,Scleraxisisexpressedinthe mesenchyme fromthe sclerotome,inthe
facial mesenchymethatformscartilaginousprecursorstobone,andinthe limbmesenchyme .
Schematicdiagramof endochondral ossification.(A,B) Mesenchymal cellscondenseanddifferentiate
intochondrocytestoformthe cartilaginousmodelof the bone.(C) Chondrocytesinthe centerof the
shaftundergohypertrophyandapoptosiswhile they
Localizationof the scleraxis message (lightareas) atthe sitesof chondrocyte formation.(A)Expression
of scleraxis inthe somitesof a12.5-day mouse embryo.Thissectionwascuttangentially,andthe neural
tube runs alongthe anterior-posterior
Duringthe secondphase of endochondral ossification,the committedmesenchyme cellscondense into
compact nodulesanddifferentiate into chondrocytes,the cartilage cells.N-cadherinappearstobe

6. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
importantinthe initiationof these condensations,andN-CAMseemstobe critical formaintainingthem
. In humans,the SOX9gene,whichencodesaDNA-bindingprotein,isexpressedinthe precartilaginous
condensations.Mutationsof the SOX9gene cause camptomelicdysplasia,arare disorderof skeletal
developmentthatresultsindeformitiesof mostof the bonesof the body.Most affectedbabiesdie from
respiratoryfailure due topoorlyformedtracheal andribcartilage .
Duringthe third phase of endochondral ossification,the chondrocytesproliferate rapidlytoformthe
model forthe bone.Astheydivide,the chondrocytessecrete acartilage-specificextracellularmatrix.In
the fourthphase,the chondrocytesstopdividingandincrease theirvolume dramatically,
becominghypertrophicchondrocytes.These large chondrocytesalterthe matrix theyproduce (by
addingcollagenXandmore fibronectin) toenable ittobecome mineralizedbycalciumcarbonate.The
fifthphase involvesthe invasionof the cartilage modelbybloodvessels.The hypertrophicchondrocytes
die byapoptosis.Thisspace will become bone marrow.Asthe cartilage cellsdie,agroupof cellsthat
have surroundedthe cartilage model differentiate intoosteoblasts.The ostoblastsbeginformingbone
matrix on the partiallydegradedcartilage.Eventually,all the cartilage isreplacedbybone.Thus,the
cartilage tissue servesasamodel forthe bone that follows.The skeletalcomponentsof the vertebral
column,the pelvis,andthe limbsare firstformedof cartilage andlaterbecome bone.
The replacementof chondrocytesbybone cellsisdependentonthe mineralizationof the extracellular
matrix.Thisisclearlyillustratedinthe developingskeletonof the chickembryo,whichutilizesthe
calciumcarbonate of the eggshell asitscalciumsource.Duringdevelopment,the circulatorysystemof
the chick embryotranslocatesabout120 mg of calcium fromthe shell tothe skeleton.Whenchick
embryosare removedfromtheirshellsatday3 and grownin shell-lesscultures(inplasticwrap) forthe
durationof theirdevelopment,muchof the cartilaginousskeletonfailstomature intobonytissue ; Tuan
and Lynch . A numberof eventsleadtothe hypertrophyandmineralizationof the chondrocytes,
includinganinitial switchfromaerobictoanaerobicrespiration,whichalterstheircell metabolismand
mitochondrial energypotential .Hypertrophicchondrocytessecrete numeroussmall membrane-bound
vesiclesintothe extracellularmatrix.These vesiclescontainenzymesthatare active inthe generationof
calciumand phosphate ionsandinitiatethe mineralizationprocesswithinthe cartilaginousmatrix.The
hypertrophicchondrocytes,theirmetabolismandmitochondrial membranes altered,thendie by
apoptosis.
Skeletal mineralizationin19-daychickembryosthatdeveloped(A) inshell-lessculture and(B) inside the
eggduringnormal incubation.The embryoswere fixedandstainedwithalizarinredtoshow the
calcifiedbone matrix.(FromTuanandLynch1983
In the longbonesof manymammals(includinghumans),endochondralossificationspreadsoutwardin
bothdirections fromthe centerof the bone.If all of our cartilage were turnedintobone beforebirth,
we wouldnotgrow anylarger,and our boneswouldbe onlyaslarge as the original cartilaginousmodel.
However,asthe ossificationfrontnearsthe endsof the cartilage model,the chondrocytesnearthe
ossificationfrontproliferate priortoundergoinghypertrophy,pushingoutthe cartilaginousendsof the

7. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
bone.These cartilaginousareasatthe endsof the longbonesare called epiphyseal growthplates.
These platescontainthree regions: aregionof chondrocyte proliferation,aregionof mature
chondrocytes,anda regionof hypertrophicchondrocytes. Asthe innercartilage hypertrophiesandthe
ossificationfrontextendsfartheroutward,the remainingcartilageinthe epiphyseal growthplate
proliferates.Aslongasthe epiphysealgrowthplatesare able toproduce chondrocytes,the bone
continuestogrow.
Proliferationof cellsinthe epiphyseal growthplate inresponse togrowthhormone.(A) Epiphyseal
growthplate ina youngrat that was made growthhormone-deficientbyremoval of itspituitary.(B)
Same regioninthe rat afterinjectionof growthhormone.
Meckel'scartilage
In humans,the cartilaginousbarof the mandibulararch is formedbywhatare knownas Meckel’s
cartilages (rightandleft) alsoknownas Meckeliancartilages;above thisthe incus and malleus are
developed. The dorsal endof eachcartilage isconnectedwiththe ear-capsule andisossifiedtoform
the malleus;the ventral endsmeeteachotherinthe regionof the symphysismenti,andare usually
regardedas undergoingossification toformthatportionof the mandiblewhichcontainsthe incisor
teeth.The interveningpartof the cartilage disappears;the portionimmediatelyadjacenttothe malleus
isreplacedbyfibrousmembrane,whichconstitutesthe sphenomandibularligament,while fromthe
connective tissuecoveringthe remainderof the cartilage the greaterpartof the mandible isossified.
Growth theories
The major theoriesexplaininggrowth are 1.GeneticTheory2.Sutural Theory3.CartilageneousTheory
4.Functional matrix Theory.
GENETIC theory
Growth iscontrolledbygeneticinfluence andispreplanned.
Sutural dominance theory
Statedthat cranio facial growthoccurs at sutures.sutural growthisthe proliferationof the connective
tissue betweenthe twobones. Growthof the cranial vault – expansive proliferative growthbysutural
connective tissuethatforcesthe bonesof the vaultawayfrom eachother.
Cartilaginoustheory
The Irish anatomist,JamesH.Scott,proposedanexplanation,the nasal septumtheoryorScotts
hypothesissuturesplaylittle ornodirectrole inthe growth of the craniofacial skeleton.Rather,sutures

8. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
are secondary,andcompensatorysitesof bone formationand growth.Scottconcluded:- thatthe nasal
septumismostactive and importantforcraniofacial skeletal growthlate prenatallyandearlypost
natally,throughapproximatelythreetofouryearsof age inhumans.
COTT‟S HYPOTHESIS
Intrinsicgrowth-controllingfactorsare incartilage & periosteum.Suturesare secondary&dependent
on extrasutural influences.Cartilaginouspartof skull mustbe recognizedasprimarycentersof growth,
withnasal septumbeingamajorcontributorinmaxillarygrowth.
FUNCTIONALMATRIX HYPOTHESIS
It isGivenby MELVIN MOSS IN 1969 and reviewedbyhimin1990s. The origin,growthand
maintenance of all skeletal tissuesandorgansare alwayssecondary,compensatoryandobligatory
response toall the temporallyandoperationalprioreventsandprocessesthatoccurin specifically
relatednon- skeletal tissues,organsorfunctional spaces.
Enlow’sexpanding“V” principle
ExpandingV shapedprinciplewasbutforwardbyEnlow.The enlow pricple isimportantfacial skeletal
growthmechanismsince manyfacial andcranial boneshave a V configurationorv shapedregions.inv
shapedbonesthe bone resorptionoccursatthe outersurface and the depositioninthe innersurface.
Most of the craniofacial bonesincludingMaxiila,mandibleandpalate isof the bestexamplesof V
principle.
.Synchondrosis
A synchondrosisisajointthatis connectedwithcartilage.Suchjointsare stiff andverystrongandthey
can be foundinseveral areasof the body.Many appearinchildhoodonly,disappearing aspeople
mature intoadulthood.Suchjointsprovide limitedflexibilitywhere itisneeded,withoutthe range of
motionfoundinothertypesof joints.Thismakesasynchondrosismore stable andsupportive.
A famousexample of asynchondrosisisthe sternocostal jointwhere the ribsmeetthe sternum.The rib
cage isdesignedtoprotectthe sensitive organsinsidethe chestwhile allowingsome roomfor
expansion.The synchondrosisallows the ribcage to absorband distribute energyfromimpacts,while
alsopermittingthe chesttoopenupwhenpeople take abreath.The stiff nature of thisjointexplains
whypeople sometimesdevelopfracturesfromcardiopulmonaryresuscitation,especially if theyare
olderadults,asthe jointisnot alwaysflexibleenoughtowithstandthe repeatedpressureof vigorous
chestcompressions.

9. Assignment
COURSE: orthodontics
Lecturer: DR.SELVA KUMAR
mawlid xamud sh.mumin
Otherexamplescanbe foundatsiteson the longbones,knownasepiphyseal growthplates.The growth
platesallowbones togrowas people getolder,whilestill providingsupporttothe body.Overtime,the
hyaline cartilage inthese synchondroses ossifies,turningintobone.Growthplatescanprovide
informationabouthowoldsomeone is,dependingonthe degree of ossification.These jointsharden
entirelyinto bone bythe time people reachtheir20s.
Show references
1. Orthodonticprinciples
2. Slide sharesby - Dr.chiranjeevsingh orthodontics
3. Americandental journal