dosarul medical al clinicii de chirurgie din FMV Bucuresti
UNIVERSITATEA DE STIINTE AGRICOLE SI MEDICINĂ VETERINARĂ – BUCURESTI
FACULTATEA DE MEDICINĂ VETERINARĂ
CLINICA DE CHIRURGIE
Splaiul Independenţei Nr. 105, sector 5, BUCURESTI, ROMÂNIA
TELEFON: 4.11.27.87; 4.10.14.05; Fax : 4.11.98.02
RAPORTUL STIINTIFIC AL CATEDREI DE CHIRURGIE DIN CADRUL USAMV -FMV BUCURESTI CU PRIVIRE LA ASPECTELE MEDICALE SPECIFICE
intalnite la rasele de caini ciobaneşti
romanesti mioritic şi carpatin necesare a fi cunoscute in cadrul activitatilor de omologare internationala a acestor doua rase
In Romania activitatea de cercetare chinologica din punct de vedere stiintific nu s-a executat decat foarte rar in cadrul unitatilor Facultatilor de Medicina Veterinara – FMV din tara mai ales in Bucuresti si deloc in cadrul formatiunilor chinologice existente pana in 1998
Caracteristicile morfo-fiziologice ale raselor de caini ciobanesti romanesti mioritic si carpatin precum si dezvoltarea chinologiei nationale de dupa 1998 au facut imperios necesare aparitia si dezvoltarea unor studii, concepte, tehnici si metode de lucru noi sub acest aspect. In acest sens, Universitatea de Stiinte Agricole si Medicina Veterinara din Bucuresti, prin intermediul FMV Bucuresti a inceput odata cu anul 1998 o colaborare pe multiple planuri cu Clubul National de Caini Ciobanesti din Bucuresti – CNCCR in vederea realizarii in comun a procesului de omologare internationala a celor doua rase nationale.
A fost aleasa aceasta organizatie datorita specificului activitatii sale non profit, a scopului sau legat de omologarea celor doua rase, a caracterului sau unic la data repectiva fiind singurul organism chinologic din Romania unic specializat in aceste 2 rase, dar si datorita nominalizarii oficiale venite din partea Ministerului Agriculturii si Alimentatiei - MAA prin ordinul 17178/1998 , ordin prin care acesta recunoaste CNCCR ca fiind „unicul organism abilitat sa se ocupe de toate problemele legate de rasele de caini ciobanesti romanesti in plan intern si international .”
In urma vizitei oficiale a presedintelui in exercitiu la acea data a Comisiei de Omologari si Standarde a Federatiei Chinologice Internationale - FCI, dr.Jean Maurice Paschoud, din dec 1998 in cadrul lucrarilor conferintei stiintifice conduse de domnia sa si desfaurate la sediul FMV pe aceasta tema a realizarii din punct de vedere stiintific a dosarelor de omologare internationala a celor doua rase de caini ciobanesti romanesti, impreuna cu membrii catedrelor FMV si ai conducerii CNCCR, s-au relevat o serie de apecte importante de urmarit in alcatuirea doarelor de omologare din punct de vedere medical si stiintific.
Concluziile trase atunci au fost puse in practica in cadrul Programului National de Selectie si Reproductie Dirijata realizat intre 1999 si anul curent de catre FMV- Bucuresti si CNCCR.
Din punctul de vedere al Clinicii de Chirurgie acest lucru s-a materializat prin urmatoarele apecte:
1. Punerea la punct a bazei tehnico-materiale si a tehnicilor de masurare a indicilor si parametrilor morfo-fiziologici la cele doua rase incepand 04.04.1998 dupa criteriile solicitate de catre FCI,in premiera nationala in Romania.
2. Crearea unor baze de date impreuna cu CNCCR legate de numarul si calitatea reproducatorilor autorizati de catre club si a produsilor lor. Aceste baze de date
s-au obtinut prin verificarea unui numar de 2675 exemplare apartinand ambelor rase din punct de vedere al existentei displaziei coxofemurale, a diverselor forme de rahitism, a heterocromiei oculare, a atrofiei retiniene progresive, a .formelor de epilepsie, etc .
3. Stabilirea unor metode de consiliere a proprietarilor si crescatorilor de astfel de caini cu privire la avantajele folosirii reproducatorilor autorizati si atestati de catre CNCCR, in vederea scaderii si a eliminarii factorilor de risc in ceea ce priveste aparitia si/sau perpetuarea unor maladii si boli cu transmisibilitate genetica.
4. Formarea unor linii de sange sub strict control medical in scopul eludarii frecventelor fraude intalnite sub acest apect in chinologia romana
5. Publicarea de articole stiintifice in presa de specialitate pentru popularizarea acestui program si a avantajelor sale prin extinderea si la celelalte rase de caini
6. Pregatirea, atestarea si reciclarea anuala a arbitrilor si candidatilor de arbitrii pentru cele doua rase de caini ciobanesti romanesti din cadrul CNCCR se face si cu participarea directa a unui reprezentant al catedrei in scopul ridicarii nivelului de pregatire teoretica si practica a acestora
1. Punerea la punct a bazei tehnico-materiale si a tehnicilor de masurare a indicilor si parametrilor morfologici la cele doua rase incepand 04.04.1998 in premiera nationala in Romania.
Prima incercare de standardizare a acestor doua rase naturale dateaza din anul 1984 cand membrii Facultatii de Medicina Veterinara din Iasi impreuna cu Centrul
National de Crestere, Selectie si Reproductie in Agricultura din subordinea Ministerului Agriculturii si Alimentatiei – MAA, filiala judetului Suceava a initiat la Suceava prima actiune de standardizare a raselor de caini ciobanesti romanesti mioritic si carpatin prin efectuarea unor masuratori pe un lot neprecizat de exemplare din acea zona geografica.
Din pacate desi cererea de inregistrare a acestor prime standarde a fost inregistrata, aprobata si publicata in Monitorul Oficial – ziarul oficial al Guvernului Romaniei, ea nu fost insotita si de textul acestor standarde, chinologii de la acea data necunoscand procedurile tehnice si juridice legate de inregistrarea unei atfel de documentatii.
Aceasta situatie delicata a necesitat implicarea ulterioara a FMV Buc in rezolvarea din punct de vedere stiintific a problemelor ridicate de restandardizarea corecta a acestor doua rase.
Prima restandardizare corecta din punct de vedere stiintific si chinotechnic a fost efectuata odata cu prima etapa a primului Campionat National organizat de catre CNCCR impreuna cu FMV in 04.04.1998, data cand membrii catedrei au efectuat masuratori zoometrice pe un ention de 436 de caini din ambele rase .
In baza rezultatelor acestor masuratori s-au intocmit si inregistrat de catre CNCCR la MAA primele standarde oficiale ale celor doua rase in conformitate cu cerintele FCI si normele OSIM.Astfel s-au masurat un numar de peste 36 de parametrii definitorii pentru rasa dintre care enumeram: inaltimea la greaban si la spate; lungimea botului, craniului, urechilor, gatului, trunchiului, membrelor anterioare si posterioare si oaselor ce le compun- jaretul,tibie, femur,etc si a cozii;angulatiile articulatiilor; rapoartele craniene; latimea botului, craniului, pieptului, toracelui si a zonei posterioare;lungimea, densitatea, gradul de acoperire, culoarea si tipul firului de par; modul de prindere si purtare in actiune si repaos a cozii; forma, dispunerea si culoarea ochilor si incidenta aparitiei heterocromiei oculare, a depigmentarilor pleoapelor, trufei si buzelor, si a prolapsului pleopei a-III-a; numarul, forma, culoarea si marimea unghiilor si procentajul si numarul de pinteni posteriori; forma si marimea amprenrei plantare /labelor; dantura ca numar si asezare,etc
2. Crearea unor baze de date impreuna cu CNCCR legate de numarul si calitatea reproducatorilor autorizati de catre club si a produsilor lor. Aceste baze de date s-au obtinut prin verificarea unui numar de 2675 exemplare apartinnd ambelor rase din punct de vedere al existentei displaziei coxofemurale, a diverselor forme de rahitism, a heterocromiei oculare, a atrofiei retiniene progresive, a .formelor de epilepsie, etc .
CONTROLUL DISPLAZIEI SOLDULUI
Consideram ca displazia de dezvoltare a soldului se realizeaza in anume conditii la anume indivizi de caini si ea reprezinta o inbcompleta dezvoltare a soldului (a articulatiei coxofemurale) ceea ce poate duce la o defectiune majora tradusa prin defecte de aplomb, durere si nu de putine ori a agravarii acestei situatii prin dezarticularea spontana a capului femural de cavitatea acetabulara aparand de aceasta data luxatia coxofemurala.
Displazia inseamna anomalia de dezvoltare pe de o parte a cavitatii acetabulare, pe de alta parte a capului si gatului femural articular proximal, sau o dezvoltare redusa a gatului femurului (portiunea dintre capul articular si corpul femural) in asa fel incat unghiul ce se formeaza intre suprafata articulara si verticalizarea femurului sa nu mai cuprinda 120-130grade si astfel sa apara o imperfecta cuplare a celor doua suprafete articulare una din partea coxalului celalta din partea femurului.
Iata ca de la inceput problema displaziei de sold se imparte in doua: o displazie de dezvoltare a cavitatii acetabulare care este numita DDH (development dyspasia
of za sip) sau o diplazie de col femural. Facem precizarea expresa ca aceasta afectiune este transmisa genetic, ca este semnalata la om si animale deopotriva si ca ea poate fi diagnosticata atunci cand este majora in primele zile de viata la ambele specii dar se manifesta la o varsta relativ inaintata pentru specia canina si anume intre (5-6 )–(11-12) luni
La caine, prin selectii repetate si consangvinizari repetate, atunci cand s-a incercat a se creea rase noi si a se obtine exemplare cu calitati deosebite au aparut frecvent si structuri defecte, structuri care se refereau in special la parti anatomice si fiziologice determinate de imperfectiuni ale matricei genetice, defecte cu caracter recesiv cu exprimare mai mult sau mai putin completa dar cel mai important cu
transmitere la descendenti.
Iata de ce pentru animalele care sunt diagnosticate cu displazie de sold este impetuos necesara pe langa repararea individuala pentru aceasta afectiune tradusa printr-o interventie chirurgicala sau un tratament conservator care nu de putine ori poate duce la rezultate de ameliorare semnificativa, acesta trebuie exclus de la reproductie iar medicul ce face interventia chirurgicala sau cea conservatoare ar trebui in mod obligatoriu sa castreze exemplarul respectiv indiferent de vointa proprietarului. Consecintele majore ale displaziei de sold la caine sunt traduse printr-o coaptare defectuoasa a capului femural in cavitatea acetabulara cu o evolutie rapida catre o artroza a acestei articulatii.
Semnele clinice ale displaziei de sold pot fi sistematizate in doua faze:
- o prima faza este determinata de durere in timpul miscarii (locomotiei) la sfarsitul perioadei de crestere, durere ce este insotita de o pozitie anormala a aplombului membrului afectat, tradusa prin departarea articulatiei grasetului de trunchi si apropierea jaretelor (tibio-tarso-metatarsiena) refuzul miscarilor ce solicita aceste articulatii cum ar fi mersul la trap, sarituri, oboseala accentuata si prematura.
-faza a doua apare in jurul varstei de doi ani, atunci cand artroza este deja prezenta, animalul refuzand in marea majoritate a timpului sa faca sprijin pe piciorul afectat iar la o inspectie atenta si fortarea articulatiei animalul prezinta durere vie.
Displazia poate fi diagnosticata de la o varsta amintita anterior(5-6 luni) atat clinic,cat si prin investigatii paraclinice si anume examenul radiologic.
Din punct de vedere al angrenajului intre cavitatea acetabulara si capul articular al femurului displazia de sold se imparte in 4 grade (de la 1 la 4) a caror gravitate creste in ordine numerica.
Criterii de selectie pentru evitarea displaziei de sold.
Printre criteriile majore de selectie in vederea evitarii acestei tare genetice se numara excluderea de la reproductie a animalelor diagnosticate prin examen radiologic cu displazie de sold.
Un alt criteriu este evaluarea gradului de risc genetic al unui reproducator efectuata asupra tuturor descendentilor acestuia, lucru foarte greu de rezolvat.
O problema majora o prezinta faptul ca displazia poate fi diagnosticata cu certitudine la o varsta de 12-18 luni timp, in care nu de putine ori masculul este folosit la reproductie iar la alegerea si selectia puilor aceasta boala nu se poate manifesta clinic cu certitudine in asa fel incat puiul sa poata fi eliminat.
Revenind la problema arzatoare a displaziei de sold, la exemplarele din rasele ciobanesc mioritic si carpatin facem precizarea ca selectia naturala care a facut sa dainuie si sa mentina aceste rase sute de ani, omul intervenind mai mult sau mai putin agresiv in potrivirea perechilor si selectia artificiala, a condus la exemplare sanatoase la care displazia de sold nu este manifesta.
Vorbind in continuare de selectia naturala putem face precizarea ca exemplarele
care eventual au fost purtatoare de aceasta maladie nu au putut face fata conditiilor naturale de mediu: inaltimile subalpine si alpine , dusmanilor oilor si a ciobanilor, tranhumantei in sine,iar in lupta cu salbaticiunile datorita faptului ca ele nu puteau sa stea bine infipte pe picioare atat in urmarirea dusmanului cat si in lupta propriuzisa cu acesta, erau rapuse.
Iata cum in mediul natural al acestor rase selectia naturala a actionat la nivelul pastrarii calitatilor fizice de forta, viteza, echilibru, agilitate, rezistenta dar mai putin la nivelul pastrarii caracteristicilor chinologice legate de aspectul exterior acest lucru fiind ca intotdeauna sarcina chinologilor.
Aceasta lipsa a gravei afectiuni despre care este vorba, displazia de sold ,poate fi confirmata la exemplarele inregistrate a celor doua rase de caini ciobanesti romanesti in cadrul CNCCR (Clubul National de Caini Ciobanesti Romanesti) in care au fost verificate cu ajutorul Clinicii de Chirurgie un numar reprezentativ de animale –peste 3000 in 5 ani de zile
Este necesar sa precizam ca la rasa ciobanesc romanesc mioritic a fost diagnosticat clinic si radiologic, ca manifestand displazie de sold de gradul 1 spre 2, un singur exemplar provenind din canisa de Brillantim , acesta fiind eliminat de la reproductie prin castrare.
La ciobanescul carpatin s-au intalnit pana in prezent 7 exemplare provenind din canisele de Humor, de Baltag, de Cimbru, in general din zonele Bucovinei de Nord si Bistritei.
Din pacate acesti crescatori nu fac parte din CNCCR si nu s-au putut lua masuri suplimentare de protectie a rasei decat de excludere de la reproductie si de urmarire si
diagnoticare a tuturor produsilor proveniti din aceste canise.
Tinand cont de faptul ca standardele acestor doua rase prevad o inaltime la greban minima, iar pentru inaltimea maxima limita nu este precizata aceste exemplare putand ajunge la inaltimi impresionante si datorita cresterii lor rapide intr-un timp relativ scurt trei pana la 6-7 luni, sunt detul de multe exemplarele care pot avea malformatii dobandite dar nu congenitale ale osaturii traduse prin sechele de rahitism care pot duce in final dupa o examinare succinta si mai putin competenta la un diagnostic fals de displazie de sold.
Pentru a intelege cat de greu se poate pune un diagnostic pentru displazia de sold putem aminti aici metoda germana de selectie si eliminare a exemplarelor cu displazie in cadrul rasei de caini Ciobanesc German conform careia ar fi nevoie de intrunirea unei comisii medicale formata din cinci specialisti care da examineze clinic si radiologic un anume exemplar. Animalul ar fi considerat cu displazie de sold daca trei din cei cinci specialisti opteaza pentru diagnostic de displazie si doi nu. Daca raportul este invers animalul ar fi considerat sanatos.
CONCLUZII
In incheiere putem afirama ca aceasta grava maladie frecvent intalnita la rasele selectionate de caini cum ar fi Ciobanesc German, Rotwailer, Doberman etc. nu este prezenta in cadrul celor doua rase de caini ciobanesti Romanesti si nu se impune introducerea in standardul raselor a obligativitatii controlului radiologic si clinic al exemplarelor inainte de selectiile pentru reproductie si concursurilor de frumusete.
3. Stabilirea unor metode de consiliere a proprietarilor si crecatorilor de astfel de caini cu privire la avantajele folosirii reproducatorilor autorizati si atestati de catre CNCCR, in vederea scaderii si a eliminarii factorilor de risc in ceea ce priveste aparitia si/sau perpetuarea unor maladii si boli cu transmisibilitate genetica.
Initiativa CNCCR de a introduce in premiera nationala, ca tipizat in activitatea de reproductie, contractul de monta – fatare a fost un pas important in marirea sigurantei in ceea ce priveste executarea montelor cu cainii inscrisi ca fiind genitori.Ideea inscrierii in acest tipizat a felului inseminarii : natural, artificial, ambele metode, a permis reprezentantilor catedrei noastre sa verifice si sa autentifice lipsa unor malformatii congenitale sau a unor tare ereditare inainte de executarea montelor la parteneri atunci cand ele aveau loc in clinica de ginecologie-obstetrica a FMV.
Reprezentantul CNCCR lua parte la controlul medical efectuat, certificand prin semnatura sa atat controlul partenerilor cat executarea montei alaturi de semnaturile proprietarilor. Inca din perioda de inceput proprietarul unui exemplar de ciobanesc romanesc este indrumat de catre club catre Clinica noastra pentru verificarea si inregistrarea parametrilor de crestere,stabilirea corecta a medicamentatiei de crestere si intretinere. La clinica proprietarul este informat depre avantajele si dezavantajele diverselor metode de tratament si profilaxie a bolilor si maladiilor specifice raselor canine de catre personalul calificat al clinicii si se face si verificarea primara cu privire la aceste maladii si malformatii cu transmie ereditara...
Reprezentantul Clinicii de Chirurgie explica deasemenea importanta actului din punct de vedere medical si stiintific prezentand proprietarului de caine ciobanesc romanesc intreg ciclul de activitati desfasurate in cadrul clinicii si ajuta atat animalul cat si proprietarul sa se familiarizeze cu prezenta medicului si a arbitrului evitand stresul tipic unei astfel de intalniri .Astfel s-a explicat si inteles mult mai usor una din problemele specifice ridicate in intretinerea exemplarelor rasei de ciobanesc romanesc mioritic si anume tendinta de aparitie a otitelor infectioase , ca urmare a incorectei curatiri si toaletari a pavilionului urechii.
O alta metoda adoptata in comun cu CNCCR de catre clinica de chirurgie a fost aceea de gasi modalitatile optime de reducere a aparitiei exemplarelor din rasa ciobanesc romanesc mioritic care nu au par pe bot si pe labe, fapt ce este considerat un defect eliminatoriu de la reproductie si care este foarte frecvent intalnit in canisele de Brillantim, de Radauti, de Casa Gheorghe Cretu, de Greycib dintre cele mai cunoscute, si la exemplarele provenind de la detinatori si crescatori ( ciobani ) neinregistrati de catre CNCCR din zona Moldovei si a Transilvaniei. Acest defect este coroborat uneori si cu alte defecte ca heterocromia oculara – canisa de Casa Gheorghe Cretu si/sau cu depigmentari masive ale ochilor si pleoapelor celelalte canise enumerate mai sus.
4. Formarea unor linii de sange sub strict control medical in scopul eludarii frecventelor fraude intalnite sub acest apect in chinologia romana
Prin activitatea de dirijare si control a reproductiei CNCCR, avand la dispozitie si mijloacele de stiintifice si tehnice de investigare si executare a inseminarilor artificiale puse la dipozitie de catre clinica de ginecologie - obstetrica a putut forma 67 linii de sange pe 3 generatii cunocute si fara consangvinizare si 17 linii de consangvinizare
destinate ameliorarii rasei. Totodata prin participarea reprezentantilor Clinicii de Chirurgie si ai CNCCR a crescut drastic increderea in aceste institutii si in calitatea performantelor lor pe fondul unei scaderi generale a increderii in activitatile de reproductie efectuate in celelalte organizatii chinologice in care abunda greselile si falsurile in declaratii in ceea ce priveste genitorii asa dupa cum reiese din nota ministrului agriculturii din anul 2000 sau prin compararea diverselor acte de origine eliberate pentru caini ciobanesti romanesti de organizatii neautorizate in acest sens de Guvernul Romaniei si recunoscute sau nu de FCI. Pentru a intelege cat de greu se poate pune in cadrul actualei miscari chinologice din Romania, exceptand CNCCR, un diagnostic corect pentru displazia de sold putem sa ne gandim doar la faptul ca se folosesc, atunci cand se folosesc, radiografii si adeverinte neverificabile pentru cainii prezentati, eliberate de medici nespecialisti. Desi credem noi, cel putin pentru selectia si eliminarea exemplarelor cu displazie in cadrul rasei de caini Ciobanesc German din Romania ar fi nevoie teoretic de copierea modelului german ( intrunirea unei comisii medicale formata din cinci specialisti care sa examineze clinic si radiologic un anume exemplar. Animalul ar fi considerat cu displazie de sold daca trei din cei cinci specialisti opteaza pentru diagnostic de displazie si doi nu. Daca raportul ar fi invers animalul ar fi considerat sanatos).
Din pacate inexitenta dorintei de colaborare cu clinicile de specialitate ale FMV au condus la aparitia unui numar foarte mare de produsi la celelalte rase cu grave malformatii genetice si de aceea consideram salutar acest exemplu de colaborare intre FMV, CNCCR si crescatorii si detinatorii de ciobanesti romanesti
Intre 1998 si 2003 dupa verificarea ,cu ajutorul acestor procedee, doar in cadrul FMV clinica de chirurgie a calitatilor de reproducatori a peste 1200 de exemplare de caini ciobanesti romanesti mioritici si carpatini, Cartea de Origine Romana COR - CNCCR a putut acorda recomandarea pentru reproductie R(++) si implicit a confirmat obtinerea titlurilor de Campion Romania a unui numar de 28 masculi si femele; recomandarea pentru reproductie dirijata R(-) unui numar de 400 de reproducatori masculi, si a exclus de la reproductie un numar de 120 de exemplare masculi ( pentru talie substandard, calitate si acoperire insuficienta a parului, heterocromie oculara, etc).
COR – CNCCR are inregistrate la acest moment in evidentele sale 2650 de exemplare de mioritici si 1234 de carpatini.Toti acesti caini au fost inregistrati dpdv chinologic incepand cu anul 1984.
Astfel au fost create pe baza acestor verificari a calitatii reproducatorilor un numar de linii de consangvinizare destinate excluiv ameliorarii raselor si un numar de 67 linii pe 3 generatii fara consangvinizare destinat realizarii cerintelor FCI pentru dosarul de omologare internationala.
5. Publicarea de articole stiintifice in presa de specialitate pentru popularizarea acestui program si a avantajelor sale prin extinderea si la celelalte rase de caini
In cadrul FMV în ultimul timp s-au dezvoltat ca o necesiate specializarile pentru animalele de companie in cadrul carora câinii ocupă primul loc.
Dacă la aceasta se mai adaugă şi faptul că Facultatea de Medicină Veterinară din Bucureşti a fost propusă pentru acreditare în Comunitatea Europeană şi pentru aceasta în programa de învăţămînt au apărut discipline noi pentru uniformizarea procesului didactic cum ar fi : Clinica animalelor de companie; se vede interesul crescut în ultima perioadă atât pentru specializarea medicilor pe problematic patologiei canine cât şi a unei discipline predate separat în acest domeniu.
La ultimul Congres Naţional de Medicină Veterinară numarul lucrărilor ce au avut ca subiect patologia animalelor de companie au ocupat peste 50% din totalul lucrărilor prezentate.
În prezent personalul didactic al Facultâţii este angrenat în realizarea unor proiecte de popularizare a patologiei animalelor de companie ale mass-mediei dintre care putem aminti : două emisiuni săptămânale cu caracter informativ şi publicitar şi două reviste cu caracter ştiinţific .
Pe lîngă toate acestea Facultate de Medicină Veterinară din Bucureşti patronează lunar sau bilunar seminarii legate de patologia animalelor de companie sponsorizante de firme de medicamente şi hrana pentru animale de companie unde sunt invitate să susţină conferinţe atât cadrele didactice din facultate căt si invitaţi din alte ţări cum ar fi : Ungaria, Belgia, Franţa, Slovacia, Austria, Polonia etc.
6. Pregatirea, atestarea si reciclarea anuala a arbitrilor si candidatilor de arbitrii pentru cele doua rase de caini ciobanesti romanesti din cadrul CNCCR se face si cu participarea directa a unui reprezentant al catedrei in scopul ridicarii nivelului de pregatire teoretica si practica a acestora
Inca din momentul initial al pregatirii viitorilor candidati de arbitrii si arbitrii interni si internationali ai CNCCR atestati pentru rasele de ciobanesti romanesti acestia parcurg un curs de pregatire si informare in cadrul clinicii de chirurgie care are rolul de a informa corect si de a pune la dispozitie un bagaj de cunostiinte stiintifice si medicale strict necesar in buna desfasurare a activitatii de arbitru chinolog autorizat pentru aceste 2 rase canine.
In cadrul reciclarilor si examenelor anuale de atestare arbitrii CNCCR trebuie sa parcurga un chestionar cu intrebari din domeniul anatomiei si patologiei canine alcatuit de catre specialistii clinicii.
In vederea cresterii interactivitatii relationale dintre Clinica de Chirurgie a FMV si CNCCR un membru al clinicii a fost atestat ca si arbitru intern si 2 membrii ca si candidati de arbitru pentru cele 2 rase inca din anul 1998
Canine hip dysplasia is a complex disease. It is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodeling and degenerative joint disease. The degree of involvement varies from minute changes in bone structure to total destruction of the hip joint. Investigators have searched intensively for genetic, chemical, and metabolic defects, but the cause has remained obscure.
Hip dysplasia affects humans and all other domestic mammals. In humans, 1.3 children in 1000 are affected. In dogs the prevalence may run over 50% in large dogs if control measures have not been practiced. Few data are available on the prevalence of hip dysplasia in other mammals, but it is thought to be low. The disease is undoubtedly rare in undomesticated animals.
No specific genetic pattern of inheritance has been demonstrated in this variable disease. It has been demonstrated that both genetic and environmental influences contribute to development, regardless of the species affected.(15,31, 32,40,74,76) Consequently, the disease has been designated as polygenic or multigenic.(28) As in most polygenic diseases, there are both major and minor causative factors. There is no evidence that a primary defect of bone exists but rather the disease is a failure of the muscles and other soft tissues to hold the hip joint in full congruity.(31,32) This is further supported by the fact that bony dysplasia can be increased, decreased, or prevented by controlling the degree of joint instability and incongruity.(53) No other malformations are associated with the disease.(79) A causal relationship between muscles and soft tissue defects or pathologic changes other than lack of muscle mass or strength has not been established.(40,41)
Experimentally, hip dysplasia may be produced in many ways.(43,56,74,76,87,88) These include any circumstances that contribute to an unstable hip joint, namely, adductor forces, lack of muscle strength, chemical relaxation of the pelvic soft tissues, traumatic injury to the hip joint, and overloading of the joint by weight. Hip dysplasia is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodeling and degenerative joint disease.
The general cause of hip dysplasia, when defined, must be broad enough to explain its development, not only in dogs, but also in all other affected animals. Many genetic and environmental factors can trigger events that bring about the condition secondarily.(74,77,79,88) Hip dysplasia, therefore, is not one disease but many diseases that result in common degenerative lesions of the hip joints.(77)
Hip dysplasia has been observed in cats (27,35) and in most breeds of dogs; however, it is a greater problem in some breeds(65) than in others. The true prevalence of hip dysplasia among breeds of purebred dogs is not known, but data from the Orthopedic Foundation for Animals (OFA) on the first 36,000 pelvic radiographs evaluated has given insight into answering this question (Table 83-1).
The percentage of dogs of various breeds affected by hip dysplasia is not a true representation of the prevalence of the disease in these breeds because radiographs depicting obvious dysplasia were screened by referring veterinarians and not submitted. Therefore, the overall prevalence of hip dysplasia is higher than that represented in the analysis (Table 83-1). The rankings of the breeds are consistent with those obtained previously from smaller populations.(36) All breeds were screened in a similar manner.
Table 83-1 Pelvic Radiographic Diagnosis
Body Size
The breeds with the lowest prevalence of hip dysplasia are near the size of the ancestral dog. The bones are small in diameter and smooth, the feet are small and well arched, and the shape of the head is long and narrow.
The giant breeds with the highest prevalence of hip dysplasia are two to three times larger than the ancestral dog. Their bones are coarse and large in diameter, with prominent protrusions and depressions. The feet are large and splayed, and the head is wide and oversized.
Body Type
In general, the body conformation of the breeds with the lowest prevalence of hip dysplasia is slender and trim. The skin is thin, smooth, and stretched tightly over the underlying tissues. The muscles are prominent, hard, and full-bellied. At dissection in these breeds, the skin and subcutaneous tissues and fascia rarely contain over 1% to 2% fat by weight. The joint ligaments are well developed; the fibers are coarse, closely packed, and relatively free of fat. The well-formed pelvic and thigh muscles are attached to broad, coarse tendons that are attached securely to the bones. These dogs are fleet-footed and well-coordinated in their movements.
Of the high-risk group, the four breeds of the giant type are not only two to three times the size of the ancestral dog, but their body conformation is heavy, round, and stocky. Acromegalic characteristics are present to some extent in all four breeds. Fat is abundant in the subcutaneous and fascial spaces and commonly accounts for 5% to 10% of the weight of the soft tissues of the hindquarters. In comparison with the low-dysplasia group, the muscles are less prominent and less developed. Fat is infiltrated into the tendons and ligaments. The fibers of these two structures are smaller in diameter than those of the low-risk group. The gait of the giant breeds is less graceful and slower than that of the smaller breeds.
Growth Pattern
Breeds with the highest prevalence of hip dysplasia grow and mature more rapidly than those in the low-risk group. Starting at birth, this group gains rapidly. The pups of these breeds are aggressive eaters, both as they nurse and as they take supplemental food. In a study involving 222 German shepherds, 63% of the dogs that weighed more than the mean of this group at 60 days of age were dysplastic at 1 year of age, whereas only 37% of those less than the mean became dysplastic. The same rapid rise in weight in other breeds of the group at high-risk for dysplasia has been observed.(63)
Hip dysplasia has not been reported in the wild undomesticated carnivorous animals, such as wolves and foxes. A study of their pattern of growth found that the pups were slow-growing and late maturing. The young pups were whelped in dens. As newborns, they received their nourishment by nursing during the first few weeks. When more food was required, the mother killed rodents and either brought them to the den or ate the animal where it was killed and then returned to the den where the ingested rodents were regurgitated for the young to eat.(61) Young carnivores were quite mature and 6 to 10 months old before they began to hunt. The amount of food available for the growing members of a litter was limited. This caused the young to mature slowly and remain thin and light for their body size. Such an environment favored the completion of ossification and developmental maturity of the joint before the hips could be subjected to possible injury, incongruity, or subluxation from excessive extrinsic forces (e.g., excessive body weight) (65,69)
Genetic Influences and Heritability
Few genes analyzed thus far directly affect osseous structures.(17) The shape of bones reflects changes by biomechanical stresses.(15)
In the dog no clear-cut pattern of inheritance has been recognized.(23,28,30) This means that many genes are affected, and polygenic traits are subject to environmental modifications. New data have substantiated these findings.(29)
The spread of hip dysplasia centers around the genetic transmission and heritability of a particular body size, type, conformation, movement, growth pattern, and temperament. This conclusion is based on the facts that the prevalence of hip dysplasia is approximately the same in a number of breeds with similar body characteristics and there is no gene flow between these purebred breeds. Since these facts must be respected, biomechanical and environmental factors associated with certain body conformation and size must be considered as causes.(69)
Critical evaluation of the heritability of hip dysplasia has been made in the German shepherd in 244 offspring from 54 full subfamilies. In one report, "heritability was defined as a property not only of the character (trait) but also the population and the environmental circumstances to which individuals are subjected. Heritability, because it represents the proportion of the total phenotypical variance, receives the attributes of a positive number which may range from 0 to 1.0 in magnitude".(29) On this scale and based on evaluations of radiographs from 2 year-old dogs, the heritability was given an average estimate of 0.25. The conclusions were that canine hip dysplasia be termed a moderately heritable diseased.(30)
In a study involving 236 German shepherds, it was demonstrated that the most reliable way to eliminate canine hip dysplasia was through the establishment of "pedigree depth," that is, by the use of ancestral lines of dogs radiographically free of hip dysplasia.(33)
Results of controlled breeding programs in Sweden further indicated that the prevalence of hip dysplasia in the German shepherd was substantially reduced by mating only dogs with radiographically normal hips.(7,50) Similar decreases in prevalence have occurred in another controlled breeding program in a colony of guide dogs (Seeing Eye, Inc. Morristown, NJ).
In another account, with 584 progeny in a closed colony of German shepherds, it was shown that the prevalence of hip dysplasia was noticeably reduced by selectively breeding dogs proved radiographically to have normal hips at 1 year of age or older. In 3-1/2 years the incidence of hip dysplasia was lowered from 39% to less than 17%.(64) The male dogs in this colony had a wide variation in their ability to transmit normal hips to their progeny. For example, only 8.7% of the progeny of one dog with radiographically normal hips at 2 years of age developed hip dysplasia, whereas 37.8% of the pups of another dog with similar radiologic evaluation mated to the same bitches developed hip dysplasia.(20)
Environmental and Man-Made Influences
Embryologically, articular joints are differentiated as units in situ from a mass of skeletal mesenchyme.(90) Development progresses normally in each joint as long as there is full congruity between the parts. The congruity remains as long as the supporting tissues are strong enough to withstand the mechanical or physiological factors that tend to pull them apart.(77)
In humans, intrauterine stress has been cited as contributing to hip dysplasia, particularly if the fetus is positioned with the legs in adduction and extension.
Hip dysplasia in humans is rarely associated with teratology abnormalities. Other hip abnormalities distinctive from dysplasia, however, are frequently associated with such deformities as clubfoot, hyperextension of the knees, spinal deformities, arthrogryposis multiplex, and chondro-osteodystrophy.(22)
In the young child, the position of the legs during infant care is found to be very important to normal hip development.(71,73,75) Abduction and flexion of the legs has a stabilizing effect on the hip joints. The square diaper favors greater abduction of the legs than does the three cornered diaper. The Bantu baby, who is carried with its front side bound to the mother's back with its legs in acute abduction and flexion, seldom has abnormal hip joints.(71,75) In contrast, the Navajo Indian baby, who spends its first years of life strapped to a cradleboard with the legs in abduction and extension, has a high rate of hip joint instability.(70)
Other factors such as femoral anteversion and spastic shortening of the psoas muscle have been shown to favor acetabular dislocation when the leg was extended.(44) These observations indicate that both environmental and hereditary influences are important.(28,42)
In the dog, the hip joints are normal at birth.(43,68) The long bones of the pup are short during prenatal life, and mechanical stresses that bring about dislocation of the femoral heads are minimal. Teratologic abnormalities of the joints are rare in the dog, except for congenitally dislocated elbows and an occasional clubfoot deformity. Congenital malformation of the hips is also rare.
Extrauterine Influences
EARLY WEIGHT GAIN
In 222 German shepherds born consecutively, 100 were dysplastic, and the prevalence of hip dysplasia at 1 year had a direct correlation with their weight at 60 days of age. The heavier dogs, that is, the heaviest males and heaviest females at 60 days of age, had the highest incidence of hip dysplasia at maturity.(63) (See Fig. 83-2.)
These data suggested a number of indirect genetic factors influencing the rate of hip dysplasia. The aggressiveness in nursing may be inherited, as may be the quality and quantity of the supporting tissues around the hip joint. It was concluded that when growth, gain in weight, and nursing aggressiveness exceeded the strength of the supporting tissues, subluxation and hip dysplasia occurred.(63)
The first subluxating stress on the hips occurs when the pup supports itself while nursing, and the hindlegs are in forceful adduction and extension. The heaviest pups were the more aggressive, worked the hardest while nursing, and spent the most time feeding.(63)
PELVIC MUSCLE MASS
Data indicate that here is a positive correlation between the amount of pelvic muscle mass and the prevalence of hip dysplasia. Of three large breeds of dogs, the greyhound is relatively free of hip dysplasia; over half of the German shepherds are affected with hip dysplasia, and nearly all the July foxhounds are dysplastic.(69)
These data further emphasize that hip dysplasia encompasses biologic height, weight, and muscle bracing. The builder, before architecture was a science, learned that when the height of a structure was doubled, the bracing had to be tripled or the structure would fall of its own weight.(82) This basic rule, learned many years ago, illustrates clearly why a low foot stool fits solidly on the floor and the tall stool of the same area wobbles when supporting weight.(82) Similarly, it has been found that dogs less than 30.5 cm in height and less than 11.3 kg in weight (dachshund) are relatively free of hip dysplasia. On the other hand, at least half the large dogs, those 34 kg or more in weight and more than 50.8 cm in height, are affected with dysplasia.(66)
MUSCLE MYOPATHIES
All newborn mammals, including human infants, undergo many metabolic changes during their transition from intrauterine to extrauterine life. The muscle tissues are relatively immature both anatomically and biochemically at birth. Lack of muscular maturation in the newborn influences the manner in which the newborn responds to function. This immaturity accounts for the failure of many mammals, including the human, dog, and cat, to walk at birth.(88)
There is evidence that the wide range of acetabular and femoral changes occurring in hip dysplasia is the consequence of joint laxity. The possibility that this may be associated with or influenced by the rate of muscle maturation has not been explored. The rate of muscle maturation may be an inherited factor.(12,43) Consequently, the degree of subluxation in the young may be influenced by subnormal muscular function. In humans, the possibility of iliopsoas muscle spasm in the infant has been explored. (41,44)
In the adult dog, the light microscope was used to examine histologically the individual pelvic muscles associated with hip joint motion. Evidence of muscle disease was not recognized. In dogs with advanced hip dysplasia and associated osteoarthritis, atrophy of the pelvic muscles was present but changes such as muscular necrosis, inflammation, and extensive fibrosis were not found.(66,69)
One observer suggested that in young dogs with developing dysplasia, the pectineus muscles were in spasm and contained a degenerative lesion.(4) The pectineus muscle (an adductor), when in spasm, was thought to favor forcing the femoral heads out of the acetabula. This observer further suggested that if the pectineus were cut in the dog at an early age, the occurrence of hip dysplasia would be drastically lowered.(4)
A causal relationship between the pectineus muscles and hip dysplasia was not established in an experiment using the pelvic muscles from Labrador retrievers, German shepherds, Alaskan malamutes, and beagles.(40) Pectineus muscles in these dogs with both normal and dysplastic hips were examined and compared. The relationship between pectineus muscle abnormality and hip dysplasia remains undefined. The pectineus muscles from some young pups showed both hypotrophic and hypertrophic changes. It was suggested that the alterations seen in the pectineus muscles of dysplastic dogs probably represented secondary manifestations associated with a disease of developing hip joints (hip dysplasia).(4,12) The available evidence does not support the concept that abnormal pectineus muscle behavior is a cause of hip dysplasia. (39)
Developmental myopathy with type II fiber hypotrophy has been described in the pectineus muscles of very young dysplastic German Shepherds These investigators failed to establish a relationship between this muscle change, joint laxity, and dysplasia but have suggested the possibility of such a relationship. In their experiments using an enzyme stain, the small fibers stained as type I (white) and the large fibers as type II (dark). They considered the differentiation between small and large fibers in young dogs to be a myopathy. No myopathies were present in either the normal or dysplastic adult dogs in their study.(12) This change in the young dog resembles muscle fiber hypotrophy, which follows the cutting of the nerve to a muscle. These hypotrophied muscles become functional again and the fibers become normal in size when the nerve unites and use is restored.(34) Atrophied muscle due to a severed nerve and immature muscle are similar in appearance. (34)
Metabolic Influences
SEX
In humans, the female is affected with hip dysplasia four to eight times more often than the male.(22) In the dog an equal number of females and males are affected. The reasons for this difference have not been explained. Of 100 dysplastic German shepherds at the Armens Hund Skula (Sweden), 49 were males and 51 were females.(63)
CHEMICAL AND HORMONAL INFLUENCES
Pelvic tissue relaxation is a well-known physiological phenomenon that occurs during the terminal phase of pregnancy in mammals. This reaction has been associated with the female hormone, estrogen. Experimentally, this reaction has been studied by injecting ovarian extracts into dogs to produce pelvic tissue relaxation resembling that seen at the termination of pregnancy. The specific polypeptide hormone that is commonly used is called relaxin. Male and spayed and virgin females when "primed" with estrogen before relaxin was administered responded sufficiently to relax pelvic tissues around the hip joints.(43,55)
The urine of newborns was examined to see if there was a correlation between high estrogen levels and the unstable hip. From the first tests, it appeared that such a correlation existed, but the use of more refined tests failed to verify these findings. (1,3,81) The conclusion is that hormonal influence is not associated with the development of congenital hip dysplasia in humans or animals.(1,3,71,81)
In the dog it has been possible to increase the incidence of hip dysplasia by giving relaxin to newborn pups and to produce hip dysplasia in the greyhound. (18,43,51,55) "It does not prove, however, that estrogens have anything to do with etiology and pathogenesis of spontaneously occurring hip dysplasia."(19) There is no evidence that estrogen levels within the biologic range have a relationship to the incidence of hip dysplasia in dogs.(19,52,55,81)
Defective protein biosynthesis of collagen was suggested as a cause for increasing articular cartilage degradation in osteoarthritic joints. Soluble collagen was reported to be found in the acetabular cartilage of dysplastic dogs, while predominantly insoluble collagen was present in dogs with normal hip joints. It was not possible to relate these changes to hip dysplasia or to osteoarthritis.(39,40)
Inborn metabolic errors of chemical or hormonal origin have not been found in human or canine hip dysplasia.(39,40,52,87)
DIET
A variety of nutritional and mineral supplements have been used in attempts to alter or prevent the course of hip dysplasia in the dog. Diet has not affected the occurrence or course of the disease other than the mechanical effect of increased or decreased weight upon the hip joint.(66)
Prevention
In the child the development of hip dysplasia can be stopped and the condition can be reversed to a stable normal hip if it is discovered early before remodeling has begun. The key to treatment is the restoration of full congruity between the femoral head and acetabulum by placing the legs in an abductor-flexed position.(76,88)
In the young dog genetically conditioned to develop hip dysplasia, confinement to a small cage (1 m3) where the dog spends most of his time sitting on his haunches (abductor-flexed position) will prevent the development of hip dysplasia.(66,68) Surgical improvement of joint congruity can also be very beneficial.
Trimite mesajÎnapoiNu poți trimite un mesaj fără conținut!Nu este permisă folosirea de cod HTML in mesaje.Mesajul nu a fost trimis din motive de securitate. Va rugam sa ne contactati prin email pe adresa office@sunphoto.roMesajul nu a fost trimis din motive de posibil spam. Va rugam sa ne contactati prin email pe adresa office@sunphoto.roMesajul nu a fost trimis din motive de posibil spam. Ati trimis prea multe mesaje in ultimul timp.A apărut o eroare în timpul trimiterii mesajului. Vă rog încercați din nou.Mesajul a fost trimis.
Canine hip dysplasia is a complex disease. It is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodeling and degenerative joint disease. The degree of involvement varies from minute changes in bone structure to total destruction of the hip joint. Investigators have searched intensively for genetic, chemical, and metabolic defects, but the cause has remained obscure.
Hip dysplasia affects humans and all other domestic mammals. In humans, 1.3 children in 1000 are affected. In dogs the prevalence may run over 50% in large dogs if control measures have not been practiced. Few data are available on the prevalence of hip dysplasia in other mammals, but it is thought to be low. The disease is undoubtedly rare in undomesticated animals.
No specific genetic pattern of inheritance has been demonstrated in this variable disease. It has been demonstrated that both genetic and environmental influences contribute to development, regardless of the species affected.(15,31, 32,40,74,76) Consequently, the disease has been designated as polygenic or multigenic.(28) As in most polygenic diseases, there are both major and minor causative factors. There is no evidence that a primary defect of bone exists but rather the disease is a failure of the muscles and other soft tissues to hold the hip joint in full congruity.(31,32) This is further supported by the fact that bony dysplasia can be increased, decreased, or prevented by controlling the degree of joint instability and incongruity.(53) No other malformations are associated with the disease.(79) A causal relationship between muscles and soft tissue defects or pathologic changes other than lack of muscle mass or strength has not been established.(40,41)
Experimentally, hip dysplasia may be produced in many ways.(43,56,74,76,87,88) These include any circumstances that contribute to an unstable hip joint, namely, adductor forces, lack of muscle strength, chemical relaxation of the pelvic soft tissues, traumatic injury to the hip joint, and overloading of the joint by weight. Hip dysplasia is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodeling and degenerative joint disease.
The general cause of hip dysplasia, when defined, must be broad enough to explain its development, not only in dogs, but also in all other affected animals. Many genetic and environmental factors can trigger events that bring about the condition secondarily.(74,77,79,88) Hip dysplasia, therefore, is not one disease but many diseases that result in common degenerative lesions of the hip joints.(77)
Hip dysplasia has been observed in cats (27,35) and in most breeds of dogs; however, it is a greater problem in some breeds(65) than in others. The true prevalence of hip dysplasia among breeds of purebred dogs is not known, but data from the Orthopedic Foundation for Animals (OFA) on the first 36,000 pelvic radiographs evaluated has given insight into answering this question (Table 83-1).
The percentage of dogs of various breeds affected by hip dysplasia is not a true representation of the prevalence of the disease in these breeds because radiographs depicting obvious dysplasia were screened by referring veterinarians and not submitted. Therefore, the overall prevalence of hip dysplasia is higher than that represented in the analysis (Table 83-1). The rankings of the breeds are consistent with those obtained previously from smaller populations.(36) All breeds were screened in a similar manner.
Table 83-1 Pelvic Radiographic Diagnosis
Body Size
The breeds with the lowest prevalence of hip dysplasia are near the size of the ancestral dog. The bones are small in diameter and smooth, the feet are small and well arched, and the shape of the head is long and narrow.
The giant breeds with the highest prevalence of hip dysplasia are two to three times larger than the ancestral dog. Their bones are coarse and large in diameter, with prominent protrusions and depressions. The feet are large and splayed, and the head is wide and oversized.
Body Type
In general, the body conformation of the breeds with the lowest prevalence of hip dysplasia is slender and trim. The skin is thin, smooth, and stretched tightly over the underlying tissues. The muscles are prominent, hard, and full-bellied. At dissection in these breeds, the skin and subcutaneous tissues and fascia rarely contain over 1% to 2% fat by weight. The joint ligaments are well developed; the fibers are coarse, closely packed, and relatively free of fat. The well-formed pelvic and thigh muscles are attached to broad, coarse tendons that are attached securely to the bones. These dogs are fleet-footed and well-coordinated in their movements.
Of the high-risk group, the four breeds of the giant type are not only two to three times the size of the ancestral dog, but their body conformation is heavy, round, and stocky. Acromegalic characteristics are present to some extent in all four breeds. Fat is abundant in the subcutaneous and fascial spaces and commonly accounts for 5% to 10% of the weight of the soft tissues of the hindquarters. In comparison with the low-dysplasia group, the muscles are less prominent and less developed. Fat is infiltrated into the tendons and ligaments. The fibers of these two structures are smaller in diameter than those of the low-risk group. The gait of the giant breeds is less graceful and slower than that of the smaller breeds.
Growth Pattern
Breeds with the highest prevalence of hip dysplasia grow and mature more rapidly than those in the low-risk group. Starting at birth, this group gains rapidly. The pups of these breeds are aggressive eaters, both as they nurse and as they take supplemental food. In a study involving 222 German shepherds, 63% of the dogs that weighed more than the mean of this group at 60 days of age were dysplastic at 1 year of age, whereas only 37% of those less than the mean became dysplastic. The same rapid rise in weight in other breeds of the group at high-risk for dysplasia has been observed.(63)
Hip dysplasia has not been reported in the wild undomesticated carnivorous animals, such as wolves and foxes. A study of their pattern of growth found that the pups were slow-growing and late maturing. The young pups were whelped in dens. As newborns, they received their nourishment by nursing during the first few weeks. When more food was required, the mother killed rodents and either brought them to the den or ate the animal where it was killed and then returned to the den where the ingested rodents were regurgitated for the young to eat.(61) Young carnivores were quite mature and 6 to 10 months old before they began to hunt. The amount of food available for the growing members of a litter was limited. This caused the young to mature slowly and remain thin and light for their body size. Such an environment favored the completion of ossification and developmental maturity of the joint before the hips could be subjected to possible injury, incongruity, or subluxation from excessive extrinsic forces (e.g., excessive body weight) (65,69)
Genetic Influences and Heritability
Few genes analyzed thus far directly affect osseous structures.(17) The shape of bones reflects changes by biomechanical stresses.(15)
In the dog no clear-cut pattern of inheritance has been recognized.(23,28,30) This means that many genes are affected, and polygenic traits are subject to environmental modifications. New data have substantiated these findings.(29)
The spread of hip dysplasia centers around the genetic transmission and heritability of a particular body size, type, conformation, movement, growth pattern, and temperament. This conclusion is based on the facts that the prevalence of hip dysplasia is approximately the same in a number of breeds with similar body characteristics and there is no gene flow between these purebred breeds. Since these facts must be respected, biomechanical and environmental factors associated with certain body conformation and size must be considered as causes.(69)
Critical evaluation of the heritability of hip dysplasia has been made in the German shepherd in 244 offspring from 54 full subfamilies. In one report, "heritability was defined as a property not only of the character (trait) but also the population and the environmental circumstances to which individuals are subjected. Heritability, because it represents the proportion of the total phenotypical variance, receives the attributes of a positive number which may range from 0 to 1.0 in magnitude".(29) On this scale and based on evaluations of radiographs from 2 year-old dogs, the heritability was given an average estimate of 0.25. The conclusions were that canine hip dysplasia be termed a moderately heritable diseased.(30)
In a study involving 236 German shepherds, it was demonstrated that the most reliable way to eliminate canine hip dysplasia was through the establishment of "pedigree depth," that is, by the use of ancestral lines of dogs radiographically free of hip dysplasia.(33)
Results of controlled breeding programs in Sweden further indicated that the prevalence of hip dysplasia in the German shepherd was substantially reduced by mating only dogs with radiographically normal hips.(7,50) Similar decreases in prevalence have occurred in another controlled breeding program in a colony of guide dogs (Seeing Eye, Inc. Morristown, NJ).
In another account, with 584 progeny in a closed colony of German shepherds, it was shown that the prevalence of hip dysplasia was noticeably reduced by selectively breeding dogs proved radiographically to have normal hips at 1 year of age or older. In 3-1/2 years the incidence of hip dysplasia was lowered from 39% to less than 17%.(64) The male dogs in this colony had a wide variation in their ability to transmit normal hips to their progeny. For example, only 8.7% of the progeny of one dog with radiographically normal hips at 2 years of age developed hip dysplasia, whereas 37.8% of the pups of another dog with similar radiologic evaluation mated to the same bitches developed hip dysplasia.(20)
Environmental and Man-Made Influences
Embryologically, articular joints are differentiated as units in situ from a mass of skeletal mesenchyme.(90) Development progresses normally in each joint as long as there is full congruity between the parts. The congruity remains as long as the supporting tissues are strong enough to withstand the mechanical or physiological factors that tend to pull them apart.(77)
In humans, intrauterine stress has been cited as contributing to hip dysplasia, particularly if the fetus is positioned with the legs in adduction and extension.
Hip dysplasia in humans is rarely associated with teratology abnormalities. Other hip abnormalities distinctive from dysplasia, however, are frequently associated with such deformities as clubfoot, hyperextension of the knees, spinal deformities, arthrogryposis multiplex, and chondro-osteodystrophy.(22)
In the young child, the position of the legs during infant care is found to be very important to normal hip development.(71,73,75) Abduction and flexion of the legs has a stabilizing effect on the hip joints. The square diaper favors greater abduction of the legs than does the three cornered diaper. The Bantu baby, who is carried with its front side bound to the mother's back with its legs in acute abduction and flexion, seldom has abnormal hip joints.(71,75) In contrast, the Navajo Indian baby, who spends its first years of life strapped to a cradleboard with the legs in abduction and extension, has a high rate of hip joint instability.(70)
Other factors such as femoral anteversion and spastic shortening of the psoas muscle have been shown to favor acetabular dislocation when the leg was extended.(44) These observations indicate that both environmental and hereditary influences are important.(28,42)
In the dog, the hip joints are normal at birth.(43,68) The long bones of the pup are short during prenatal life, and mechanical stresses that bring about dislocation of the femoral heads are minimal. Teratologic abnormalities of the joints are rare in the dog, except for congenitally dislocated elbows and an occasional clubfoot deformity. Congenital malformation of the hips is also rare.
Extrauterine Influences
EARLY WEIGHT GAIN
In 222 German shepherds born consecutively, 100 were dysplastic, and the prevalence of hip dysplasia at 1 year had a direct correlation with their weight at 60 days of age. The heavier dogs, that is, the heaviest males and heaviest females at 60 days of age, had the highest incidence of hip dysplasia at maturity.(63) (See Fig. 83-2.)
These data suggested a number of indirect genetic factors influencing the rate of hip dysplasia. The aggressiveness in nursing may be inherited, as may be the quality and quantity of the supporting tissues around the hip joint. It was concluded that when growth, gain in weight, and nursing aggressiveness exceeded the strength of the supporting tissues, subluxation and hip dysplasia occurred.(63)
The first subluxating stress on the hips occurs when the pup supports itself while nursing, and the hindlegs are in forceful adduction and extension. The heaviest pups were the more aggressive, worked the hardest while nursing, and spent the most time feeding.(63)
PELVIC MUSCLE MASS
Data indicate that here is a positive correlation between the amount of pelvic muscle mass and the prevalence of hip dysplasia. Of three large breeds of dogs, the greyhound is relatively free of hip dysplasia; over half of the German shepherds are affected with hip dysplasia, and nearly all the July foxhounds are dysplastic.(69)
These data further emphasize that hip dysplasia encompasses biologic height, weight, and muscle bracing. The builder, before architecture was a science, learned that when the height of a structure was doubled, the bracing had to be tripled or the structure would fall of its own weight.(82) This basic rule, learned many years ago, illustrates clearly why a low foot stool fits solidly on the floor and the tall stool of the same area wobbles when supporting weight.(82) Similarly, it has been found that dogs less than 30.5 cm in height and less than 11.3 kg in weight (dachshund) are relatively free of hip dysplasia. On the other hand, at least half the large dogs, those 34 kg or more in weight and more than 50.8 cm in height, are affected with dysplasia.(66)
MUSCLE MYOPATHIES
All newborn mammals, including human infants, undergo many metabolic changes during their transition from intrauterine to extrauterine life. The muscle tissues are relatively immature both anatomically and biochemically at birth. Lack of muscular maturation in the newborn influences the manner in which the newborn responds to function. This immaturity accounts for the failure of many mammals, including the human, dog, and cat, to walk at birth.(88)
There is evidence that the wide range of acetabular and femoral changes occurring in hip dysplasia is the consequence of joint laxity. The possibility that this may be associated with or influenced by the rate of muscle maturation has not been explored. The rate of muscle maturation may be an inherited factor.(12,43) Consequently, the degree of subluxation in the young may be influenced by subnormal muscular function. In humans, the possibility of iliopsoas muscle spasm in the infant has been explored. (41,44)
In the adult dog, the light microscope was used to examine histologically the individual pelvic muscles associated with hip joint motion. Evidence of muscle disease was not recognized. In dogs with advanced hip dysplasia and associated osteoarthritis, atrophy of the pelvic muscles was present but changes such as muscular necrosis, inflammation, and extensive fibrosis were not found.(66,69)
One observer suggested that in young dogs with developing dysplasia, the pectineus muscles were in spasm and contained a degenerative lesion.(4) The pectineus muscle (an adductor), when in spasm, was thought to favor forcing the femoral heads out of the acetabula. This observer further suggested that if the pectineus were cut in the dog at an early age, the occurrence of hip dysplasia would be drastically lowered.(4)
A causal relationship between the pectineus muscles and hip dysplasia was not established in an experiment using the pelvic muscles from Labrador retrievers, German shepherds, Alaskan malamutes, and beagles.(40) Pectineus muscles in these dogs with both normal and dysplastic hips were examined and compared. The relationship between pectineus muscle abnormality and hip dysplasia remains undefined. The pectineus muscles from some young pups showed both hypotrophic and hypertrophic changes. It was suggested that the alterations seen in the pectineus muscles of dysplastic dogs probably represented secondary manifestations associated with a disease of developing hip joints (hip dysplasia).(4,12) The available evidence does not support the concept that abnormal pectineus muscle behavior is a cause of hip dysplasia. (39)
Developmental myopathy with type II fiber hypotrophy has been described in the pectineus muscles of very young dysplastic German Shepherds These investigators failed to establish a relationship between this muscle change, joint laxity, and dysplasia but have suggested the possibility of such a relationship. In their experiments using an enzyme stain, the small fibers stained as type I (white) and the large fibers as type II (dark). They considered the differentiation between small and large fibers in young dogs to be a myopathy. No myopathies were present in either the normal or dysplastic adult dogs in their study.(12) This change in the young dog resembles muscle fiber hypotrophy, which follows the cutting of the nerve to a muscle. These hypotrophied muscles become functional again and the fibers become normal in size when the nerve unites and use is restored.(34) Atrophied muscle due to a severed nerve and immature muscle are similar in appearance. (34)
Metabolic Influences
SEX
In humans, the female is affected with hip dysplasia four to eight times more often than the male.(22) In the dog an equal number of females and males are affected. The reasons for this difference have not been explained. Of 100 dysplastic German shepherds at the Armens Hund Skula (Sweden), 49 were males and 51 were females.(63)
CHEMICAL AND HORMONAL INFLUENCES
Pelvic tissue relaxation is a well-known physiological phenomenon that occurs during the terminal phase of pregnancy in mammals. This reaction has been associated with the female hormone, estrogen. Experimentally, this reaction has been studied by injecting ovarian extracts into dogs to produce pelvic tissue relaxation resembling that seen at the termination of pregnancy. The specific polypeptide hormone that is commonly used is called relaxin. Male and spayed and virgin females when "primed" with estrogen before relaxin was administered responded sufficiently to relax pelvic tissues around the hip joints.(43,55)
The urine of newborns was examined to see if there was a correlation between high estrogen levels and the unstable hip. From the first tests, it appeared that such a correlation existed, but the use of more refined tests failed to verify these findings. (1,3,81) The conclusion is that hormonal influence is not associated with the development of congenital hip dysplasia in humans or animals.(1,3,71,81)
In the dog it has been possible to increase the incidence of hip dysplasia by giving relaxin to newborn pups and to produce hip dysplasia in the greyhound. (18,43,51,55) "It does not prove, however, that estrogens have anything to do with etiology and pathogenesis of spontaneously occurring hip dysplasia."(19) There is no evidence that estrogen levels within the biologic range have a relationship to the incidence of hip dysplasia in dogs.(19,52,55,81)
Defective protein biosynthesis of collagen was suggested as a cause for increasing articular cartilage degradation in osteoarthritic joints. Soluble collagen was reported to be found in the acetabular cartilage of dysplastic dogs, while predominantly insoluble collagen was present in dogs with normal hip joints. It was not possible to relate these changes to hip dysplasia or to osteoarthritis.(39,40)
Inborn metabolic errors of chemical or hormonal origin have not been found in human or canine hip dysplasia.(39,40,52,87)
DIET
A variety of nutritional and mineral supplements have been used in attempts to alter or prevent the course of hip dysplasia in the dog. Diet has not affected the occurrence or course of the disease other than the mechanical effect of increased or decreased weight upon the hip joint.(66)
Prevention
In the child the development of hip dysplasia can be stopped and the condition can be reversed to a stable normal hip if it is discovered early before remodeling has begun. The key to treatment is the restoration of full congruity between the femoral head and acetabulum by placing the legs in an abductor-flexed position.(76,88)
In the young dog genetically conditioned to develop hip dysplasia, confinement to a small cage (1 m3) where the dog spends most of his time sitting on his haunches (abductor-flexed position) will prevent the development of hip dysplasia.(66,68) Surgical improvement of joint congruity can also be very beneficial.
Linkul catre documentul intreg cal.vet.upenn.edu/projects/saortho/chapter_83/83mast.htm