Condyle secondary cartilage-a misnomer /certified fixed orthodontic courses by Indian dental academy


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Condyle secondary cartilage-a misnomer /certified fixed orthodontic courses by Indian dental academy

  1. 1. Condyle- secondary cartilage-a misnomer INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. Cartilage It’s a type of connective tissue found on the ends of bones, which protects and cushions them, and absorbs the forcses transmitted throughout the body;a living tissue without a direct blood supply.
  3. 3. Facts about cartilage Mesenchymal in origin Consists of cartilage cells called chondrocytes and a ground substance Rigid and firm, but not hard Matrix is noncalcified and avascular Can grow both interstitially and appositionally Is covered by perichondrium but can exist without one. Uniquely Pressure tolerant.
  4. 4. Types of Cartilage and their Distribution Hyaline cartilage - 1. Costochondral Junctions 2. Articular surfaces of most joints 3. Some laryngeal cartilages 4. Walls of Trachea and large bronchi 5. Epiphyseal plate of long bones
  5. 5. Fibrocartilage – 1. Secondary cartilaginous joints or symphysis 2. Articular discs of Synovial joints 3. Shoulder and hip joints Elastic cartilage – 1. Auricle 2. Medial part of auditory tube 3. Epiglottis
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  7. 7. Methods of Ossification Endochondral Ossification Intramembranous Ossification
  8. 8. Steps in Endochondral Ossification Mesenchymal condesation at site of bone formation Differentiation of mesenchymal cells to form chondroblasts. Those on the surface form perichondrium Calcification of intercellular substance Formation of PRIMARY AREOLAE Invasion of calcified cartilaginous matrix by the PERIOSTEAL BUD
  9. 9. Formation of SECONDARY AREOLAE Differentiation of osteogenic cells to osteoblasts Formation of Osteoid and it’s subsequent calcification
  10. 10. Primary Vs Secondary Cartilage According to Stutzmann (1976) Primary Cartilage – exists in the axial skeleton, skull base and limbs; the dividing cells , the differentiated chondroblasts are surrounded by a cartilaginous matrix that isolates them from local factors able to restrain or stimulate cartilaginous growth
  11. 11. Secondary Cartilages – exist in the condylar and coronoid processes and sometimes in sutures;the dividing cells ,prechondroblasts, are not surrounded by a cartilaginous matrix and thus are not isolated from local growth modifications
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  13. 13. Origin of the term “Secondary Cartilage A common theory of the 18th and 19th century – that cartilage always preceded and turned into bone. That most bone was not transformed cartilage but formed by an independent process ( intramembranous ossification) – gave forth the revolutionary idea of “Secondary Cartilages “.
  14. 14. Schaffer’s Definition of Secondary cartilages Schaffer defined as secondary or accessory any cartilage forming after and separate from the primary cartilaginous skeleton. Examples – mandibular symphysis, condyle, coronoid process , ends of clavicle,on several bones of the cranial vault, cartilage participating temporarily in callus formation. Heterotrophic cartilage – secondary cartilages that are occasional abnormal malformations not typical of the site and species – eg.cartilage in human arterial walls.
  15. 15. Apart from differing times of first formation can one otherwise justify a separation of secondary cartilage from primary?
  16. 16. Fuch’s refutation of Secondary cartilage Argued that the relation between secondary cartilages and pressure / mechanical stimulation was inconsistent. Noted that the mechanical action of the condyle played no role in the formation of cartilage. That no criterion – whether of timing, histology or etiology precisely seperated the two categories. Contended that he had positive evidence that secondary cartilages were in fact primary. Claimed to have recognized a CHONDROBLASTEM at sites of futures secondary cartilage.
  17. 17. Key points of Fuch Mechanical forces cannot be seen to play a role in the origin of all secondary cartilages. There is overlap between the first appearance of primary and secondary cartilages. The secondary cartilages vary greatly in their histologic appearance. He called to attention the secondary nature of structures not included by Schaffer -
  18. 18. If the boundaries of Schaffer’s class of secondary cartilages so vulnerable, has the concept any value?
  19. 19. Differences between condylar and epiphyseal cartilages Biologic criteria Epiphyseal growth plates Condyle Origin Derivative of primordial cartilage Secondary cartilage formation on original membrane bone Growth Interstitial Peripheral in Fibrocartilage covering; proliferating cells are not cartilage cells but undifferentiated mesenchymal cells. Mechanical Stimuli Unresponsive Responsive
  20. 20. Biologic Criteria Epiphyseal Growth Plates Condyles Maturation Secondary ossification centers,final fusion and disappearance of all cartilage Conversion from hypertrophic to non hypertrophic state but not complete conversion to bone Histology Only the degenrative zone is mineralizing Whole hypertrophic area is in state of mineralization, structural organization is lacking Hormonal control Marked response to thyroxine deficiency,after final fusion no further response to growth hormone Minimal response to thyroxine deficiency.Mature condyle can be reawakened by growth hormone
  21. 21. Growth of Mandible
  22. 22. Effects of Orthodontic forces on the Mandible It is fair to say that controlling excessive mandibular growth is an important unsolved problem in orthodontics. If growth stimulation is defined as producing a larger mandible at the end of total growth period than would have existed without treatment; it is much harder to demonstrate a positive effect. The ultimate size of mandible in treated and untreated patients is remarkably similar. Muscle activity is not necessary to obtain growth modification. When the mandible is protruded or restrained, changes occur on the temporal as well as the mandibular side of the TMJ. The Herbst appliance is potentially the most effective of functional appliances in altering jaw growth probably because of its full time action, but is also rather unpredictable in terms of the amount of skeletal versus dental changes likely to be produced.
  23. 23. Acceleration of mandibular growth often occurs but a long term increase in size is difficult to demonstrate and,if it exists at all, is so small to be clinically significant. Functional appliances that are aimed at stimulating mandibular growth produce a highly variable response,but the growth acceleration that sometimes occurs can be useful
  24. 24. Tentative interpretation of the method of operation of functional appliances Functional Appliance Increased contractile activity of the LPM Intensification of repetitive activity of the retrodiscal pad Increase in growth stimulating factors
  25. 25. Increase in growth stimulating factors .Change in condylar trabecular orientation .Additional Growth of condylar cartilage .Additional subperiosteal ossification of the posterior border of The mandible Supplementary lengthening of the mandible
  26. 26. Functional Appliances believed to stimulate growth of condylar cartilage Class II elastics – believed to stimulate growth rate and amount of condylar cartilage; the stimulating action mediated primarily through the retrodiscal pad. Herren (L.S.U activator) – increase growth of condylar cartilage if the appliance is worn for 12 – 18 hours. Increased repititive activity of retrodiscal pad produces hypertrophy of condylar chondroblasts. Neither the functional regulator nor the Harvold activator are capable of altering the size of the mandible.
  27. 27. Condylar Cartilage before and after resection of LPM and retrodiscal Pad Resection of LPM and retrodiscal pad produces a significant slowdown of condylar cartilage growth rate Interruption of blood supply to the differentiating skeletoblasts;originating from the LPM may be the probable cause.
  28. 28. Demise of the Lateral Pterygoid Hypothesis Anatomic research has not found significant attachments of the LPM to the condylar head. Hyperactivity of the LPM during mandibular advancement thereapy is doubtful as the muscle actually shortens during this procedure.
  29. 29. New bone formation at the condyle was associated with decreased postural EMG activity in the LPM, masseter and digastric muscles This has led to the evolution of NON MUSCULAR HYPOTHESIS.
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  31. 31. Lateral Functional Shift of the mandible – effects on condylar cartilage thickness and proliferation Condyle on the side opposite the direction of shift is displaced anteriorly or protruded while the condyle on the side towards the shift is more stable positionally and is less likely to be retruded. Growth of the Mandibular Condylar Cartilage (MCC) adapts to its local functional biomechanical environment Thus differential changes in the metabolic activity of the MCC would be expected on the non protruded and protruded sides. Increased thickness of the MCC was followed by temporary increased proliferation of prechondroblastic cells on the protruded side.
  32. 32. Clinical implications Functional appliances which protrude or retrude the mandible and alter the local functional-biomechanical environment; can alter the growth of the MCC.
  33. 33. What exactly affects the growth of the condylar head? Genetic theory - suggests that condylar growth is strongly under the influence of genes. Functional Matrix Theory – though attractive could not satisfactorily explain how condylar growth would be stimulated by the growth of the soft tissues. Endow and Hans – mandibular growth is a composite of regional forces and functional agents of growth control that interact in response to specific extracoronal activating signals.
  34. 34. Growth Relativity Hypothesis – John Voudouris Based on three main foundations – Glenoid fossa promotes condylar growth with the use of mandibular advancement thereapy.
  35. 35. Growth Relativity Hypothesis Viscoelastic tissues anchored between glenoid fossa and the condyle insert directly into condylar fibrocartilage and affect its growth. Transduction of forces over the fibrocartilaginous cap of condylar head occurs as the viscoelastic tissues are stretched during mandibular advancement
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  38. 38. Light Bulb Analogy of Condylar growth and Retention The condyle lights up like a LIGHT BULB on a dimmer switch when it is continuously advanced. The reactivated muscle activity dims the light bulb and returns it to normal growth activity at the end of
  39. 39. Conclusions of John Voudouris Propulsive mandibular appliances such as herbst and twinblock cause growth modification of the condyle fossa region that involves– Displacement of mandible Viscoelastic tissue extension forces to the condyle Transduction of forces radiating beneath the fibrocartilage of the condyle and glenoid fossa. Condylar growth modifications occur relative to the glenoid fossa and not necessarily as an independent and isolated phenomenon. New bone formation at the condyle and glenoid fossa is associated with decreased postural EMG activity in the LPM, masseter and anterior digastric muscles. Fixed functional appliances (Herbst) produce consistent and reproducible condyle fossa changes compared with inconsistent results reported for removable functional appliances. Bone formation in the glenoid fossa and condyle was statistically significant compared to controls. Condylar response appears to be age determined.
  40. 40. Unique features of the mandibular condyle A major site of growth having considerable clinical significance. Not a pacesetting “master center” with all other regional growth fields subordinate to and dependant on it . The condylar cartilage has a secondary type of cartilage which developed because of changed functional and developmental conditions imposed on this part of the mandible. The condylar cartilage is not the pacemaker for the growth of the mandible. It functions to provide regional adaptive growth. The condyle performs a dual role – Provides pressure tolerant articular contact.
  41. 41. Makes possible a multidimensional growth capacity in response to ever changing developmental conditions and variations. The condylar cartilage does have some measure of intrinsic genetic programming.The cartilage cells are coded to divide and divide but extracondylar features are needed to sustain this activity. Condylar prechondroblasts are randomly arranged providing an opportunity for selected multidirectional growth potential in contrast to long bones.
  42. 42. Conclusions Secondary cartilages resemble each other in many respects eg-the clavicle and mandibular condyle have a similar layering and disorder in their growth cartilages. Secondary cartilages alike in many ways differ in others. No one secondary cartilage can represent all the properties in it’s class. The argument that secondary cartilage can validly be distinguished from primary one has hinged not only on morphology and histochemistry but on whether a mechanical factor underlies secondary chondrogenesis. Secondary cartilages have no manifest unity being in the first place non primary cartilages.They cannot be unified by a known mechanical etiology. Condylar cartilage can at best be considered a modified periosteum. Condylar cartilage is rather like an epiphysis at the end of a long bone but unlike the clavicle it has no secondary center of ossification.
  43. 43. Cartilage matrix production and chondrocyte enlargement as contributors to mandiular growth in Animals ( AJODO Oct.1991) Mandibular growth in length at the condyle results from Perichondral and Chondral components Matrix production depends on systemic influences while chondrocyte enlargement might be affected by local factors. One could speculate that chondrocyte enlargement rather than matrix production should be primarily affected by orthopedic appliances aimed at altering condylar growth though this aspect has never been investigated.
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