Asociación Mexicana de Ortopedia Maxilar A.C.



Reserach Scientist. Divition of Growth and Development Sciences
Depart. Of Othodontics University of New York and Priv. Practice in Toronto. Canada
Member. AAO, WFO. Canada

Malden M. Kuftinec

MLADEN M. KUFTINEC, DMD (Harv), Dstom, ScDb.
Prof. and Director Dept. of Orthodontics University of New York. USA.
Member. AAO. WFO.
Chairman and Coordinator U.S.A
Congreso Euro-Americano de Ortopedia Dentofacial AMOM 2001
Nov.29.2- Dic. 2 Ixtapa, México


USA Simposium Internacional de Articulación Temporomandibular y Trastornos Craneofaciales

Improved clinical use of Twin-block and Herbst as a resulradiating viscoelastic tissue forces on the condyle and fossa in treatment and long-term retention: Growth relativity

Understanding mechanisms of action for orthopedic appliances is critical for orthodontists who hope to treat and retain the achieved corrections in patients with initial Class II mandibular retrognathism.

That Knowledge can help orthodontists produce clinically significant bone formation and avoid compression at the condyle-glenoid fossa region. It also assists us to understand the differences between short-term and long-term treatment results. It was previously thought that increased activity in the postural masticatory muscles was the key to promoting condyle-glenoid fossa growth. Bey analyzing results from several studies, we postulate that growth modification is associated with decreased activity, which leads to our nonmuscular hypothesis. This premise has its foundation on 3 key specific findings: significant glenoid fossa bone kformation occurs during treatment that includes mandibular displacement; glenoid fossa modification is a result of the strech forces of the retrodiskal tissues, capsule, and altered flow of viscous synovium; observations that glenoid fossa bone formation takes place a distance from the soft tissue attachment. The latter observation is explained by transduction or referral of forces. Evidence is presented, therofore, that the 3 trigger switches for glenoid fossa growth can similarly initiate short-term condylar growth modifications because the 2 structures are contiguous.

These are displacement, several direct viscoelastic tissues may be highly significant and should be considered along with the standard skeletal, dental, neuromuscular, and age factors that influence condyle-glenoid fossa growth with orthopedic advancement. These biodynamic factors are also capable of reversing effects of treatment on mandibular growth direction, size, and morphology. Relapse occurs as a result of release of the condyle and ensuing compression against the newly proliferated retrodiskal tissues together with the reactivation of muscle activity.

To describe condyle-glenoid fossa growth modification, an analogy is made to a light bulb on a dimmer switch. The condyle illuminates in treatment, dims down in the retention period, to near base levels over the long-term. (Am J Orthod Dentofacial Orthop 2000;117:247-66). According to Aristotle, to be successful in theorizing is to realize the highest excellence, for practical applications. The purpose of this article is to improve dentofacial orthopedic tratments by describing a specific, nonmuscular hypothesis that explains histologically the way the condyle modifies beyond the level that can be explained by displacement alone (fig 1). As orthodontists pursue more ambitious treatments for their patients with mandibular retroghathism, they are increasingly turning to orthopedic appliances such as the Herbst, Twin-block, and other auxiliaries.

Part of the rationale is to augment edgewise appliances with fixed intermaxillary elastic and coils, although it has been reported that these edgewise systems also produce condylar growth modification. Some claim orthopedic appliances assist in the growth of mandibles and promote their use in this manner. As a responsibility to our patients to achieve the highest standards of treatment possible we need to understand exactly why and how those appliances work.

“Can we aid in the growth of condyles to a clinically significant degree?” This commonly asked question must always be qualified in terms of time before being answered intelligently.

This is because the clinically significant results of short-term treatment have been shown to be quite different from the findings on long-term stability. It is important to differentiate between 3 conditions that often everlap: normal condyle-glenoid fossa (C-GF) growth, orthopedic remodeling as a result of condylar advancement, and pathosis at the condyle. Pathologic adaptations show the C-GF region´s ability to be modified significantly (Fig 2). This type of growth is distinctly different from the limited shortterm growth modification observed with orthopedic displacement therapy.

Interpreting literature on C-GF modification can challenging, mainly because of the variation in the study designs, analyses, range of orthopedic appliances used, and compliance. A literature overview (Table I) classifies studies with continuous versus intermittent orthopedic displacement of the condyle and distinguishes between those conducted on animals and human beings.


Over the years, several theories have emerged attempting to shed light on condylar growth.
One of the earliest theories, the genetic theory, suggests the condyle is under strong genetic control like and epiphysis that causes the entire mandible to grow downward and forward.

Although this may by related more to development of the prenatal than postnatal condyle, the theory does indirectly question the effectiveness of orthopedic appliances in condylar growth as proposed by Brodie. Several long-term investigations actually showed clinically insignificant condylar growth modification after continuous mandibular advancement with a reasonable retention period in human beings although the initial treatment results appeared encouraging.

This leads to the conclusion that the general growth of the condyle appears relatively unalterable in long-term studies. In contrast, one similar study of primates showed significant condylar growth modifications over the long-term but only after retention periods that were far too long to be feasible for human beings.


A second hypothesis, based on the earliest available acute and blind EMG monitoring technique, suggests that hyperactivity of the lateral pterygoid muscles (LPM) promotes condylar growth.

Rees reported that other muscles and tendons, including those of the deep masseter and temporalis, also attach to the articular disk region. Attachments of the LPM to the condylar head or articular disk may be expected to cause condylar growth, but anatomic research has not found evidence that significant attachments actually exist. The LPM tendon is observed attaching. However, to the anterior boder of the fibrous capsule that in turn attaches to the fibrocartilage of the condylar head and nec anteriorly. At the same tisme, it is doubtful that initial hyperactivity could occur where the LPM muscle has been shortened by continuous mandibular displacement therapy.

By using LPM myectomy in rats, which may have disrupted condylar blood supply, Whetten and Johnston found little evidence that LPM traction had any pronounced effect on condylar growth.

More recently, permanently implanted longitudinal muscle monitoring techniques have found that the condylar growth is actually related to decreased postural and functional LPM activity.

This notion was also supported in human studies by Auf der Maur, Pancherz and Anehus-Pancherz, and Ingervall and Bitsanis that reported decreased muscle activity. The LPM hyperactivity theory brought forward by Charlier et al, Petrovic, and later espoused by McNamara however, was important in prompting further investigations in muscle-bone interactions. Petrovic studied the removal of the lateral pterygoid muscles and retrodiskal tissues “condylar frenum” for the effect on condylar growth. WHAT SPECIFICALLY AFFECTS THE GROWTH AT THE CONDYLAR HEAD?

A third hypothesis, the functional matrix theory, postulates the principal control of bone growth is not the bone itself, but rather the growth of soft tissues directly associated with it. Although this was supported in part by investigations testing the different growth and developmental responses between the condyle and epiphysis, there has been no explanation as to exactly how condylar growth would be stimulated. Thus, this theory´s validity has been questioned. One of the reasons was that there was little explanation of the specific mechanism by which the condyle was stimulated to grow. Endow and Hans presented and excellent overall perspective suggesting that mandibular growth is a compsite of regional forces and functional agents of growth control that interact in response to specific extracondylar activating signals. These extrinsic signals are the main focus of this article. They are the foundation of the growth relativity hypothesis.

Growth relativity refers to growth that is relative to the displaced condyles from actively relocating fossae. Growth is discussed relative to long-term retention results, rathe than short-term treatment outcomes that are clearly different. Viscoelasticity is conventionally applied to elastic tissue,

primarity muscles. In this article viscoelasticity refers to all noncalcified tissues. Specifically, viscoelasticity addresses the viscosity and flow of the synovial fluids,s the elasticity of the retrodiskal tissues, the fobrous capsule and other nonmuscular tissues including LPM perimysium, TMJ tendons and ligaments, other soft tissues, and bodily fluids. VERTICAL DIMENSION INCREASES AND DECREASED LPM ACTIVITY

The examination of soft tissues (fascina and tendons attachments, the perioral muscles of the lips, cheeks, and tongue) has also been undertaken. Investigations of active patients with chronic oral respiration with resultant skeletall maxillary constriction, together with increased lower vertical face height, showed significant effects caused primarily by disturbance in the equilibrium of soft tissue.

In addition to breathing pattern, a possibility of altered salivary flow and not necessarily of muscle activity alone has been implicated. Some studies suggested a form of condylar pull “stress” that resulted in a significant mandibular growth. Conversely, condylar compression demonstrated decreased C-GF modification, as shown by Graber and Joho. Interestingly, increases in the vertical dimension have accompanied decreased postural EMG masticatory muscle activity as demonstrated by Storey and others. With evidence of decreased muscle activity during the use of propulsive orthopedic appliances, one can ask the question: what is causing the observed growth modifications?

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