Condylar Hyperplasia Type 1

CH Type 1 creates mandibular prognathism (Figures 12.6.1a–c, 12.6.2a–c, 12.6.3a) usually beginning during pubertal growth causing the mandible to grow at an accelerated rate, occurring more frequently in females (2:1 ratio). Growth is self‐limiting but can continue into the early to mid‐20s before cessation (Obwegeser and Makek 1986; Wolford and LeBanc 1986; Wolford 2002; Wolford et al. 2002c, 2009, 2014c). Patients begin with a Class I skeletal and occlusal relationship and develop into a Class III relation, or start as Class III, but develop a worse Class III relationship as the mandible grows predominantly in a horizontal direction, although sometimes there can be a vertical growth vector (Obwegeser and Makek 1986; Wolford et al. 2009, 2014c). Asymmetry of the mandible can occur by CH Type 1B (Obewegeser’s hemimandibular elongation) (Obwegeser and Makek 1986) or CH Type 1A where one condyle grows at a faster rate than the opposite side. The mandible, dental midline, and chin become deviated toward the contralateral side; there is a Class III occlusion on the ipsilateral side and a crossbite on the contralateral side. Pubertal onset of CH Type 1 strongly suggests a hormonal etiology. However, trauma, infection, heredity, intrauterine factors, and hypervascularity have also been implicated as causative factors (Wolford et al. 2009, 2014c). Approximately 1/3 of CH Type 1 cases have a familial history (Gottlieb 1951).

Cone‐beam computed tomography (CBCT) and computed tomography (CT) scans usually show a relatively normal condylar architecture, although an increased length of the condylar head, neck, and mandibular body (Figure 12.6.3a). In the coronal view, the top of the ipsilateral condyle may have a more global morphology (Wolford et al. 2009, 2014c). The normal pubertal growth rate measuring from condylion to point B in females is a mean of 1.6 mm per year with 98% of growth complete by the age of 15 years. Males grow at a mean rate of 2.2 mm per year with 98% of growth complete by the age of 17–18 years (Riolo et al. 1974). An increased rate and prolonged growth may indicate active CH Type 1. Bone scans may not be of value in diagnosing CH Type 1 because the growth center (proliferative layer) is very narrow where the cellular activity is located (Chan and Leung 2018; Xiao et al. 2022) with minimal differentiation in the amount of isotope uptake compared to a normal joint. Serial radiographs (lateral cephalograms, cephalometric TMJ tomograms, etc.), dental models, and clinical evaluations are usually the best methods to determine if the growth process is active. Magnetic resonance imaging (MRIs) may show thin discs that may be difficult to identify. On the ipsilateral side, the disc can become posteriorly displaced. About 62% of these patients will show a displaced disc on the contralateral side from increased joint loading created by the ipsilateral CH (Wolford et al. 2009, 2014c).

Histologically, CH Type 1 condyles appear similar to normal condylar architecture, but in some cases, the proliferative layer may demonstrate greater thickness with cartilage‐producing cells prevalent at the lower level. In normal condyles, the cartilage formation from the proliferative layer and the replacement of cartilage by bone ceases by approximately age 20, where the marrow cavity is occluded from the remaining cartilage by the closure of the bone plate. The inability of this plate to close in the presence of an active proliferative cartilage layer may be a major etiological factor for prolonged growth in CH Type 1 (Wolford 2002; Wolford et al. 2002c, 2009, 2014c).

Treatment of this deformity depends on whether the condylar growth is active or quiescent. If jaw growth has stopped, orthognathic surgery can correct the asymmetry. TMJ surgery would only be indicated if disc displacement is present. If active growth is confirmed, then there are two predictable treatment options. The most predictable option is to perform a high condylectomy removing 4–5 mm of the top of the condylar head on the involved side(s), reposition the articular discover the remaining condyle using the Mitek anchor (Mitek Products, Westwood, MA, USA) technique (Wolford et al. 1995, 2002c; Mehra and Wolford 2001) and perform orthognathic surgery to correct the associated dentofacial deformity (Figure 12.6.3b) (Wolford and LeBanc 1986; Wolford 2002; Wolford et al. 2002c, 2009, 2014c). This will stop mandibular growth with stable long‐term functional and esthetic outcomes (Figures 12.6.1d–f and 12.6.2d–f) (Wolford and LeBanc 1986; Wolford 2002; Wolford et al. 2002c, 2009, 2014c). The recommended age for unilateral CH surgery is 15 years for females and 17 years for males. Performing a unilateral high condylectomy earlier during normal growth will result in arresting the growth on the CH side, but the normal side can continue to grow until normal cessation, with the potential of causing asymmetry by the mandible shifting toward the original CH side (Wolford et al., 2001a, 2001b; Wolford and Rodrigues, 2012a, 2012b; Mehra and Wolford 2016).

The second option is to delay surgery until growth is complete. However, since these cases often continue to grow into the early to mid‐20s, the surgery would be delayed until it is confirmed that the growth has stopped. The longer the asymmetric growth proceeds, the worse the facial deformity, asymmetry, and dental compensations affecting both the hard and soft tissues. This may increase the difficulties in obtaining an optimal functional and esthetic result, as well as adversely affect the patient’s psychosocial development.

Wolford et al. (2009) presented a study of 54 CH Type 1 patients with confirmed active growth divided into two groups. Group 1 (12 patients) only had orthognathic surgery without high condylectomy, and all grew into Class III skeletal and occlusal relationships. Group 2 (42 patients) treated with high condylectomies and orthognathic surgery maintained stable Class I skeletal and occlusal relationships, confirming the efficacy of this treatment protocol.

Condylar Hyperplasia Type 2

CH Type 2 is a unilateral mandibular benign condylar tumor (osteochondroma, also referred to as hemimandibular hyperplasia) (Obwegeser and Makek 1986; Wolford et al. 2002a, 2014b, 2014c) initiated at any age, although 67% of cases start between ages 10 and 20 years (Wolford et al. 2014b), creating unilateral vertical enlargement of the condyle and mandible, creating facial asymmetry (Wolford et al. 2002a, 2014b, 2014c). Common characteristics of CH type 2 include: (i) enlarged, elongated, deformed ipsilateral condyle (CH type 2A; Figures 12.6.4a–c, 12.6.5a–c, 12.6.6a), often with exophytic extensions of the tumor of the condyle (CH type 2B; (ii) increased thickness of the ipsilateral condylar neck; (iii) progressive increasing vertical height of the ipsilateral mandibular condyle, neck, ramus, body, symphysis, and dentoalveolus; (iv) an increased vertical height of the ipsilateral maxillary dentoalveolus; (v) transverse cant in the occlusal plane; (vi) coronoid process will be a normal size and displaced below the zygomatic arch; (vii) loss of ipsilateral antigonial notching with downward bowing of the inferior border of the mandible; (viii) the inferior alveolar nerve canal commonly positioned toward the inferior border of the mandible; and (ix) the chin vertically longer on the ipsilateral side and prominent in profile. Bone scintigraphy may show increased uptake, particularly, in the more active tumors. MRI will show the enlarged ipsilateral condyle (Figure 12.6.7a). Usually, the articular disc will be in position. The contralateral TMJ will commonly have an anteriorly displaced disc (76% of cases) and associated arthritic condylar changes created by the functional overload (Figure 12.6.7b). In CH type 2A, the articular disc can become posteriorly displaced on the ipsilateral side (Wolford et al. 2002a, 2014b, 2014c).

Histologically, CH type 2 will include a cartilaginous cap similar to that seen in normal growth cartilage, endochondral ossification, and cartilaginous islands in the subcortical bone. The cartilage islands are mini‐growth centers producing bone, causing enlargement of the condyle. As more bone is produced from these islands, additional separation occurs between them, making it more difficult to identify these islands histologically in larger and older tumors (Wolford et al. 2002a, 2014b, 2014c).

The highly predictable treatment protocol for CH Type 2 includes: Ipsilateral low condylectomy recontour the condylar neck (neo‐condyle), reposition the disc over the neo‐condyle, and reposition the articular disc on the contra‐lateral side, if displaced, with the Mitek anchor technique; orthognathic surgery to correct the maxillary and mandibular asymmetries; and an inferior border ostectomy on the ipsilateral side if indicated, with preservation of the inferior alveolar nerve, to reestablish vertical balance of the mandible (Figure 12.6.6b) (Wolford et al. 2002a, 2014b, 2014c). This treatment approach will allow removal of the tumor yet still use the enlarged condylar neck as the new condyle thus providing predictable and stable outcomes (Figures 12.6.4c, d and 12.6.5d–f). Other treatment considerations include condylar replacement with autogenous tissue grafts (not recommended by the author because of complications), or preferably, total joint prostheses, particularly if the articular disc(s) are non‐salvageable (Wolford et al. 2002a, 2014a).

Wolford et al. (2014b) evaluated 37 CH Type 2 patients. The study showed that 74% of the patients were females, 68% had onset between ages 10 and 20 years, left and right sides equally involved, and 76% had displaced discs on the contralateral side. The treatment protocol of single‐stage surgery for low condylectomy, disc repositioning with Mitek anchor, double jaw orthognathic surgery, and ipsilateral inferior border ostectomy when indicated, resulted in stable skeletal and occlusal outcomes, as well as significant improvement in TMJ pain, headaches, myofascial pain, jaw function, diet, and disability.