## 13 Discussion  
The prevalence of pectus excavation reported in the literature ranges from 1 in 1000 to 3400 [1,2]. Males are more frequently affected than females, with the male:female ratio ranging from 3:1 and 5:1 [2]. Our own sample also contained predominantly male patients (with a ratio of 5.5:1). As reported in the literature [3,4], the deformity was congenital in most cases (80.1%). Other authors have found a preponderance of asymmetric deformities, with a ratio of 1.5:1 [2,3]. This was also observed in our collective results (ratio 1.3:1). As described in previous studies [5, 6, 7, 8], the most common symptoms in our patients were dyspnea on exertion, lack of endurance, palpitations, early fatigue, and back pain. Over time, several theories have been proposed regarding the etiology of pectus excavation. It has been hypothesized that the overgrowth of costal cartilage causes indrawing of the sternum [2]. Several groups have performed histologic and biochemical studies of costal cartilage in patients with pectus excavation. The reports are inconsistent, but most describe degenerative changes and impaired chondrogenesis which may weaken the stability of the cartilage during the growth spurt [2,20, 21, 22]. Comprehensive studies of cartilage from pectus patients have also shown significantly lower levels of zinc and other trace elements that play a role in chondrogenesis [23]. Studies indicate that 5.3% of PE patients are affected by Marfan syndrome and 2.7% by neurofibromatosis type 1 [24,25], and approximately 20 genetic disorders have already been described to be associated with PE. A familial predisposition to chest wall deformities has long been known, with reported rates of 12-50%. Family trees suggest dominant inheritance with incomplete penetrance. Most cases are thought to be multifactorial [1,26], and single genes have been identified that may cause PE [27,28]. Analysis of gene expression in the costal cartilage of affected patients has not definitively elucidated the underlying genetic changes [23]. These disorders of chondrogenesis and their subsequent etiologically-based therapeutic approaches have had strong implications for issues of radical treatment based on the age of the patient. Early open techniques ([PERSON]: Lit) therefore focused on radical resection of the anomalous cartilage in the belief that by leaving the perichondrial sheaths intact, new cartilage would develop to stabilize the thorax and to allow for sufficient growth of the chest. Children were often operated on at an early age, and in many cases the resulting impairments caused typical forms of postcorrectional thoracic dystrophy. As a result, etiologic attempts at treatment were abandoned in favor of corrective methods based on biomechanical principles. These contemporary concepts also imply and explain a noticeable shift toward treating older patients for pectus correction at the time of cessation of their bone growth. In principle, modern methods of corrective surgery can be performed at any age, and in cases of severe and debilitating compression symptoms, surgery may be justified even in young children. Especially in these cases, surgical invasiveness must be kept to a minimum to avoid the risks mentioned above. Today, however, most authors recommend surgery at the end of the pubertal growth spurt [3] and to reshape rather than eliminate the malformed segments of the anterior chest wall. In addition, at an older age, the patients can decide for themselves whether or not to undergo surgery. The use of surgery too early carries the risk of developing new or recurrent deformities [3; 13; 29]. The mean age of our patient population at the time of surgery was 21.5 years (range: 4 years-60 years). This wide age range illustrates the applicability of the Hummer technique at any age. The Nuss procedure was developed for young adults and the implant should be placed just before the cessation of bone growth.