Tissue engineering strategies combining molecular targets against inflammation and fibrosis, and umbilical cord blood stem cells to improve hampered muscle and skin regeneration following cleft repair.

Cleft lip with or without cleft palate is a congenital deformity that occurs in about 1 of 700 newborns, affecting the dentition, bone, skin, muscles and mucosa in the orofacial region. A cleft can give rise to problems with maxillofacial growth, dental development, speech, and eating, and can also cause hearing impairment. Surgical repair of the lip may lead to impaired regeneration of muscle and skin, fibrosis, and scar formation. This may result in hampered facial growth and dental development affecting oral function and lip and nose esthetics. Therefore, secondary surgery to correct the scar is often indicated. We will discuss the molecular and cellular pathways involved in facial and lip myogenesis, muscle anatomy in the normal and cleft lip, and complications following surgery. The aim of this review is to outline a novel molecular and cellular strategy to improve musculature and skin regeneration and to reduce scar formation following cleft repair. Orofacial clefting can be diagnosed in the fetus through prenatal ultrasound screening and allows planning for the harvesting of umbilical cord blood stem cells upon birth. Tissue engineering techniques using these cord blood stem cells and molecular targeting of inflammation and fibrosis during surgery may promote tissue regeneration. We expect that this novel strategy improves both muscle and skin regeneration, resulting in better function and esthetics after cleft repair.

Pseudoaneurysm of the left ventricle with moderate left-to-right shunt.

A 79 year old man was admitted to the hospital with increased breathlessness and fatigue on minimal exertion, and this since a few weeks. Transthoracic and transesophageal echocardiography, followed by cardiovascular magnetic resonance imaging, demonstrated a cardiac pseudoaneurysm connected with both ventricular cavities resulting in an extracardiac left-to-right shunt, with even re-perforating into the right atrium. These findings were suggested to be sequels from an inferior myocardial infarction. Given the age and the complex characteristics of the aneurysm, conservative management was the treatment of choice. At one year follow-up the patient was still doing well.