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Biomedical subjects

M T Longaker

Publications and source records attributed to M T Longaker.

At least 163 records · Page 9Linked to original sources
PubMed1997

Reconstruction of breast asymmetry in Poland's chest-wall deformity using microvascular free flaps.

Poland's syndrome comprises a spectrum of chest-wall deformities affecting, to various degrees, the rib cage, the chest-wall muscles, the neurovascular structures of the ipsilateral arm, and the overlying breast. This study details our experience with nine female Poland's syndrome patients who had chest-wall and breast asymmetry corrected by microvascular free-tissue transfer. Nine female patients with Poland's chest deformity underwent 12 microvascular free flaps between 1989 and 1994. Donor sites for free-tissue transfer included eight transverse rectus abdominis flaps, two superior gluteal flaps, one inferior gluteal flap, and one contralateral latissimus dorsi flap. Recipient vessels were branches of the subscapular vascular axis in all patients. Patients' ages ranged from 18 to 47 years at the time of reconstruction. Chest-wall and breast asymmetry varied from accompanying severe pectus and rib cage deformities to isolated breast involvement. Complications were limited to a superior gluteal flap loss due to anomalous subscapular venous drainage. This patient underwent a successful second superior gluteal flap reconstruction utilizing the cephalic venous outflow system. Chest-wall and breast symmetry was restored in all patients. This study demonstrates that microsurgical reconstruction of chest-wall and breast asymmetry in Poland's syndrome yields excellent results with a high degree of patient satisfaction. Careful intraoperative assessment of the recipient vessels prior to flap transfer is mandatory. Because Poland's chest-wall deformity may include anomalies of the vascular system, preoperative vascular assessment with duplex ultrasonography should be considered in all patients, and use of preoperative angiography or venography in selected patients also appears justified.

Adolescent↗
PubMed1997

Blood supply of the Le Fort I maxillary segment: an anatomic study.

The vascular supply of the Le Fort I osteotomy segment was studied by utilizing standard latex injection techniques. Anatomic dissections in 10 fresh cadavers demonstrated interruption of the descending palatine arteries with preservation of the ascending palatine branch of the facial artery and the anterior branch of the ascending pharyngeal artery within the attached posterior palatal soft-tissue pedicle in all specimens following Le Fort I maxillary osteotomy. These ascending arterial branches entered the soft palate at a position approximately 1 cm posterior to the pterygomaxillary junction, which was disrupted during the Le Fort I maxillary osteotomy. Separate ink injections of total maxillary osteotomy segments confirmed vascular perfusion of the ipsilateral hemimaxillary segment by the ascending palatine artery. Thus vascular supply of the mobilized Le Fort I maxillary segment is by means of the ascending palatine branch of the facial artery and the anterior branch of the ascending pharyngeal artery in addition to the rich mucosal alveolar anastomotic network overlying the maxilla.

Arteries↗
PubMed1997

Gene expression of transforming growth factor beta-1 in rabbit zone II flexor tendon wound healing: evidence for dual mechanisms of repair.

The postoperative outcome of hand flexor tendon repair can be complicated by adhesions between the repair site and surrounding tissue. To date, the biology of hand flexor tendon wound healing remains controversial--both intrinsic (resident tenocyte) and extrinsic (tendon sheath fibroblast and inflammatory cell) processes may contribute to repair. Transforming growth factor beta-1 is a cytokine that plays multiple roles in wound healing but is also implicated in the pathogenesis of excessive scar formation. This study examines the activation of transforming growth factor beta-1 mRNA in a rabbit zone II flexor tendon wound-healing model. Forty New Zealand White rabbit forepaws underwent complete transection and repair of the middle digit flexor digitorum profundus tendon in zone II. Tendons were harvested at increasing time intervals (1, 3, 7, 14, 28, and 56 days) and analyzed by in situ hybridization and immunohistochemistry to determine the expression patterns of transforming growth factor beta-1. A small number of tenocytes exhibited expression of transforming growth factor beta-1 mRNA at baseline in nonwounded control tendon specimens. The surrounding tendon sheath in these control specimens also revealed low numbers of fibroblasts and inflammatory cells expressing transforming growth factor beta-1 mRNA. In contrast, flexor tendons subjected to transection and repair exhibited increased signal for transforming growth factor beta-1 mRNA in both resident tenocytes and infiltrating fibroblasts and inflammatory cells from the tendon sheath. These data demonstrate that (1) normal unwounded tenocytes and tendon sheath cells are capable of transforming growth factor beta-1 production, (2) this cytokine is activated in the tendon wound environment, as evidenced by mRNA upregulation, and (3) the upregulation of this cytokine in both "intrinsic" tenocytes and "extrinsic" tendon sheath fibroblasts and inflammatory cells supports dual mechanisms for tendon repair. Because transforming growth factor beta-1 is thought to contribute to the pathogenesis of excessive scar formation, the findings presented here suggest that perioperative biochemical modulation of transforming growth factor beta-1 levels may help limit flexor tendon adhesion formation.

Animals↗
PubMed1997

Studies in cranial suture biology: regional dura mater determines in vitro cranial suture fusion.

Craniosynostosis results in alterations in craniofacial growth that create cosmetic abnormalities and functional deficits, yet the biology underlying cranial suture fusion remains unknown. The purpose of the present study was to show that regional dura mater can induce suture fusion while in an organ culture system in cranial sutures programmed to remain patient. To accomplish this, we studied mouse cranial sutures, since in this model the posterior frontal suture (analogous to the human metopic suture) fuses in both in vivo and in vitro environments while all other sutures remain patent. We demonstrated that when mouse sagittal sutures (programmed to remain patent) were rotated or translocated to overlie the posterior frontal dura then grown in organ culture systems, suture fusion occurred. Twenty-four-day-old CD-1 mice (time when the posterior frontal suture was patent) were divided into three groups of 50 (n = 165: three groups of 50 cultured and three groups of 5 uncultured controls). Group A (unrotated control group) was characterized by a strip of posterior frontal and sagittal suture with underlying dural tissue grown in organ culture systems for up to 30 days and resulted in persistent patency of the sagittal suture and fusion of the posterior frontal suture in an anterior-to-posterior direction. Group B (rotated experimental group) was characterized by 180-degree suture rotation while in vitro and resulted in patency of the posterior frontal suture over the sagittal dura and fusion of the sagittal suture over the posterior frontal dura in a posterior-to-anterior suture direction. Group C (translocated experimental group) was characterized by translocation or shifting of sutures while in vitro and resulted in patency of the posterior frontal suture over the sagittal dura and fusion of the sagittal suture over the posterior frontal dura in an anterior-to-posterior suture direction. These data from the in vitro rotation and translocation experiments indicate that the "regional" posterior frontal dura determined in vitro cranial suture fusion. Molecular mechanisms behind this process are thought to involve inductive tissue interactions of the dural cells with the suture cells by means of growth factor-mediated signal pathways.

Animals↗
PubMed1997

The inferior retinacular lateral canthoplasty: a new technique.

Lateral canthoplasty is a useful method of restoring lower eyelid position and thereby protecting the ocular surfaces. The success of the lateral canthoplasty procedure depends on the proper analysis of periorbital anatomy. Newer lateral canthoplasty techniques have become progressively refined in an attempt to avoid the drawbacks and pitfalls of older procedures. We present the inferior retinacular lateral canthoplasty, developed to effectively address the problems associated with lower lid laxity and/or malposition. The inferior retinacular lateral canthoplasty is a versatile reconstructive procedure that also can be used as an adjunct to aesthetic surgery. The evolution of the inferior retinacular lateral canthoplasty from over 15 years of clinical experience is discussed.

Blepharoplasty↗
PubMed1997

Evolution of the lateral canthoplasty: techniques and indications.

Lateral canthoplasty is a useful method to restore eyelid function and to protect the ocular surfaces. The success of the procedure depends on the proper analysis of periorbital anatomy as it relates to the specific indication for lateral canthoplasty. We report the experience with 1565 lateral canthoplasties with emphasis on the evaluation of newer techniques that better address anatomic and functional requirements. Between 1981 and 1994, 1565 lateral canthoplasties were performed in 684 patients. Of these, 1369 "reconstructive" lateral canthoplasties were performed in 586 patients and 196 "cosmetic" lateral canthoplasties were performed in 98 patients. All operations were performed by a single surgeon (Jelks), and follow-up ranged from 1 to 14 years. The evolution of the operative technique for lateral canthoplasty has been toward an operation that corresponds with the anatomy of the individual. Indications for the procedure include lateral canthal dystopia, horizontal lid laxity, ectropion, entropion, lid margin eversion, lid retraction with or without soft-tissue deficiency, and aesthetic improvement. The types of procedures performed will be reviewed in detail. The evaluation of the newer forms of lateral canthoplasty as unique reconstructive tools and as adjuncts to aesthetic surgery will be discussed.

Adult↗
PubMed1997

Vascular lip enlargement: Part I. Hemangiomas--tenets of therapy.

Vascular lesions involving the lips pose a difficult problem for both the surgeon and patient. Their removal by surgery may result in greater disfigurement and impairment than the original lesion. When nonsurgical modalities fail, using a well-planned strategy of sequential procedures can provide excellent results. Many hemangioma patients require judicious serial debulking of excess tissue mass, whereas enlargement from port-wine lesions may require direct aggressive surgery. Over a 10-year period, 38 patients underwent surgery for treatment of vascular lip enlargement. In 27 patients, the lip deformities were caused by hemangiomas. The remaining 11 patients had macrocheilia associated with port-wine vascular malformations. This paper specifically addresses hemangiomas of the lips, tenets for their removal, and reduction strategies. Of the 27 patients with hemangiomas involving the lips, 12 had had some form of previous treatment including corticosteroids (4 patients), embolization (3 patients), laser (3 patients), and interferon (2 patients). All 12 of these patients had unsatisfactory results. Specific tenets for the surgical management of these patients are presented. The distribution of the facial hemangiomas was as follows: 15 patients had isolated involvement of the upper lip, 7 lesions involved the lower lip alone and 5 involved both upper and lower lips. Additionally, 10 of these lesions involved the cheek(s), nose, or chin to some degree. Six patients experienced some form of functional impairment before our evaluation including difficulty with eating or drinking, visual obstruction, and psychosocial problems. All operations were performed following several principles established by the senior surgeon (B.M.Z.). By following the tenets presented in this report, he has achieved near-normal lip form, giving the patient marked improvement in appearance and function.

Adolescent↗
PubMed1997

Vascular lip enlargement: Part II. Port-wine macrocheilia--tenets of therapy based on normative values.

Port-wine (capillary) vascular malformations that enlarge the lips (port-wine macrocheilia) are challenging reconstructive problems which, as a result, often go untreated. The surgical management of these lesions is not straightforward. Scarification by laser to diminish the discoloration has been performed with good results in some cases. However, laser treatment does little to correct three-dimensional tissue deformities such as macrocheilia, which must be addressed surgically. We present our experience with the treatment of port-wine macrocheilia in 11 patients over the 10-year period between 1983 and 1994. Basic principles for surgical and nonsurgical treatment of these patients are also discussed. Normative data about lip dimensions are important to surgical planning. We used 40 male and female volunteers, all less than 30 years of age, as a source for measuring normal lip dimensions, thereby creating a normative database. Preestablished points in the labial and perioral region were marked. Measurements were taken and then averaged. This information was used as a guide for surgical excision of large defects in some patients. In addition, in both the lower and the upper lip, if the opposite side is uninvolved, this database could serve as a template for reconstruction of the affected side. Between 1983 and 1994, 11 patients underwent surgery for port-wine macrocheilia. Of the 11 patients, 1 had previous treatment consisting of laser scarification. Four patients had port-wine vascular malformations involving the upper lip alone, four involved the lower lip alone, and three involved both lips. In six patients, other areas of the face and body were also involved. Our experience has led us to perform earlier surgical intervention than has previously been described for these patients. Basic reconstructive surgical principles and planning based on normative data and templates can lead to excellent results.

Adolescent↗
PubMed1997

Reduced expression of PDGF and PDGF receptors during impaired wound healing.

A series of studies has shown that application of platelet-derived growth factor (PDGF) to a wound enhances the process of wound repair, especially in animals with wound-healing defects. In the current study, we investigated the regulation of PDGF A and PDGF B and their receptors during wound repair in mice. Both ligands and both types of receptor were expressed in normal and wounded skin, whereby PDGF A and PDGF B proteins were found at different sites in the healing wound. Surprisingly, no significant induction of these genes was observed after skin injury in normal mice, and expression levels were similar at all stages of the repair process. To determine a possible role of endogenous PDGF in normal wound healing, we subsequently analyzed the regulation of PDGF and PDGF receptors during wound healing in healing-impaired animals. Genetically diabetic db/db mice showed a significant reduction in PDGF A and A-type receptor expression in nonwounded and wounded back skin. Furthermore, expression of the B-type receptor was also reduced during the repair process. Systemic glucocorticoid treatment caused a severe defect in wound repair that was accompanied by reduced expression of PDGF A and B and of the B-type receptor in the early phase of wound healing. These results provide an explanation for the beneficial effect of exogenous PDGF in the treatment of wound-healing disorders. Furthermore, our data suggest that a certain expression level of PDGF and its receptors is essential for normal repair.

Animals↗
PubMed1997

Studies in cranial suture biology: Part I. Increased immunoreactivity for TGF-beta isoforms (beta 1, beta 2, and beta 3) during rat cranial suture fusion.

The mechanisms involved in normal cranial suture development and fusion as well as the pathophysiology of craniosynostosis, a premature fusion of the cranial sutures, are not well understood. Transforming growth factor-beta isoforms (TGF-beta 1, beta 2, and beta 3) are abundant in bone and stimulate calvarial bone formation when injected locally in vivo. To gain insight into the role of these factors in normal growth and development of cranial sutures and the possible etiology of premature cranial suture fusion, we examined the temporal and spatial expression of TGF-beta isoforms during normal cranial suture development in the rat. In the Sprague-Dawley rat, only the posterior frontal cranial suture undergoes fusion between 12 and 22 days of age, while all other cranial sutures remain patent. Therefore, immunohistochemical analysis of the fusing posterior frontal suture was compared with the patent sagittal suture at multiple time points from the fetus through adult. Whereas the intensity of immunostaining was the same in the posterior frontal and sagittal sutures in the fetal rat, there was increased immunoreactivity for TGF-beta isoforms in the actively fusing posterior frontal suture compared with the patent sagittal suture starting 2 days after birth and continuing until approximately 20 days. There were intensely immunoreactive osteoblasts present during fusion of the posterior frontal suture. In contrast, the patent sagittal suture was only slightly immunoreactive. A differential immunostaining pattern was observed among the TGF-beta isoforms; TGF-beta 2 was the most immunoreactive isoform and was also most strongly associated with osteoblasts adjacent to the dura and the margin of the fusing suture. Since the increased expression of TGF-beta 2 during suture fusion suggested a possible regulatory role, recombinant TGF-beta 2 was added directly to the posterior frontal and sagittal sutures in vivo to determine if suture fusion could be initiated. Exogenously added TGF-beta 2 stimulated fusion of the ectocranial surface of the posterior frontal suture. These data provide evidence for a regulatory role for these growth factors in cranial suture development and fusion. Additionally, the intense immunostaining for TGF-beta 2 in the dura mater underlying the fusing suture supports a role for the dura mater in suture fusion. It is possible that premature or excessive expression of these factors may be involved in the etiopathogenesis of craniosynostosis and that modulation of the growth factor profile at the suture site may have potential therapeutic value.

Animals↗
PubMed1997

Type I (RI) and type II (RII) receptors for transforming growth factor-beta isoforms are expressed subsequent to transforming growth factor-beta ligands during excisional wound repair.

Transforming growth factor (TGF)-beta isoforms (TGF-beta 1, -beta 2, and -beta 3) regulate cell growth and differentiation and have critical regulatory roles in the process of tissue repair and remodeling. Signal transduction for TGF-beta function is transmitted by a heteromeric complex of receptors consisting of two serine/threonine kinase transmembrane proteins (RI and RII). We have previously shown that each TGF-beta isoform is widely expressed in a distinct spatial and temporal pattern throughout the processes of excisional and incisional wound repair. As the presence of TGF-beta receptors determines cellular responsiveness, we have currently examined, by immunohistochemistry, the localization of RI (ALK-1, ALK-5) and RII throughout repair of full-thickness excisional wounds up to 21 days after wounding. The expression of RI (ALK-5) and RII co-localized in both the unwounded and wounded skin and was present in the same cell types as TGF-beta ligands. However, immunoreactivity for TGF-beta receptors, throughout repair, occurred 1 to 5 days later than TGF-beta isoform immunostaining. This implies that the presence of TGF-beta ligands may up-regulate TGF-beta receptors for function and/or may reflect a lag due to local processing of latent TGF-beta. As observed for the immunohistochemical localization of TGF-beta isoforms in unwounded skin, RI and RII were expressed throughout the four layers of the epidermis, showing a wavy pattern of slight to moderate immunostaining, and hair follicles, sweat glands, and sebaceous glands were moderately immunoreactive. The extracellular matrix, fibroblasts, and blood vessels in the dermis were not immunoreactive. After injury, as observed for TGF-beta ligands, RI and RII expression was increased in the epidermis adjacent to the wound and the epithelium migrating over the wound was completely devoid of TGF-beta receptor immunoreactivity until re-epithelialization was completed by day 7 after wounding. The dermis was only slightly immunoreactive for RI and RII until day 5 when, immediately under the wound, immunostaining for fibroblasts, connective tissue cells, and newly forming vasculature began to increase and remained intense until day 14. Consistent with the role for TGF-beta in scarring, numerous fibroblasts, ostensibly active in the production of extracellular matrix components, continued to be slightly immunoreactive for RI and RII at 21 days. The ALK-1 (TSR-1) type I receptor, which binds both activin and TGF-beta, showed slight immunostaining early in repair (days 1 to 7) that progressively became more intense later in repair after day 10 and through day 21. This suggests that there may be a switch to a different type I receptor, implying different functions for the ALK-1 and ALK-5 receptors. The concomitant expression of TGF-beta isoforms and their signal-transducing receptors denote potential spatial and temporal activity of TGF-beta. Thus, although TGF-beta ligand is present, TGF-beta would not function in wound repair until a later time when RI and RII appear. This information should aid in the development of receptor antagonists as a therapeutic approach to scarring and fibrosis. In addition, these studies underscore the importance of defining the expression of proteins in vivo to establish a basis for the analysis of mechanisms in vitro.

Animals↗
PubMed1997

Reconstruction of Tessier no. 4 clefts revisited.

Atypical craniofacial clefts present a surgical challenge. Little is published about their treatment because of their rarity. Such is the nature of Tessier no. 4 clefts and others with shortened oculoalar and oculo-oral distances requiring multiple operative interventions. The soft-tissue abnormalities include a cleft of the lip with possible extension into the check, orbital dystopia, and globe abnormalities and a decreased oculo-oral distance. Typically, multiple local cheek and nasal flaps are used to close the soft-tissue defects, elevate the medial canthus, and protect the globe. However, this approach creates traction on the lower eyelid, suboptimal location of the scar, and poor color match between the flaps. We present two cases of Tessier no. 4 clefts and one case of a multiply clefted (Tessier nos. 1/13, 2/12, 3/11) child with the typical contracted oculoalar and oculo-oral distances. Reconstruction with a superiorly based nasolabial flap transposed 90 degrees under the eye was performed in all three as a primary procedure. This technique respects aesthetic units and places the resulting scars in less conspicuous areas on the face.

Child, Preschool↗
PubMed1997

Secondary craniofacial management following skeletal correction in facial asymmetry. Application of microsurgical techniques.

Based upon our experience with microvascular reconstruction of facial contour problems in 116 patients, we have developed an operative approach that emphasized both donor site and facial aesthetics and reliably restores symmetry. This allows correction of the obvious facial symmetry along the jawline as well as the more subtle problems in the midface, temporal, and periorbital areas. A state-of-the-art approach for reconstruction of facial deformities should include standard craniofacial techniques with or without bone expansion followed by soft-tissue microvascular reconstruction when required. This marriage of both hard and soft tissue maximizes the aesthetic results by restoring facial harmony in these difficult craniofacial patients.

Adult↗
PubMed1997

Enophthalmos revisited.

As an alternative to the conventional craniofacial approach with its coronal incision, a limited access technique has evolved. Its advantages and disadvantages are discussed. The method should not be used unless one is well versed in the correction of enophthalmos and has previous experience using the traditional craniofacial approach.

Enophthalmos↗
PubMed1996

Step expansion of the frontal bar: correction of trigonocephaly.

In severe trigonocephaly, metopic suture synostosis extends inferiorly to involve the frontoethmoid suture, resulting in orbital hypotelorism. To correct this growth disturbance, a nasofrontal osteotomy with bone graft interposition has been advocated. We describe an alternative procedure, supraorbital bar step expansion, which does not require a bone graft or metallic miniplate fixation. The supraorbital bar step expansion avoids donor site morbidity and the potential for plate migration. This procedure not only corrects orbital distopia, but also improves the anterolateral position of the brows, lateral canthus, and temporal regions.

Craniosynostoses↗
PubMed1996

Microsurgical correction of facial asymmetry in 60 consecutive cases.

Restoring soft-tissue contour in patients with facial asymmetry is a difficult problem for plastic surgeons. We report our experience with 57 consecutive patients who underwent 60 microvascular free flaps for the correction of facial asymmetry between July of 1989 and June of 1994. Etiologies of facial asymmetry included hemifacial microsomia, hemifacial atrophy, postradiation sequelae, burns and trauma, and selected congenital anomalies. Thirty-eight patients were reconstructed with a customized parascapular flap incorporating extensions of dorsal thoracic fascia. Other donor sites utilized were as follows: six superficial inferior epigastric flaps, three myocutaneous flaps, seven muscle flaps, and six fasciocutaneous flaps with bone. To correct facial asymmetry, the recipient site was dissected through a limited preauricular incision whenever feasible, and the superficial temporal artery and vein were used as recipient vessels. A monitoring skin paddle was rarely used. There were no flap losses in this series. Six patients experienced a postoperative hematoma, three of which were drained at the bedside. Limited skin slough occurred in three patients. No donor-site complications other than hypertrophic scarring were encountered. Flap revisions were performed in 22 of the 57 patients to maximize aesthetic results. Based on our experience, we feel that the operative approach presented here allows excellent and stable correction of facial asymmetry due to a variety of etiologies. Furthermore, this technique is applicable to other congenital craniofacial deformities such as Treacher-Collins syndrome and orbital-facial clefts.

Adolescent↗
PubMed1996

Studies in cranial suture biology: part II. Role of the dura in cranial suture fusion.

The biology underlying normal and premature cranial suture fusion remains unknown. The purpose of this study was to investigate the role of the dura mater in cranial suture fusion. In the Sprague Dawley rat model, the posterior frontal cranial suture fuses between 10 and 20 days of postnatal life. The effect of separating the posterior frontal cranial suture from its underlying dura mater with an intervening silastic sheet was studied. Sixty rat pups, age 8 days, were divided into four groups of 15. Group A served as unoperated controls. Group B, the experimental group, underwent craniotomy, dural elevation, and insertion of a silicone sheet between the posterior frontal cranial suture and the underlying dura. Two operative sham groups were included. Group C underwent craniotomy and dural deflection only. Group D underwent craniotomy alone without dural deflection. The rats were sacrificed at 15, 22, and 30 days of age. The results showed that the unoperated animals (group A) demonstrated normal initiation of suture fusion at 15 days and complete fusion by 22 days. Group B animals, with silicone sheet barriers placed, showed persistent patency of sutures at 22 days. Initiation of suture fusion was delayed until 30 days. Sham group C, animals with craniotomy and dural deflection, showed that initiation of fusion was delayed until 22 days with complete fusion by 30 days of age. Sham group D, craniotomy alone, had the same normal temporal sequence of suture fusion as the unoperated control group A. These data indicate that normal cranial suture fusion is delayed when the suture-dural interaction is interrupted by a surgically place barrier or by simple dural deflection. Furthermore, interaction between the dura and the overlying suture appears to direct suture fusion.

Animals↗