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At least 811 records · Page 45Linked to original sources
PubMed1997

Operative versus closed treatment of primary dislocation of the patella. Similar 2-year results in 125 randomized patients.

To assess whether initial surgery is beneficial for patients with primary dislocation of the patella, we carried out a prospective randomized study. Knee stability was examined under anesthesia, and associated injuries were excluded by diagnostic arthroscopy. 55 patients then had closed treatment and 70 patients were operated on with individually adjusted proximal realignment procedures. Surgery gave no benefit based on 2 years of follow-up. The subjective result was better in the non-operative group in respect of mean Houghston VAS knee score (closed 90, operative 87), but similar in terms of the patient's own overall opinion and mean Lysholm II knee score. Recurrent instability episodes (redislocation or recurrent subluxation) occurred in 20 nonoperated and in 18 operated patients. Of these, 15 and 12, respectively, then suffered redislocations. Function was better after closed treatment. Serious complications occurred after surgery in 4 patients. In conclusion, the recurrence of patellar dislocation may be more frequent than reported, whatever the form of treatment. Routine operative management cannot be recommended for primary dislocation of the patella.

Adolescent↗
PubMed2000

Microanatomy and ultrastructure of the protonephridial system in the larva of the limpet, Patella vulgata L. (Mollusca, Patellogastropoda).

The microanatomy and ultrastructure of the larval excretory system of Patella vulgata L., 1758 has been examined by means of semithin and ultrathin serial sections, reconstructions, and transmission electron microscopy. The protonephridial system appears after torsion and consists of two terminal flame bulbs with narrow, ciliated ducts. Whereas the polyciliary terminal cells (cyrtocytes) are only slightly asymmetrically placed below the mantle cavity, the distal excretory ducts and their openings show remarkable asymmetry due to torsion. Further larval ultrafiltration sites with identical fine-structure (meandering slits with diaphragms covered by extracellular matrix) are present in the solitary rhogocytes (pore cells). The presence of larval protonephridia is regarded as plesiomorphic for Mollusca and the Trochozoa (Spiralia) as a whole and the specific conditions (asymmetry, simplicity) in Patella are probably plesiomorphic for the Gastropoda.

Animals↗
PubMed2004

Viability of allogeneic bone marrow stromal cells following local delivery into patella tendon in rabbit model.

Bone marrow stromal cells are potentially useful for tendon repair and regeneration. To provide lasting benefits, the seeded cells must survive implantation at local tendon sites. Our objective was to determine the in vivo fate of allogeneic bone marrow stromal cells (bMSCs) at different time points after implantation into patella tendon defects (i.e., at 2, 3, 5, and 8 weeks). The protocol involved the labeling of bMSCs with green fluorescent protein (GFP) or carboxyfluorescein diacetate (CFDA) before implantation. A window defect (5 x 5 mm) was created at the central portion of rabbit patella tendon and subsequently treated with GFP- or CFDA-marked bMSCs. The marked bMSCs were loaded into the window defect with fibrin glue. Upon sacrifice of the rabbits at the different time points, the implant site of the patellar tendon was immediately retrieved and the viability of the labeled cells was assessed under confocal microscopy. The results showed that the seeded bMSCs remained viable within the tendon wound site for at least 8 weeks after implantation. The cell morphology was changed from a round shape at 2 weeks to a spindle shape at 5 weeks after implantation. This study demonstrated that the bMSCs remained viable for prolonged periods after implantation and therefore have the potential to influence the formation and remodeling of neotendon tissue after tendon repair.

Adipocytes↗
PubMed2006

[Arthroscopic management of traumatic luxation of the patella].

AIM: The authors present a restrospective assessment of acute traumatic patellar luxation. MATERIAL: From 1999 to 2003, the authors treated 57 patients with acute traumatic patellar luxations, including 36 females and 21 males, the age range was 16-40 years. In cases of marked lateralization of the patella, the injured medial retinaculum was sutured under arthroscopic control. Furthermore, should the lateralization persist, lateral release of the patella was conducted. Early patellar cartillage injuries were detected in 34 subjects (59%), injuries of the lateral femoral condyle in 19 subjects (33 %). Patellar chondromalacia, grade 1-2 was diagnosed in 16 subjects. Free cartillagenous particles within the joint were detected in 18 subjects. Reconstruction of the cartillage was conducted in extensive injuries in 13 subjects. RESULTS: The subjects were assessed 1-4 years after the injuries and surgery. In one case (2%), a relaps of the patellar luxation, due to a new contact sport injury (a direct impact), was recorded. Assessment results, using the Lysholm score, were defined as follows: 93%-excellent and good, 7% fair. CONCLUSION: Sparing surgical techniques, followed by appropriate rehabilitation care, may optimalize the healing process of the injured tissue and prevent relapses of patellar luxations, as well as further wearing of femoropatellar cartillages.

Adolescent↗
PubMed2002

Nail-patella syndrome. Overview on clinical and molecular findings.

Nail-patella syndrome (NPS) is a rare autosomal dominant pleiotropic disorder characterized by dysplasia of the nails, patellar aplasia or hypoplasia, iliac horns, dysplasia of the elbows, and frequently glaucoma and progressive nephropathy. The recent identification of the causative gene for this syndrome has initiated further studies of the phenotype and molecular pathogenesis of kidney disease in NPS. The gene underlying NPS, LMX1B, is a LIM-homeodomain transcription factor involved in normal patterning of the dorsoventral axis of the limb during development and early morphogenesis of the glomerular basement membrane. Molecular studies of Lmx1b, combined with genetic and immunohistochemical investigation of different alpha chains of type IV collagen in the Lmx1b null mice kidney, a mouse model for NPS, have provided evidence that Lmx1b is involved in the pathogenesis of NPS glomerulopathy. At present evidence for a correlation between the presence and severity of the renal and extrarenal anomalies and LMX1B genotype is lacking. This review focuses on the recent advances in clinical and molecular genetic studies of NPS.

Collagen Type IV↗
PubMed2005

Second-look arthroscopy of cartilage changes of the patellofemoral joint, especially the patella, following acute and recurrent patellar dislocation.

OBJECTIVE: The purpose of this study was to clarify some pathogenesis of the cartilage changes of the patellofemoral joint in patellar dislocation knees. METHODS: A first arthroscopy was performed in a total of 60 knees, including 30 knees of acute patellar dislocation (APD) and 30 knees of recurrent patellar dislocation (RPD). At the time of the first arthroscopy, 58 knees sustained open medial patellofemoral ligament repair/reconstruction, and 2 knees had only arthroscopy examination. In APD knees, the second-look arthroscopy was performed 16.7 months after the first arthroscopy, and in RPD knees, 25.2 months after the first arthroscopy. RESULTS: In most APD knees, cracking primarily on the central dome of the patella did not have a remarkable change but in several knees that had a high number of cracking or interlaced cracking, cracking became worse with fibrillation. Osteochondral defect site primarily on the medial facet showed fibrillation and/or ulceration (erosion). In most RPD knees, fissuring primarily on the central dome did not have a remarkable change, and fibrillation and/or erosion mainly on the medial facet also did not have a remarkable change. However, in four knees with the continuation of patellar dislocation, the patellar cartilage changes had definitely worsened. On the other hand, in the first and second-look arthroscopy, most APD and RPD knees had no remarkable cartilage lesions or cartilage changes of the femoro-trochlear aspect. CONCLUSIONS: One of the pathogenesis of fissuring in RPD knees seems to be cracking occurring at the time of APD. Two of the pathogenesis of fibrillation may result from the reparative reaction of the cartilage in osteochondral defect site and the cartilage change due to a high degree of cracking damage mainly on the central dome in APD injury. The continuation of patellar dislocation definitely makes the patellar cartilage lesions worse.

Acute Disease↗
PubMedDate not supplied

[Nail-patella syndrome. A 4-generation family study].

Five cases of hereditary onycho-osteodysplasie are reported. All of the family members presented dysplastic nails. Hypoplastic patella, elbow dysplasia or iliac horns were shown in variable expression. We've seen no other anomalies especially nephropathy did not occur.

Adult↗
PubMed2003

[From gene to disease; the nail-patella syndrome and the LMX1B gene].

Nail-patella syndrome (NPS) is an autosomal dominant hereditary disorder characterised by nail dysplasia, patellar apoplasia/hypoplasia, iliac horns, elbow dysplasia, and frequently primary open angle glaucoma and progressive nephropathy. The gene underlying NPS, LMX1B on chromosome 9q34.1, is a transcription factor involved in the normal dorsoventral patterning of the limb and normal development of the glomerular basement membrane in the kidney. Recent studies suggest a role for LMX1B in the regulation of collagen IV expression and in the transcriptional regulation of podocyte specification and differentiation. At present, no evidence for a correlation between the presence and severity of the clinical anomalies and the LMX1B genotype has been found.

Chromosomes, Human, Pair 9↗
PubMed1976

[Dislocation of patella also a symptom of other diseases or consequence of local primary alteration of the scelet (author's transl)].

According to a large group of patients there is demonstrated the "symptomatic" dislocation of patella. It is a part of a system-disease, especially Onycho-osteo-arthro-dysplasia. Arthrogryposis multiplex. Freeman-Sheldon-syndrome, mongolism and children with debility or imbecility. There are discussed their pathogenesis and any consequences for diagnosis and treatment.

Abnormalities, Multiple↗
PubMed1980

Triangular lunulae. A clue to nail-patella syndrome.

The nail-patella syndrome has been of interest to dermatologists because the diagnosis of this multisystem complex may be suggested simply by observing the patient's abnormal nails. It is the purpose of this article to call attention to triangular lunulae and other nail abnormalities associated with this syndrome, as well as other causes of triangular lunulae.

Adult↗
PubMed1984

An autosomal recessive disorder with glomerular basement membrane abnormalities similar to those seen in the nail patella syndrome: report of a kindred.

We present a 9-year-old boy, the product of a consanguineous marriage, with proteinuria, edema, and microscopic hematuria with mild renal impairment since age 2 yr. Renal biopsy showed the histopathologic electron microscopic changes seen in hereditary osteo-onchyodysplasia (HOOD) [Hoyer et al, 1972; Bennet et al, 1973; DelPozo and Lapp 1970; Vernier et al, 1974; Morita et al, 1973] or "nail-patella syndrome." Neither the patient nor his relatives had bone or nail abnormalities; however, 2 other sibs had died of complications of end-stage renal disease at age 6 and 9, leading us to suspect autosomal recessive inheritance of a severe nephropathy or glomerulodysplasia.

Basement Membrane↗
PubMed1992

Nail-patella syndrome in a spontaneously aborted 18-week fetus: ultrastructural and immunofluorescent study of the kidneys.

Nail-patella syndrome (NPS), hereditary onycho-osteodysplasia, is an autosomal dominant disorder of nail dystrophy, patellar absence or hypoplasia, incomplete elbow extension, conical posterior iliac horns, and nephropathy. We studied the kidneys of an 18-week spontaneously aborted fetus of a mother with the NPS. Ultrastructural examination of the kidney showed thickening of the capillary walls of the glomeruli and mesangium. There was irregular thickening of basement membranes with subendothelial fibrillar electron-dense deposits. Immunofluorescence showed fibrinogen deposition in glomerular basement membranes. Fibrinogen deposition in utero may ultimately lead to glomerular fibrosis and intrabasement membrane collagen deposition as seen in the adult renal lesion of this syndrome. This is the first report of the NPS in which the renal abnormalities have been studied in a fetus. These findings provide support for possible prenatal diagnosis of NPS by intra-uterine kidney biopsy.

Abortion, Spontaneous↗
PubMed2004

Interstitial deletion 9q22.32-q33.2 associated with additional familial translocation t(9;17)(q34.11;p11.2) in a patient with Gorlin-Goltz syndrome and features of Nail-Patella syndrome.

The phenotype of Gorlin-Goltz syndrome or basal cell nevus syndrome (BCNS, #109400, OMIM), a Mendelian trait due to PTCH mutations has been reported in a few cases of interstitial deletion of chromosome 9q. We present an 11-year-old girl with clinical features consistent with BCNS including bridging of sella turcica, biparietal bossing, downward slanting palpebral fissures, mandible prognathism, pectus excavatum, thumb abnormalities, occult spina bifida at L5-S4, numerous basal cell nevi, and single basal cell carcinoma. Cytogenetic analysis using high-resolution banding techniques and fluorescence in situ hybridization (FISH) revealed interstitial chromosome deletion 9q22.32-q33.2 involving the PTCH gene as a secondary breakage event to a chromosome translocation t(9;17)(q34.1;p11.2)mat. Further FISH studies showed the translocation breakpoint on 9q34.11 maps proximal to ABL, between the BAC clone RP11-88G17 and the LMX1B gene. The latter gene encodes a transcription factor, in which loss of function mutations are responsible for the nail-patella syndrome (NPS, #161200 OMIM). Interestingly, some features of our proband (e.g., bilateral patellar dysplasia and abnormal clavicular shape), as well as her healthy sister who carries the same translocation, are also found in patients with NPS. The chromosome 17p11.2 breakpoint maps in the Smith-Magenis syndrome common deletion region, within two overlapping BAC clones, CTD-2354J3 and RP11-311F12.

Basal Cell Nevus Syndrome↗
PubMed1991

Pressure erosion of the femoral trochlea, patella baja, and altered patellar surfaces.

As knee flexion increases, so do tendofemoral and patellofemoral compression forces. Three cases of long-standing uncorrected flexion contractures of the knees are presented that resulted in marked erosion of the femoral trochlea, patella baja, and remodeled patellar articular surfaces likely reflecting increased angles of flexion. It is probable that the deep femoral grooves are the result of adaptation under high-level persistent contact loads from the quadriceps tendon. These examples expand our knowledge of bone remodeling and offer information of potential use in studying ancient skeletal samples.

Adult↗
PubMed2001

Twenty-two novel LMX1B mutations identified in nail patella syndrome (NPS) patients.

We report twenty-two novel mutations in the gene encoding the transcription factor LMX1B, previously shown to be mutated in persons with Nail Patella Syndrome (NPS). The mutations comprised eight missense, one splice-site, three insertion/deletion and ten nonsense or frameshift mutations. A sub-set of five recurrent mutations within the homeodomain represents over one-quarter of the described NPS mutations. The type and distribution of the mutations is consistent with the hypothesis that NPS is the result of haploinsufficiency for LMX1B.

Codon, Nonsense↗
PubMed1996

Expression of osteocalcin in the patella of experimentally immobilized and remobilized rats.

The exact mechanisms by which mechanical loading-unloading affects bone tissue are mostly unknown. Recently, osteocalcin, a direct product of osteoblasts, has been shown to reflect the activity of the mineralization phase of the newly formed bone matrix, and therefore, the in situ detection of osteocalcin could be used for studying the effects of physical activity-inactivity on the osteoblast function or bone formation in the target bone. In this study, the effect of various loading states (immobilization and three forms of subsequent remobilization) on the in situ expression of osteocalcin in the rat patellas and their osteotendinous junctions was studied immunohistochemically using a polyclonal rat antiosteocalcin as the primary antibody. Following immobilization for 3 weeks, the immunoreactivity of osteocalcin was markedly decreased or was completely absent in all the patellar areas which normally show intense reaction as a sign of mineralization of the newly formed bone, that is, in the subperiosteal and subchondral regions, in the osteoid tissue that lies on the surface of the trabecular bone, and around the cortical lacunae. The same was true in the mineralized fibrocartilage zone of the osteotendinous junction of the quadriceps tendon. Free remobilization for 8 weeks (free cage activity) could not improve the situation, but after intensified remobilization of the same duration (low and especially high intensity treadmill running) high osteocalcin expression was observed in the above-mentioned anatomic sites. These findings indicate that formation of new bone tissue is rapidly regulated by the loading states of the bone. Higher than normal activity seems to be needed to restore the bone formation from the disuseinduced depression to normal.

Animals↗