Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “instability”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1996

Microsatellite instability and loss of heterozygosity at the hMLH1 locus on chromosome 3p21 occur in a subset of nonsmall cell lung carcinomas.

Microsatellite alterations observed in tumor specimens may reflect genomic instability due to defective mismatch repair genes. To investigate whether this occurs in human nonsmall cell lung carcinomas we have analyzed microsatellite instability at 5 marker loci and loss of heterozygosity (LOH) at the hMLH1 locus on chromosome 3p21 using the polymerase chain reaction. Of a total of 49 nonsmall cell lung carcinomas examined, 43% (13 of 30 informative cases) showed LOH at 3p21 and 29% (14 of 49) exhibited microsatellite instability at one or multiple loci. LOH of the mismatch repair gene hMLH1 at 3p21 occurred in 82% (9 of 11 informative cases) of the tumors with microsatellite instability. This suggests that defects in the mismatch repair gene hMLH1 at 3p21 may be involved in microsatellite instability and tumorigenesis of a subset of nonsmall cell lung carcinomas. However, in those nonsmall cell lung carcinomas without microsatellite instability LOH at 3p21 probably involved another tumor suppressor gene(s) in this chromosomal region.

Carcinoma, Non-Small-Cell Lung↗
PubMed1996

Detection of chromosome instability of tissue fields at risk: in situ hybridization.

Many human tumors are thought to develop along a multistep pathway in tissues that have encountered long periods of carcinogen exposure and thus have accumulated genetic hits in functional targets relevant to tumor evolution. The cumulative degree of genetic change is dependent on both exogenous (e.g., degree of carcinogen exposure) and endogenous factors (e.g., metabolism of procarcinogens, repair or misrepair capacity, proliferation properties of the tissue, capability of damaged cells to survive). Thus one approach to risk estimation is to measure the accumulated amount of genetic damage in a target tissue at risk for tumor development. Since one cannot predict the exact site of the future tumor, the risk assay must detect a generalized ongoing process of genetic instability from small, random biopsies. The technique of chromosome in situ hybridization involves the use of chromosome- or region-specific probes and provides an ability to directly visualize genetic change (e.g., random or clonal chromosome polysomy and monosomy) on thin tissue sections (where tissue architecture is maintained) or exfoliated cells. Analyses of normal and premalignant lesions adjacent to tumors (e.g., head and neck, lung, bladder, cervix, breast) have demonstrated that chromosome instability can be detected in the field of the tumor (i.e., in normal and premalignant cells in a tissue at 100% risk of tumor development) and the degree of chromosome instability increases with the degree of histologic progression toward cancer. Analyses of premalignant lesions (e.g., oral leukoplakia and erythroplakia from individuals at risk for aerodigestive tract cancer) by chromosome in situ hybridization have uncovered varying degrees of chromosome instability. However, approximately half of those individuals who showed a high degree of chromosome instability in biopsies subsequently developed aerodigestive tract cancer. Of interest, half of these tumors have developed away from the biopsied site, suggesting that the detection of a chromosome instability process in one aspect of the tissue might yield risk information for the total tissue field. These studies also suggest that chromosome in situ hybridization might be useful for identifying individuals with high tumor risk who might benefit from chemopreventive intervention.

Bronchi↗
PubMed1997

Differential induction of chromosomal instability by DNA strand-breaking agents.

To investigate the role of DNA strand breakage as the molecular lesion responsible for initiating genomic instability, five different strand-breaking agents, bleomycin, neocarzinostatin, hydrogen peroxide, restriction endonucleases, and ionizing radiation, were examined for their capacity to induce delayed chromosomal instability. These studies used GM10115 human-hamster hybrid cells, which contain one copy of human chromosome 4 in a background of 20-24 hamster chromosomes. Chromosomal instability was investigated using fluorescence in situ hybridization to visualize chromosomal rearrangements involving the human chromosome. Rearrangements are detected multiple generations after treatment, in clonal populations derived from single progenitor cells surviving treatment of the specified DNA-damaging agents. Clastogenic and cytotoxic activities of all agents were tested by examining chromosome aberration yields in first-division metaphases and by clonogenic survival assays. Analysis of over 250 individual clones representing over 50,000 metaphases demonstrates that when compared at comparable levels of cell kill, ionizing radiation, bleomycin, and neocarzinostatin are equally effective at eliciting delayed genomic instability. These observations document, for the first time, the persistent destabilization of chromosomes following chemical treatment. In contrast, the analysis of nearly 300 clones and 60,000 metaphases, involving treatment with four different restriction endonucleases and/or hydrogen peroxide, did not show any delayed chromosomal instability. These data indicate that DNA strand breakage per se does not necessarily lead to chromosomal instability but that the complexity or quality of DNA strand breaks are important in initiating this phenotype.

Adenine Phosphoribosyltransferase↗
PubMed1996

Replication errors in hematological neoplasias: genomic instability in progression of disease is different among different types of leukemia.

Genetic alteration, including genomic instability, is an ultimate step toward the malignant process. One approach to delineating replication errors in cancer cells is to determine the alterations of microsatellites, which are short, repeated nucleotide sequences existing throughout the genomes. We used a fluorescent system to assess microsatellite changes in seven loci (D2S123, D3S643, D5S107, LPL, D17S261, TP53, and D18S34) of 73 consecutive patients with various hematological neoplasias. De novo acute leukemia patients had a low frequency (<1%) of microsatellite alterations at each locus, and none of them demonstrated multiple microsatellite changes. In chronic myeloid leukemia patients, no microsatellite instability was detected in the chronic phase, whereas a relatively high frequency (25%) of multiple microsatellite changes was evident in the blastic phase, and half of these patients had multiple microsatellite changes. About 50% of the patients with myelodysplastic syndrome (MDS) and post-MDS acute myeloid leukemia (post-MDS AML) had microsatellite alterations. We next compared microsatellite alterations in two different hematological phases (MDS and post-MDS AML phases); 5 of 11 patients with post-MDS AML had de novo appearance of microsatellite instability during disease progression. This indicates that genomic instability at multiple microsatellite loci could occur either before or after leukemic transformation in MDS patients. We concluded that genomic instability in chronic myeloid leukemia might be linked to blastic transformation in combination with cytogenetic changes. In contrast, MDS patients had replication errors as a relatively early genetic event as well as a late genetic event. These results suggest that the involvement of genomic instability in the progression of disease is different among various types of leukemia.

DNA Replication↗
PubMed2006

Patterns of genomic instability in gastric cancer: clinical implications and perspectives.

In gastric cancer (GC) the loss of genomic stability represents a key molecular step that occurs early in the carcinogenesis process and creates a permissive environment for the accumulation of genetic and epigenetic alterations in tumor suppressor genes and oncogenes. It is widely accepted that GC can follow at least two major genomic instability pathways, microsatellite instability (MSI) and chromosome instability (CIN). MSI is responsible for a well-defined subset of GCs. CIN represents a more common pathway comprising heterogeneous subsets of GC. In addition to MSI and CIN, the CpG islands methylator phenotype (CIMP) plays an important role in gastric carcinogenesis. CIMP may lead to the transcriptional silencing of various genes in gastric carcinogenesis. Intriguingly, more recently in addition to CpG island hypermethylation, a global DNA demethylation, that precedes genomic damage, has been observed in GC. Thus, epigenetic alterations may play a relevant role in gastric carcinogenesis as alternative mechanisms. Evidence suggests that although MSI, CIN and CIMP phenotypes can be distinguished from one another, there might be some degree of overlap. This review describes our current knowledge of the instability pathways in gastric carcinogenesis and the potential clinical applications for different forms of genomic instability in GC.

Chromosomal Instability↗
PubMed2025

Surprisingly frequent chromosomal instability in cultivated peanut.

This study, the third in a three-part series, investigates whether chromosomal instability persists in cultivated peanut. The allotetraploid peanut (Arachis hypogaea; genome type AABB) originated from the hybridization and polyploidization of A. duranensis (AA) and A. ipa&#xeb;nsis (BB). Our first study established that this was an extremely narrow genetic origin, likely from a single hybridization event. This raised a paradox: how did such narrow genetics give rise to the phenotypic diversity seen in cultivated peanut? The second study addressed this, showing that a single neoallotetraploid spontaneously generates striking diversity, and that homoeologous exchanges-abundant in early generations following polyploidy-are a key mechanism in creating this diversity. In contrast to this early-generation instability, cultivated peanut is generally considered to be genetically stable, presumably due to selection. This third study tests whether residual instability still occurs in modern peanut. From a single plant of the highly selfed 'genome stock' of the cultivar 'Tifrunner', we advanced lineages through seven generations in a pollinator-free greenhouse. Among 233 plants, we identified three new large-scale chromosomal instability events: a large deletion on chromosome B01, associated with reduced pod width and seed weight, and two ABBB compositions involving chromosomes A02/B02 and A05/B05. With these observations in hand, we reinterpreted previously published data from two recombinant inbred populations. Together, these results indicate that at least 1% of pure pedigree A. hypogaea plants exhibit spontaneous large-scale chromosomal changes-a surprising frequency of instability that likely contributes to peanut's long-term adaptability and evolution.

Arachis↗
PubMed2006

Chromosomal instability in microsatellite-unstable and stable colon cancer.

PURPOSE: The genomic instability in colon cancer can be divided into at least two major types, microsatellite instability (MSI) or chromosomal instability (CIN). Although initially felt to be mutually exclusive, recent evidence suggests that there may be overlap between the two. The aim of this study was to identify chromosomal alterations at high resolution in sporadic colon cancers with high-level microsatellite instability (MSI-H) and to compare them to those present in a set of matched microsatellite stable (MSS) tumors. EXPERIMENTAL DESIGN: Array-based comparative genomic hybridization was used to analyze a set of 23 sporadic MSI-H and 23 MSS colon cancers matched for location, gender, stage, and age. The arrays consisted of 2,464 bacterial artificial chromosome clones. RESULTS: MSI and MSS colon cancers differed significantly with respect to frequency and type of chromosomal alterations. The median fraction of genome altered was lower among MSI-H tumors than MSS tumors (2.8% versus 30.7%, P=0.00006). However, the MSI-H tumors displayed a range of genomic alterations, from the absence of detectable alterations to extensive alterations. Frequent alterations in MSI-H tumors included gains of chromosomes 8, 12, and 13, and loss of 15q14. In contrast, the most frequent alterations in MSS tumors were gains of 7, 13, 8q, and 20, and losses of 8p, 17p, and 18. A small, previously uncharacterized, genomic deletion on 16p13.2, found in 35% of MSI-H and 21% of MSS tumors, was confirmed by fluorescence in situ hybridization. CONCLUSION: MSI and CIN are not mutually exclusive forms of genomic instability in sporadic colon cancer, with MSI tumors also showing varying degrees of CIN.

Adenocarcinoma↗
PubMed2005

Microsatellite instability and alterations of mismatch repair protein expression in choroidal melanomas.

OBJECTIVES: To examine choroidal melanomas for genomic instability, manifested by microsatellite instability (MSI) and mismatch repair (MMR) protein alterations, and to determine the association of these alterations with selected clinicopathological features of the tumors. METHODS: Polymerase chain reaction-based microsatellite assays were applied to analyze 57 cases of choroidal melanomas using 11 microsatellite markers at 5 chromosomal regions: 1p, 2p, 4q, 9p, and 17p. Immunoperoxidase staining methods and mouse monoclonal antibodies were used to investigate the expression patterns of MMR proteins. RESULTS: Microsatellite instability was found at the 1p, 9p, and 17p regions in these lesions with an overall prevalence of 35% (20/57). The frequency of MSI ranged from 9% (1/11) to 27% (3/11), ie, low-level MSI (MSI-L). The instability was most commonly found at the 1p region (D1S2734, 55%; D1S2832, 40%; and D1S233, 20%). Two MSI banding patterns, band shifts and the appearance of additional bands, were found in 10% and 90% of the unstable lesions, respectively. The average percentages of hMLH1 and hMSH2 positively stained cells were insignificantly reduced in the unstable lesions (81.7 +/- 9.3 and 76.7 +/- 16.7) as compared with the stable lesions (84.1 +/- 15.5 and 78.6 +/- 19.6; P = .62 and 0.74 for hMLH1 and hMSH2, respectively). There was no significant difference in survival between the 2 groups; however, relative to the stable subset, the unstable tumors showed a trend (P<.10) toward occurring at a younger age and having tumor cells in vascular lakes. CONCLUSIONS: The presence of MSI-L in some choroidal melanomas defines a novel genetic subset of these tumors and suggests that MSI (genomic instability) may play a role in their molecular pathogenesis. Elucidation of the underlying mechanisms for MSI will require further investigation. CLINICAL RELEVANCE: Detection of the MSI-L pattern might prove to be useful as an adjunct to the conventional diagnosis of choroidal melanomas. Larger series are needed to determine whether any of the correlative trends noted in this study will achieve statistical significance. To the best of our knowledge, this study is the first to define both the MSI and MMR protein expression features of choroidal melanomas.

Base Pair Mismatch↗
PubMed2005

Chromosomal instability in amniocytes from fetuses of mothers who smoke.

CONTEXT: Tobacco increases the risk of systemic diseases, and it has adverse effects on pregnancy. However, only indirect data have been published on a possible genotoxic effect on pregnancy in humans. OBJECTIVES: To determine whether maternal smoking has a genotoxic effect on amniotic cells, expressed as an increased chromosomal instability, and to analyze whether any chromosomal regions are especially affected by exposure to tobacco. DESIGN, SETTING, AND PATIENTS: In this prospective study, amniocytes were obtained by routine amniocentesis for prenatal diagnosis from 25 controls and 25 women who smoke (> or =10 cigarettes/d for > or =10 years), who were asked to fill out a smoking questionnaire concerning their smoking habits. Chromosomal instability was analyzed in blinded fashion by 2 independent observers in routine chromosome spreads. Breakpoints implicated in chromosomal abnormalities were identified by G-banding. MAIN OUTCOME MEASURES: Association between maternal smoking and increased chromosomal instability in amniotic fluid cells, expressed as chromosomal lesions (gaps and breaks) and structural chromosomal abnormalities. RESULTS: Comparison of cytogenetic data between smokers and nonsmokers (controls) showed important differences for the proportion of structural chromosomal abnormalities (smokers: 12.1% [96/793]; controls: 3.5% [26/752]; P = .002) and to a lesser degree for the proportion of metaphases with chromosomal instability (smokers: 10.5% [262/2492]; controls: 8.0% [210/2637]; P = .04), and for the proportion of chromosomal lesions (smokers: 15.7% [391/2492]; controls: 10.1% [267/2637]; P = .045). Statistical analysis of the 689 breakpoints detected showed that band 11q23, which is a band commonly implicated in hematopoietic malignancies, was the chromosomal region most affected by tobacco. CONCLUSIONS: Our findings show that smoking 10 or more cigarettes per day for at least 10 years and during pregnancy is associated with increased chromosomal instability in amniocytes. Band 11q23, known to be involved in leukemogenesis, seems especially sensitive to genotoxic compounds contained in tobacco.

Adult↗
PubMed1999

CT imaging and three-dimensional reconstructions of shoulders with anterior glenohumeral instability.

Glenohumeral instability is a common occurrence following anterior dislocation of the shoulder joint, particularly in young men. The bony abnormalities encountered in patients with glenohumeral instability can be difficult to detect with conventional radiography, even with special views. The aim of our study was to evaluate the bony abnormalities associated with glenohumeral instability using CT imaging with 3-D reconstruction images. We scanned 11 patients with glenohumeral instability, one with bilateral symptoms; 10 were male, one female, and their ages ranged from 18-66 years. Contiguous 3 mm axial slices of the glenohumeral joint were taken at 2 mm intervals using a Siemens Somatom CT scanner. In the 12 shoulders imaged, we identified four main abnormalities. A humeral-head defect or Hill-Sachs deformity was seen in 83% cases, fractures of the anterior glenoid rim in 50%, periosteal new bone formation secondary to capsular stripping in 42%, and loose bone fragments in 25%. Manipulation of the 3-D images enabled the abnormalities to be well seen in all cases, giving a graphic visualization of the joint, and only two 3-D images were needed to demonstrate all the necessary information. We feel that CT is the imaging modality most likely to show all the bone abnormalities associated with glenohumeral instability. These bony changes may lead to the correct inference of soft tissue abnormalities making more invasive examinations such as arthrography unnecessary.

Adolescent↗
PubMed2006

Interventions for treating chronic ankle instability.

BACKGROUND: Chronic lateral ankle instability occurs in 10% to 20% of people after an acute ankle sprain. The initial form of treatment is conservative but if this fails and ligament laxity is present, surgical intervention is considered. OBJECTIVES: To compare different treatments, both conservative and surgical, for chronic lateral ankle instability. SEARCH STRATEGY: We searched the Cochrane Bone, Joint and Muscle Trauma Group Specialized Register (to July 2005), the Cochrane Central Register of Controlled Trials (The Cochrane Library 2005, Issue 3), and MEDLINE (1966 to April 2006), EMBASE (1980 to April 2006), CINAHL (1982 to April 2006) and reference lists of articles. SELECTION CRITERIA: All randomised and quasi-randomised controlled trials of interventions for chronic lateral ankle instability were included. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed methodological quality and extracted data. Where appropriate, results of comparable studies were pooled. MAIN RESULTS: Seven randomised trials were included and divided into three groups: surgical interventions; rehabilitation programs after surgical interventions; and conservative interventions. None of the studies were methodologically flawless. Only one study described an adequate randomisation procedure. Only two studies, both about rehabilitation programs after surgery, had a moderate risk of bias; all other studies had a high risk of bias. Due to clinical and methodological diversity, extensive pooling of the data was not possible. Surgical interventions (four studies): one study showed more complications after the Chrisman-Snook procedure compared to an anatomical reconstruction, whereas another study showed greater mean talar tilt after an anatomical reconstruction. Subjective instability and hindfoot inversion was greater after a dynamic than after a static tenodesis in a third study. The fourth study showed that the operating time for anatomical reconstructions was shorter for the reinsertion technique than for the imbrication method. Rehabilitation after surgical interventions (two studies): both studies provided evidence that early functional mobilization leads to an earlier return to work and sports than immobilisation. Conservative interventions: the only study in this group showed better proprioception and functional outcome with the bi-directional than with the uni-directional pedal technique on a cyclo-ergometer. AUTHORS' CONCLUSIONS: In view of the low quality methodology of almost all the studies, this review does not provide sufficient evidence to support any specific surgical or conservative intervention for chronic ankle instability. However, after surgical reconstruction, early functional rehabilitation was shown to be superior to six weeks immobilisation regarding time to return to work and sports.

Ankle Joint↗
PubMed1999

Increased interleukin-1beta production in the synovium of glenohumeral joints with anterior instability.

Macroscopic synovitis of the glenohumeral joint is frequently seen during arthroscopy in patients with anterior instability. Interleukin-1beta is known to be expressed in inflamed tissue, to correlate with the magnitude of inflammation, and to affect articular cartilage in the joint. We hypothesized that chronic synovitis may occur in the glenohumeral joint in patients with anterior instability. The purpose of this study was to examine the expression of interleukin-1beta in the synovium of the glenohumeral joint with anterior instability and to discuss its clinicopathologic significance. Specimens of synovial tissue around the greater tuberosity in the subacromial synovium (as controls) and around the rotator interval in the glenohumeral synovium were obtained from 10 patients who had anterior instability without signs of subacromial impingement. Semiquantitative reverse transcriptase-polymerase chain reaction was used to compare the levels of interleukin-1beta mRNA expression in the glenohumeral joint with those in the subacromial bursa. We also employed immunohistochemistry and in situ reverse transcriptase-polymerase chain reaction to detect the cells producing interleukin-1beta protein and mRNA. The levels of interleukin-1beta mRNA expression were significantly higher in the glenohumeral joint than in the subacromial bursa (p < 0.01). Histology showed nonspecific inflammation in all 10 samples of glenohumeral synovium, whereas no inflammation was seen in seven of 10 samples of subacromial synovium. Immunohistochemistry identified interleukin-1beta protein in the vessels and inflammatory and synovial cells (from lining to sublining layers) in synovium of the glenohumeral joint, whereas immunoreactivity was negative in seven subacromial bursa. The remaining three synovial specimens of subacromial bursa, however, showed positive immunoreactivity that was unremarkable and confined around the vessels. In situ reverse transcriptase-polymerase chain reaction was exclusively performed in the synovial specimens of the glenohumeral joint, which exhibited a positive reaction (in the same kinds of cells as seen with immunohistochemistry) in the lining and sublining layers and to a lesser extent in the stroma. Thus, our data confirmed the increased production of interleukin-1beta in the synovium of the glenohumeral joint in patients with anterior instability, suggesting the presence of chronic inflammation at the site. We conclude that this chronic synovitis may be partly associated with the development of dislocation arthropathy in the long term.

Acromion↗
PubMed1984

The anterior cruciate ligament of the knee: an experimental study of its importance in rotatory knee instability.

The importance of the anterior cruciate ligament (ACL) in relation to valgus-varus and axial rotation stability in the knee joint was investigated. Mobility patterns were drawn from ten osteoligamentous preparations after successive transection of the two parts of the ACL and the medial (MCL) and lateral collateral ligaments (LCL). The knee joint remained grossly stable after partial injury of the ACL, while sectioning of the entire ACL caused an increase in internal rotation in the extended-semiflexed position. Combined lesions to the ACL and the MCL caused considerable valgus instability increasing with flexion, the joints remaining stable in extension. Moreover, marked anteromedial instability occurred, while only slight posteromedial instability was found. Combined lesions to the ACL and the LCL caused varus instability, worst in the semiflexed position, and a consistent pivot shift in applying a valgus torque in flexion was noted. Moreover, moderate posterolateral instability was found, at its maximum in the semiflexed position. External rotatory stability is secured primarily by the MCL, secondarily by the posterior medial capsule, and finally by the ACL. The existence of lateral pivot shift is proof of damage to the ACL.

Humans↗
PubMed1994

[Standardized ultrasound examination for classification of instability of the acromioclavicular joint].

Anteroposterior X-ray views of both acromio-clavicular (AC-) joints with 10 kg weights in each hand are generally accepted for the diagnosis of Tossy I to III AC-joint separations. An analogue diagnosis can be made by standardized ultrasound examination. Ten individuals without AC-instability (Tossy I), eleven with Tossy II- and eight with Tossy III-instability were examined both radiographically and by B-mode ultrasound. AC-joint width was uniformly calculated by using an index (AC-index = AC-joint width of uninjured side/AC-joint width of injured side). The sonographically measured mean AC-index for Tossy I-stability was 1.0; sonographically 0.49 and radiographically measured 0.5 for Tossy II-injury; and sonographically 0.21 and radiographically measured 0.2 for Tossy III-instability. Statistical analysis resulted in significant differences for all mean AC-indices of the three groups (p < 0.0001). We conclude that ultrasound examination of AC-joint instability is as reliable as radiographic measurement. Standard X-rays of the shoulder remain mandatory to exclude fractures only. The decision for operative stabilisation of the AC-joint can be based on the side-effect free and cost-effective ultrasound examination of the grade of AC-joint instability (AC-index < 0.3 equivalent Tossy III).

Acromioclavicular Joint↗
PubMed2004

[Shoulder instability].

Shoulder instability is a common clinical feature leading to recurrent pain and limited range of motion within the glenohumeral joint. Instability can be due a single traumatic event, general joint laxity or repeated episodes of microtrauma. Differentiation between traumatic and atraumatic forms of shoulder instability requires careful history and a systemic clinical examination. Shoulder laxity has to be differentiated from true instability followed by the clinical assessment of direction and degree of glenohumeral translation. Conventional radiography and CT are used for the diagnosis of bony lesions. MR imaging and MR arthrography help in the detection of soft tissue affection, especially of the glenoid labrum and the capsuloligamentous complex. The most common lesion involving the labrum is the anterior labral tear, associated with capsuloperiostal stripping (Bankart lesion). A number of variants of the Bankart lesion have been described, such as ALPSA, SLAP or HAGL lesions. The purpose of this review is to highlight different forms of shoulder instability and its associated radiological findings with a focus on MR imaging.

Arthrography↗
PubMed1999

[Chronic recurrent ligament instability on the lateral ankle].

According to the literature, chronic ankle instability occurs after acute rupture of the lateral ankle ligaments in 10-20% of the cases. The etiology of the instability are ligamentous damage and functional neuromuscular disorder of the peroneal muscles. The standards of diagnostics are the history with the frequency of inversion trauma per period and the interval from the primary trauma, the clinical examination and radiological stress tests. Newer diagnostic methods, up to now not well established in clinical routine, include stabilometry, cybex-measurements of the pronator muscles, the evaluation of peroneal reaction time on a tilting platform and dynamic pedography. Conservative management of chronic ankle instability consists of wearing ankle braces and rehabilitation programs concerned with peroneal muscle strengthening and coordination training. The indication for surgical reconstruction of the ankle ligaments are a well-documented mechanical instability with the neuromuscular reflexes intact and a failed physiotherapeutic training program. The surgical procedure should be selected according to a priority list: 1. anatomical repair, eventually augmented with periosteum from the fibula, 2. Watson-Jones tenodesis, and 3. Chrisman-Snook tenodesis to treat a concomittant subtalar instability.

Ankle Injuries↗
PubMed2006

Trochlear osteotomy for patellar instability: satisfactory minimum 2-year results in patients with dysplasia of the trochlea.

Trochlear dysplasia is a predisposing factor for recurrent patellar instability. We evaluated the results of an anterior lateral femoral condyle open wedge osteotomy for treating patellar instability. A total of 16 consecutive patients (19 knees) with symptoms of recurrent patellar instability and trochlear dysplasia identified using a true lateral radiograph of the knee underwent an anterior lateral femoral osteotomy. Outcomes were documented at 2 years minimum follow-up using the Lysholm scale, the patellofemoral score, WOMAC score and standard conventional radiographs. In 17 knees, patients reported good improvement in stability (no dislocations) and most patients had a marked improvement in pain and functional scores at follow-up (mean follow-up 51 months). No serious complications occurred. Anterior femoral osteotomy of the lateral condyle appears to be a satisfactory and safe method for treating patients with patellofemoral joint instability caused by trochlea dysplasia. In selected cases this procedure can be used to correct trochlea dysplasia. In our opinion, the key to a successful treatment of patellofemoral instability is to successfully distinguish the anatomic deficiencies and to correct the anatomical abnormality.

Adolescent↗
PubMed2000

Gleno-humeral instabilities.

The purpose of this review is to highlight the most efficient imaging exploratory techniques depicting shoulder instability, to describe its various forms and to point out the findings which can simulate instability. In anterior recurrent dislocation, surgery is indicated and the procedure essentially depends on the importance of glenoid rim lesions. In this case, a standard X-ray evaluation is usually sufficient. The CT arthrography or MRI techniques give more specific details as to the severity of the lesions, particularly soft tissues alterations; however, these data do not alter standard therapeutic protocol. In fixed posterior dislocations, CT scan represents the most pertinent technique to evaluate the size of the humeral head defect and to determine the therapeutic follow-up. In subtle forms of instability, diagnosis or instability direction are not clearly assessed clinically and standard X-ray evaluation is usually unremarkable. In this case, further exploration, such as CT arthrography, MR imaging or MR arthrography, are recommended to confirm the diagnosis of instability and to evaluate its direction. The technique of choice is undoubtedly MR arthrography. Atraumatic voluntary painless subluxations associated with hyperlaxity of the shoulder do not require any specific exploratory method because the findings are generally limited to a capacious axillary pouch.

Humans↗