Chronic glial activation and behavioral alterations induced by acute/subacute pioglitazone treatment in a mouse model of traumatic brain injury.

Traumatic brain injury (TBI) is a disabling neurotraumatic condition and the leading cause of injury-related deaths and disability in the United States. Attenuation of neuroinflammation early after TBI is considered an important treatment target; however, while these inflammatory responses can induce secondary brain injury, they are also involved in the repair of the nervous system. Pioglitazone, which activates peroxisome proliferator-activated receptor gamma, has been shown to decrease inflammation acutely after TBI, but the long-term consequences of its use remain unknown. For this reason, the impacts of treatment with pioglitazone during the acute/subacute phase (30 min after injury and each subsequent 24 h for 5 days) after TBI were interrogated during the chronic phase (30- and 274-days post-injury (DPI)) in mice using the controlled cortical impact model of experimental TBI. Acute/subacute pioglitazone treatment after TBI results in long-term deleterious consequences, including disruption of tau homeostasis, chronic glial cell activation, neuronal pathology, and worsened injury severity particularly at 274 DPI, with male mice being more susceptible than female mice. Further, male pioglitazone-treated TBI mice exhibited increased dominant and offensive-like behavior while having a decreased non-social exploring behavior at 274 DPI. After TBI, both sexes exhibited glial activation at 30 DPI when treated with pioglitazone; however, while injury severity was increased in females it was not impacted in male mice. This work reveals that although pioglitazone has been shown to lead to attenuated TBI outcomes acutely, sex-based differences, timing and long-term consequences of treatment with glitazones must be considered and further studied prior to their clinical use for TBI therapy.

Cellular and molecular mechanisms of hepatic ischemia-reperfusion injury: The role of oxidative stress and therapeutic approaches.

Ischemia-reperfusion (IR) or reoxygenation injury is the paradoxical exacerbation of cellular impairment following restoration of blood flow after a period of ischemia during surgical procedures or other conditions. Acute interruption of blood supply to the liver and subsequent reperfusion can result in hepatocyte injury, apoptosis, and necrosis. Since the liver requires a continuous supply of oxygen for many biochemical reactions, any obstruction of blood flow can rapidly lead to hepatic hypoxia, which could quickly progress to absolute anoxia. Reoxygenation results in the increased generation of reactive oxygen species and oxidative stress, which lead to the enhanced production of proinflammatory cytokines, chemokines, and other signaling molecules. Consequent acute inflammatory cascades lead to significant impairment of hepatocytes and nonparenchymal cells. Furthermore, the expression of several vascular growth factors results in the heterogeneous closure of numerous hepatic sinusoids, which leads to reduced oxygen supply in certain areas of the liver even after reperfusion. Therefore, it is vital to identify appropriate therapeutic modalities to mitigate hepatic IR injury and subsequent tissue damage. This review covers all the major aspects of cellular and molecular mechanisms underlying the pathogenesis of hepatic ischemia-reperfusion injury, with special emphasis on oxidative stress, associated inflammation and complications, and prospective therapeutic approaches.

Molecular pathogenesis of metabolic dysfunction-associated steatotic liver disease, steatohepatitis, hepatic fibrosis and liver cirrhosis.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by intense deposition of fat globules in the hepatic parenchyma that could potentially progress to liver cirrhosis and hepatocellular carcinoma. Here, we evaluated a rat model to study the molecular pathogenesis of the spectrum of MASLD and to screen therapeutic agents. SHRSP5/Dmcr rats were fed a high-fat and cholesterol (HFC) diet for a period of 12 weeks and evaluated for the development of steatosis (MASLD), steatohepatitis, fibrosis and cirrhosis. A group of animals were sacrificed at the end of the 4th, 6th, 8th and 12th weeks from the beginning of the experiment, along with the control rats that received normal diet. Blood and liver samples were collected for biochemical and histopathological evaluations. Immunohistochemical staining was performed for α-SMA and Collagen Type I. Histopathological examinations demonstrated steatosis at the 4th week, steatohepatitis with progressive fibrosis at the 6th week, advanced fibrosis with bridging at the 8th week and cirrhosis at the 12th week. Biochemical markers and staining for α-SMA and Collagen Type I demonstrated the progression of steatosis to steatohepatitis, hepatic fibrosis and liver cirrhosis in a stepwise manner. Control animals fed a normal diet did not show any biochemical or histopathological alterations. The results of the present study clearly demonstrated that the HFC diet-induced model of steatosis, steatohepatitis, hepatic fibrosis and cirrhosis is a feasible, quick and appropriate animal model to study the molecular pathogenesis of the spectrum of MASLD and to screen potent therapeutic agents.

Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats.

Parkinson's disease (PD) is the most common progressive neurodegenerative movement disorder and results from the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Pink1 and Parkin are proteins that function together in mitochondrial quality control, and when they carry loss-of-function mutations lead to familial forms of PD. While much research has focused on central nervous system alterations in PD, peripheral contributions to PD pathogenesis are increasingly appreciated. We report Pink1/Parkin regulate glycolytic and mitochondrial oxidative metabolism in peripheral blood mononuclear cells (PBMCs) from rats. Pink1/Parkin deficiency induces changes in the circulating lymphocyte populations, namely increased CD4 + T cells and decreased CD8 + T cells and B cells. Loss of Pink1/Parkin leads to elevated platelet counts in the blood and increased platelet-T cell aggregation. Platelet-lymphocyte aggregates are associated with increased thrombosis risk, and venous thrombosis is a cause of sudden death in PD, suggesting targeting the Pink1/Parkin pathway in the periphery has therapeutic potential.

Arthroscopic Fixation of Acute Large Bony Bankart with Suture-assisted Reduction and Screw Fixation - Surgical Technique.

Introduction: Glenoid rim fractures with Bankart lesions are called bony Bankart lesions and are associated with persistent glenohumeral joint instability. Acute bony Bankart lesions can be treated by various arthroscopic techniques. Here, we present a technique of arthroscopic bony Bankart repair using suture-assisted reduction and screw fixation. Discussion: The conventional suture anchor repair does not provide compression of the fractured fragment, and the bony piece may tilt because of the single-point fixation. Conclusion: This procedure can achieve firm compression between the bony fragments and prevent rotation of fragment during screw fixation to the glenoid. The capsular plication distributes the loads to the surrounding soft tissues. Hence, this procedure should be offered to all patients presenting acutely with a large bony Bankart of size >25% of glenoid width, as it is minimally invasive as well as provides excellent outcomes and anatomical union.

Perception of congenital cardiac surgery as a career choice among cardiothoracic surgery trainees in the United Kingdom.

OBJECTIVES: Our goal was to evaluate interest among trainees in pursuing congenital cardiac surgery (CCS) as a sub-specialty career and probe for reasons in decline in interest. METHODS: An anonymized, voluntary survey of cardiothoracic surgical trainees across the United Kingdom and Ireland was conducted from October 2020 to December 2020. The questionnaire included demographics, congenital experience and career intentions. RESULTS: A total of 43 respondents from all training regions responded with a response rate of 36%. A total of 28% reported having no access to a congenital cardiac unit in their training region, reflecting that 4 out of the 14 regions do not have a congenital unit. Although only 18% of trainees have undertaken a placement, a large proportion (74%) have considered a career in CCS, predominantly (50%) before entering training or in the first half of the training programme (38%). Reasons for not pursuing included discouragement by colleagues (42%) and concerns regarding the training pathway, citing, among other reasons, length of training, limited exposure to operations and uncertainty about career progression. Respondents suggested improvements to the training programme, including increasing exposure and early mentoring and steps to dispel unduly negative perceptions about the specialty. CONCLUSIONS: A large proportion of cardiothoracic trainees have a negative perception of CCS in terms of career and training. Interest wanes substantially after entry into the United Kingdom cardiothoracic training programme for several reasons. As well as short-term measures to improve exposure to CCS and structure of training, there has to be long-term planning to improve perception about this sub-specialty at all levels.

Interaction between fatty acid oxidation and ethanol metabolism in liver.

Fatty acid oxidation (FAO) releases the energy stored in fat to maintain basic biological processes. Dehydrogenation is a major way to oxidize fatty acids, which needs NAD+ to accept the released H+ from fatty acids and form NADH, which increases the ratio of NADH/NAD+ and consequently inhibits FAO leading to the deposition of fat in the liver, which is termed fatty liver or steatosis. Consumption of alcohol (ethanol) initiates simple steatosis that progresses to alcoholic steatohepatitis, which constitutes a spectrum of liver disorders called alcohol-associated liver disease (ALD). ALD is linked to ethanol metabolism. Ethanol is metabolized by alcohol dehydrogenase (ADH), microsomal ethanol oxidation system (MEOS), mainly cytochrome P450 2E1 (CYP2E1), and catalase. ADH also requires NAD+ to accept the released H+ from ethanol. Thus, ethanol metabolism by ADH leads to increased ratio of NADH/NAD+, which inhibits FAO and induces steatosis. CYP2E1 directly consumes reducing equivalent NADPH to oxidize ethanol, which generates reactive oxygen species (ROS) that lead to cellular injury. Catalase is mainly present in peroxisomes, where very long-chain fatty acids and branched-chain fatty acids are oxidized, and the resultant short-chain fatty acids will be further oxidized in mitochondria. Peroxisomal FAO generates hydrogen peroxide (H2O2), which is locally decomposed by catalase. When ethanol is present, catalase uses H2O2 to oxidize ethanol. In this review, we introduce FAO (including α-, ß-, and ω-oxidation) and ethanol metabolism (by ADH, CYP2E1, and catalase) followed by the interaction between FAO and ethanol metabolism in the liver and its pathophysiological significance.

Therapeutic implication of human placental extract to prevent liver cirrhosis in rats with metabolic dysfunction-associated steatohepatitis.

Metabolic dysfunction-associated steatohepatitis (MASH) is always accompanied with hepatic fibrosis that could potentially progress to liver cirrhosis and hepatocellular carcinoma. Employing a rat model, we evaluated the role of human placental extract (HPE) to arrest the progression of hepatic fibrosis to cirrhosis in patients with MASH. SHRSP5/Dmcr rats were fed with a high-fat and high-cholesterol diet for 4 weeks and evaluated for the development of steatosis. The animals were divided into control and treated groups and received either saline or HPE (3.6 ml/kg body weight) subcutaneously thrice a week. A set of animals were killed at the end of 6th, 8th, and 12th weeks from the beginning of the experiment. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), hepatic malondialdehyde (MDA), and glutathione content were measured. Immunohistochemical staining was performed for α-smooth muscle actin (α-SMA), 4-hydroxy-2-nonenal (4-HNE), collagen type I, and type III. Control rats depicted progression of liver fibrosis at 6 weeks, advanced fibrosis and bridging at 8 weeks, and cirrhosis at 12 weeks, which were significantly decreased in HPE-treated animals. Treatment with HPE maintained normal levels of MDA and glutathione in the liver. There was marked decrease in the staining intensity of α-SMA, 4-HNE, and collagen type I and type III in HPE treated rats compared with control animals. The results of the present study indicated that HPE treatment mediates immunotropic, anti-inflammatory, and antioxidant responses and attenuates hepatic fibrosis and early cirrhosis. HPE depicts therapeutic potential to arrest the progression of MASH towards cirrhosis.

Longitudinal assessment of dental erosion-abrasion by cross-polarization optical coherence tomography in vitro.

This study tested a novel in vitro dental erosion-abrasion model and the performance of cross-polarization optical coherence tomography (CP-OCT) in longitudinally monitoring the simulated lesions. Thirty human enamel specimens were prepared and randomized to receive three dental erosion-abrasion (EA) protocols: severe (s-EA, lemon juice/pH:2.5/4.25%w/v citric acid), moderate (m-EA, grapefruit juice/pH:3.5/1.03%w/v citric acid) and no-EA (water, control). EA challenge was performed by exposing the specimens to acidic solutions 4x/day and to brushing 2x/day with 1:3 fluoridated toothpaste slurry, for 14 days. Enamel thickness measurements were obtained using CP-OCT at baseline (D0), 7 (D7) and 14 days (D14) and micro-computed tomography (micro-CT) at D14. Enamel surface loss was measured with both CP-OCT and optical profilometry at D0, D7 and D14. Data was analyzed with repeated-measures ANOVA and Pearson's correlation (r) (α = 0.05). CP-OCT enamel thickness decreased over time in the s-EA group (D0 >D7 > D14, p < 0.001) and m-EA group (D0 > D14, p = 0.019) but did not change in the no-EA group (p = 0.30). Overall, CP-OCT and micro-CT results at D14 correlated moderately (r = 0.73). CP-OCT surface loss was highest for s-EA (p <0.001) but did not differ between moderate and no-EA (p = 0.25). Enamel surface loss with profilometry increased with severity (no-EA>m-EA>s-EA, p < 0.001). D14 surface loss was higher than D7 for both methods except for the no-EA group with profilometry. CP-OCT and profilometry had moderate overall correlation (r = 0.70). Our results revealed that the currently proposed in vitro dental erosion-abrasion model is valid and could simulate lesions of different severities over time. CP-OCT was a suitable method for monitoring the EA lesions.

Eosinophilic Fasciitis Possibly Provoked by Exercise.

A 26-year-old woman was referred to dermatology for evaluation of "lumpy skin" for 4 months. She experienced Achilles tendon pain and muscle tightness, occurring before the skin lesions had appeared. The lesions began on her arms and progressed to her legs over 1 month.

Tension pyopneumothorax caused by Burkholderia cenocepacia: a rare case report in an immunocompetent individual.

Tension pyopneumothorax is a medical emergency that occurs when air and pus build up in the pleural space. This case report describes a 47-year-old diabetic female who presented with tension pyopneumothorax due to Burkholderia cenocepacia. The patient was successfully treated with a 24-French tube thoracostomy and antibiotics. To the best of our knowledge, this is the first case of tension pyopneumothorax caused by Burkholderia cenocepacia to be reported.

Inferior scapula avulsion fracture: an unusual presentation of winged scapula.

Inferior scapula avulsion fractures are rare injuries, with few cases reported and only a small number managed operatively discussed in the literature. We report the case of a man in his 40s who fell from a height and presented with right-sided scapular winging and point tenderness at the inferior pole of his right scapula with no neurological deficit. Radiographs and CT diagnosed avulsion fracture of the inferior scapula. The patient underwent surgical fixation and, following a course of physiotherapy, successfully recovered with no residual winging and full range of movement.

Immediate and 90-Day Clinical Outcome of Patients with Acute Stroke Treated with the NeVa-Vesalio Mechanical Thrombectomy Device: A Retrospective Case Series.

OBJECTIVE: The NeVa stent retriever is a newly designed mechanical thrombectomy device for the treatment of acute ischemic stroke caused by large vessel occlusion. We investigate the procedural characteristics and patients' clinical outcomes at discharge and at 90 days of follow-up. METHODS: We retrospectively reviewed a cohort of 75 patients (median age, 74 years) treated with the NeVa device for acute large vessel occlusion stroke. Per pass modified Treatment in Cerebral Infarction (mTICI) scores, procedural complications, and clinical outcome parameters including the National Institutes of Health Stroke Scale (NIHSS) score, modified Rankin Scale (mRS) score, and mortality were analyzed, based on patients' electronic medical records. RESULTS: Complete first pass effect was observed in 24 patients (32%). Vasospasm, repeated re-thrombosis, failure to advance the NeVa device through the microcatheter, and symptomatic intracranial hemorrhage were observed in 2, 1, 1, and 2 patient(s) respectively. The rate of complete (mTICI 2c-3) reperfusion was achieved in 61 patients (81.33%), with a median number of 2 passes (1-3). Median NIHSS score on admission, after 24 hours, and after 5-10 days or at discharge was 19 (15-23), 11 (4-19), and 3 (2-13.5), respectively. The number of patients with a functional mRS score (0-2) at 90 days follow-up was 29 (39%). CONCLUSIONS: Endovascular stroke management with use of the NeVa-Vesalio stent retriever may be associated with a 90-day functional mRS score in nearly 40% of treated patients.

Parkinson's disease relevant pathological features are manifested in male Pink1/Parkin deficient rats.

Animal disease models are important for neuroscience experimentation and in the study of neurodegenerative disorders. The major neurodegenerative disorder leading to motor impairments is Parkinson's disease (PD). The identification of hereditary forms of PD uncovered gene mutations and variants, such as loss-of-function mutations in PTEN-induced putative kinase 1 (Pink1) and the E3 ubiquitin ligase Parkin, two proteins involved in mitochondrial quality control, that could be harnessed to create animal models. However, to date, such models have not reproducibly recapitulated major aspects of the disease. Here, we describe the generation and phenotypic characterization of a combined Pink1/Parkin double knockout (dKO) rat, which reproducibly exhibits PD-relevant abnormalities, particularly in male animals. Motor dysfunction in Pink1/Parkin dKO rats was characterized by gait abnormalities and decreased rearing frequency, the latter of which was responsive to levodopa treatment. Pink1/Parkin dKO rats exhibited elevated plasma levels of neurofilament light chain and significant loss of tyrosine hydroxylase expression in the substantia nigra pars compacta (SNpc). Glial cell activation was also observed in the SNpc. Pink1/Parkin dKO rats showed elevated plasma and reduced cerebrospinal levels of alpha-synuclein as well as the presence of alpha-synuclein aggregates in the striatum. Further, the profile of circulating lymphocytes was altered, as elevated CD3+CD4+ T cells and reduced CD3+CD8+ T cells in Pink1/Parkin dKO rats were found. This coincided with mitochondrial dysfunction and infiltration of CD3+ T cells in the striatum. Altogether, the Pink1/Parkin dKO rats exhibited phenotypes similar to what is seen with PD patients, thus highlighting the suitability of this model for mechanistic studies of the role of Pink1 and Parkin in PD pathogenesis and as therapeutic targets.

Synovial Chondromatosis Ankle - A Case Report.

Introduction: Many loose bodies are present in the joint due to the uncommon benign neoplastic disorder known as synovial chondromatosis, which causes the production of intra-articular nodular cartilaginous lesions from the synovium. Synovial chondromatosis of the ankle joint is an uncommon condition. Here, we present a case of synovial chondromatosis of the ankle joint treated by surgical excision. Case Report: A 42-year-old woman who had been experiencing discomfort and edema in her left ankle for 8 years and had gotten worse during the previous 2 years visited our outpatient department. Clinical and radiological examination revealed synovial chondromatosis of the left ankle joint. Conclusion: Synovial chondromatosis of the ankle is an uncommon synovial neoplasm in an unlikely anatomic location. The diagnosis should be considered when evaluating monoarticular synovitis.

Healing pattern of subfoveal retinal pigment epithelium rip and aperture in central serous chorioretinopathy.

This report describes a rare case of spontaneous Grade-4 retinal pigment epithelium (RPE) rip of serous pigment epithelial detachment (PED) in central serous chorioretinopathy (CSC) and RPE aperture in the fellow eye, with favorable long-term outcomes. A 38-year-old man presented with defective vision (20/30) in the left eye (LE) due to bullous CSC associated with a large extramacular RPE rip located temporally and inferior exudative retinal detachment. Optical coherence tomography (OCT) confirmed a subfoveal serous PED with RPE aperture, subretinal fluid (SRF) and fibrinous exudation, and a large extramacular RPE rip temporally. The right eye (RE) had an asymptomatic large serous PED. The LE was treated with low-fluence photodynamic therapy, which resulted in the closure of RPE aperture and complete resolution of PED and SRF. Six-month later, the patient presented with sudden defective vision (20/120) in the RE secondary to a large fovea-involving (Grade-4) RPE rip with SRF as confirmed on OCT. Fluorescein angiography showed two extrafoveal active point leaks, which were treated with focal photocoagulation. He was also started on oral eplerenone. On subsequent serial follow-ups over 1 year, OCT showed SRF resolution and patchy reorganization of the subfoveal RPE-photoreceptor complex with good visual outcome (20/30).

Patient-reported outcome measures in congenital heart surgery: a systematic review.

BACKGROUND: Patient-reported outcome measures are commonly used to evaluate the effectiveness of treatments. CHD remains the most common congenital malformation. There has been a gradual shift in evaluating the outcome of surgery for CHD from mortality to morbidity and now to self-reported outcomes. AIMS: We aimed to review studies assessing patient-reported outcome measures as a useful marker of outcome for patients, both children and adults, who underwent surgery for CHD. METHODS: A systematic database search was conducted of original articles that explored the application of patient-reported outcome measures in the CHD surgical setting in PubMed and SCOPUS from inception to February 2022. RESULTS: Our search yielded 1511 papers, of which six studies were included in this review after screening abstract and full-text, with a total sample size of 5734 patients. The main areas of discussion were the utility of patient-reported outcome measures, determinants of patient-reported outcome measures, and the need for a congenital cardiac surgery-specific patient-reported outcome measure for paediatric patients and their parents/guardians and adult patients. CONCLUSION: This systematic review reports the use of patient-reported outcome measures to be a useful indicator to gain insight into the patients' perspective to provide holistic and patient-centred management. However, further studies are required to assess the utility of patient-reported outcome measures in a congenital cardiac surgical setting.

Robotic Arm-Assisted versus Manual Total Knee Arthroplasty: A Propensity Score-Matched Analysis.

The purpose of this study was to compare (1) operative time, (2) in-hospital pain scores, (3) opioid medication use, (4) length of stay (LOS), (5) discharge disposition at 90-day postoperative, (6) range of motion (ROM), (7) number of physical therapy (PT) visits, (8) emergency department (ED) visits, (9) readmissions, (10) reoperations, (11) complications, and (12) 1-year patient-reported outcome measures (PROMs) in propensity matched patient cohorts who underwent robotic arm-assisted (RA) versus manual total knee arthroplasty (TKA). Using a prospectively collected institutional database, patients who underwent RA- and manual TKA were the nearest neighbor propensity score matched 3:1 (255 manual TKA:85 RA-TKA), accounting for various preoperative characteristics. Data were compared using analysis of variance (ANOVA), Kruskal-Wallis, Pearson's Chi-squared, and Fisher's exact tests, when appropriate. Postoperative pain scores, opioid use, ED visits, readmissions, and 1-year PROMs were similar between the cohorts. Manual TKA patients achieved higher maximum flexion ROM (120.3 ± 9.9 versus 117.8 ± 10.2, p = 0.043) with no statistical differences in other ROM parameters. Manual TKA had shorter operative time (105 vs.113 minutes, p < 0.001), and fewer PT visits (median [interquartile range] = 10.0 [8.0-13.0] vs. 11.5 [9.5-15.5] visits, p = 0.014). RA-TKA had shorter LOS (0.48 ± 0.59 vs.1.2 ± 0.59 days, p < 0.001) and higher proportion of home discharges (p < 0.001). RA-TKA and manual TKA had similar postoperative complications and 1-year PROMs. Although RA-TKA patients had longer operative times, they had shorter LOS and higher propensity for home discharge. In an era of value-based care models and the steady shift to outpatient TKA, these trends need to be explored further. Long-term and randomized controlled studies may help determine potential added value of RA-TKA versus manual TKA. This study reflects level of evidence III.

Longitudinal assessment of dental erosion-abrasion by cross-polarization optical coherence tomography in vitro

Abstract: This study tested a novel in vitro dental erosion-abrasion model and the performance of cross-polarization optical coherence tomography (CP-OCT) in longitudinally monitoring the simulated lesions. Thirty human enamel specimens were prepared and randomized to receive three dental erosion-abrasion (EA) protocols: severe (s-EA, lemon juice/pH:2.5/4.25%w/v citric acid), moderate (m-EA, grapefruit juice/pH:3.5/1.03%w/v citric acid) and no-EA (water, control). EA challenge was performed by exposing the specimens to acidic solutions 4x/day and to brushing 2x/day with 1:3 fluoridated toothpaste slurry, for 14 days. Enamel thickness measurements were obtained using CP-OCT at baseline (D0), 7 (D7) and 14 days (D14) and micro-computed tomography (micro-CT) at D14. Enamel surface loss was measured with both CP-OCT and optical profilometry at D0, D7 and D14. Data was analyzed with repeated-measures ANOVA and Pearson's correlation (r) (α = 0.05). CP-OCT enamel thickness decreased over time in the s-EA group (D0 >D7 > D14, p < 0.001) and m-EA group (D0 > D14, p = 0.019) but did not change in the no-EA group (p = 0.30). Overall, CP-OCT and micro-CT results at D14 correlated moderately (r = 0.73). CP-OCT surface loss was highest for s-EA (p <0.001) but did not differ between moderate and no-EA (p = 0.25). Enamel surface loss with profilometry increased with severity (no-EA>m-EA>s-EA, p < 0.001). D14 surface loss was higher than D7 for both methods except for the no-EA group with profilometry. CP-OCT and profilometry had moderate overall correlation (r = 0.70). Our results revealed that the currently proposed in vitro dental erosion-abrasion model is valid and could simulate lesions of different severities over time. CP-OCT was a suitable method for monitoring the EA lesions.