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Objective of Work: Wrong-site tooth extraction (WSTE) is the most common serious patient safety incident in dentistry. Safety checklists have significantly reduced wrong-site surgery, although their benefit is unproven in primary care dentistry. Our quality improvement project developed and implemented a checklist optimised for oral surgery procedures in primary care to reduce WSTE risk. Material and Methods: Local best practice for tooth extraction record-keeping (LBP), using national guidelines and standards was devised. We then retrospectively audited tooth extraction record-keeping against LBP. Deficiencies in current record-keeping practice were identified and used to design a checklist aimed at improving compliance. We provided a computerised safety checklist compliant with LBP to eleven clinicians at three general dental clinics within our region. The checklist included a preoperative safety check, a pause to re-confirm the surgical site and a post-operative record-keeping proforma. The checklist was linked to our record-keeping software for use during tooth extraction. We audited checklist completion and compliance with LBP fortnightly for ten weeks. Results: The introduction of a safety checklist resulted in increased compliance with LBP for tooth extraction record keeping. At week ten, 67% of records contained the computerised safety checklist. This resulted in a 50% increase in overall compliance with LBP for tooth extraction compared to baseline. Conclusions: A computerised safety checklist for tooth extraction in primary care has potential to improve patient safety by adopting measures to prevent WSTE and standardising communication between clinicians. Checklists in general practice should be encouraged.

Advanced alveolar bone resorption in the maxillary anterior teeth is a common finding that limits the placement of implants for prosthetic rehabilitation. Autologous bone graft from the mandibular symphysis is one of the oldest techniques in horizontal ridge augmentation techniques for placement of implants in advanced resorption of the alveolar ridge in the maxillary anterior region. This case report revisits the technique carried out using piezoelectric osteotome for harvesting block graft from the mandible to augment the resorbed ridge horizontally to place implant in a young and healthy patient.

Context: Melanin pigmentation of the gingiva is a physiological process that occurs in all ethnicities. Many treatment modalities are available to treat gingival hyperpigmentation. These are based on the principle of complete removal of the epithelial layer along with a part of subepithelial connective tissue which is then permitted to heal by secondary intention. Aim: This study aims to compare the treatment outcome of laser and its effectiveness in the management of gingival hyperpigmentation over scalpel. Design: A split-mouth study. Methods: Twenty young patients, between the ages of 18–35 with no systemic comorbidities with concerns regarding of dark-colored gums were selected for the study. A split-mouth study involving treatment of melanin pigmentation using scalpel abrasion on one side (left side upper and lower jaws) and Diode laser (980 nm) on other side (right side upper and lower jaws) was carried out. Observations regarding time taken, amount of bleeding during procedure, postoperative pain, healing of wound, and recurrence were made. Statistical Analysis: Data were analyzed using SPSS version 21.0 for Microsoft Windows. Results: Pain and healing were comparable in both the groups, though intraoperative time consumed and bleeding was significantly lower for laser group. Recurrence also was significantly lower on the laser group. Conclusion: Diode lasers can give better results in the management of gingival pigmentation compared to conventional scalpel abrasion technique.

Purpose: Three related male English Cocker Spaniels (ECS) were reported to be congenitally blind. Examination of one of these revealed complete retinal detachment. A presumptive diagnosis of retinal dysplasia (RD) was provided and pedigree analysis was suggestive of an X-linked mode of inheritance. We sought to investigate the genetic basis of RD in this family of ECS., Methods: Following whole genome sequencing (WGS) of the one remaining male RD-affected ECS, two distinct investigative approaches were employed: a candidate gene approach and a whole genome approach. In the candidate gene approach, COL9A2, COL9A3, NHEJ1, RS1 and NDP genes were investigated based on their known associations with RD and retinal detachment in dogs and humans. In the whole genome approach, affected WGS was compared with 814 unaffected canids to identify candidate variants, which were filtered based on appropriate segregation and predicted pathogenic effects followed by subsequent investigation of gene function. Candidate variants were tested for appropriate segregation in the ECS family and association with disease was assessed using samples from a total of 180 ECS., Results: The same variant in NDP (c.653_654insC, p.Met114Hisfs*16) that was predicted to result in 15 aberrant amino acids before a premature stop in norrin protein, was identified independently by both approaches and was shown to segregate appropriately within the ECS family. Association of this variant with X-linked RD was significant (P = 0.0056)., Conclusions: For the first time, we report a variant associated with canine X-linked RD. NDP variants are already known to cause X-linked RD, along with other abnormalities, in human Norrie disease. Thus, the dog may serve as a useful large animal model for research., Competing Interests: Three of the authors (HJ, LF and JO) are employed by a commercial company, Dick White Referrals. This does not alter our adherence to PLOS ONE policies on sharing data and materials. The authors declare that no other competing interests exist.

This study describes clinical and histopathological features, treatment, and outcome of cats diagnosed with ocular mycobacteriosis. Cases diagnosed from 2012 to 2017 were reviewed for (a) histopathological evidence of ocular (pyo)granulomatous inflammation containing acid-fast bacilli with mycobacterial morphology, (b) positive mycobacterial culture and/or mycobacterial DNA identified by polymerase chain reaction of ocular tissue, or (c) presumed mycobacteriosis based on ophthalmic examination and positive interferon-gamma release assay. Twenty-five cats (31 eyes) were included; 14 cats (17/31 eyes, 55%) were blind at presentation (unilateral: n = 12 cats; bilateral: n = 2 cats); one unilaterally affected cat later became bilaterally blind. Another 5 cats (7/31 eyes, 23%) became blind after initially being bilaterally visual (unilateral: n = 3 cats; bilateral: n = 2 cats). The commonest ocular finding was uveitis (87%). The main histopathological features were granulomatous to pyogranulomatous chorioretinitis with retinal detachment, anterior uveitis, optic neuritis, episcleritis, scleritis, and/or retrobulbar cellulitis. Nineteen cats (76%) had systemic signs, with disseminated disease being diagnosed in 9, defined by interstitial pulmonary disease, generalized lymphadenopathy, and/or nonocular infection. Nine cats were diagnosed with Mycobacterium bovis , 2 with Mycobacterium microti , 1 with Mycobacterium tuberculosis complex, and 1 with Mycobacterium avium-intracellulare complex. The infecting species was unknown in the remaining cats. Combined surgery (enucleation: n = 5 cats; biopsy: n = 3 cats) and systemic treatment with 2 or 3 appropriate antibiotics for 2 to 7 months resulted in remission in 8 of the 10 cats treated; however, the cat treated with dual therapy relapsed after 8 months. A total of 16 cats (64%) were euthanized; 2 were lost to follow-up.

Seven Northern Inuit Dogs (NID) were diagnosed by pedigree analysis with an autosomal recessive inherited oculoskeletal dysplasia (OSD). Short-limbed dwarfism, angular limb deformities and a variable combination of macroglobus, cataracts, lens coloboma, microphakia and vitreopathy were present in all seven dogs, while retinal detachment was diagnosed in five dogs. Autosomal recessive OSD caused by COL9A3 and COL9A2 mutations have previously been identified in the Labrador Retriever (dwarfism with retinal dysplasia 1-drd1) and Samoyed dog (dwarfism with retinal dysplasia 2-drd2) respectively; both of those mutations were excluded in all affected NID. Nine candidate genes were screened in whole genome sequence data; only one variant was identified that was homozygous in two affected NID but absent in controls. This variant was a nonsense single nucleotide polymorphism in COL9A3 predicted to result in a premature termination codon and a truncated protein product. This variant was genotyped in a total of 1,232 dogs. All seven affected NID were homozygous for the variant allele (T/T), while 31/116 OSD-unaffected NID were heterozygous for the variant (C/T) and 85/116 were homozygous for the wildtype allele (C/C); indicating a significant association with OSD (p = 1.41x10-11). A subset of 56 NID unrelated at the parent level were analysed to determine an allele frequency of 0.08, estimating carrier and affected rates to be 15% and 0.6% respectively in NID. All 1,109 non-NID were C/C, suggesting the variant is rare or absent in other breeds. Expression of retinal mRNA was similar between an OSD-affected NID and OSD-unaffected non-NID. In conclusion, a nonsense variant in COL9A3 is strongly associated with OSD in NID, and appears to be widespread in this breed., Competing Interests: Two of the authors (RS and JACO) are employed by a commercial company, Dick White Referrals. This does not alter our adherence to PLOS ONE policies on sharing data and materials. The authors declare that no other competing interests exist.

Canine progressive retinal atrophies (PRA) are genetically heterogeneous diseases characterized by retinal degeneration and subsequent blindness. PRAs are untreatable and affect multiple dog breeds, significantly impacting welfare. Three out of seven Giant Schnauzer (GS) littermates presented with PRA around four years of age. We sought to identify the causal variant to improve our understanding of the aetiology of this form of PRA and to enable development of a DNA test. Whole genome sequencing of two PRA-affected full-siblings and both unaffected parents was performed. Variants were filtered based on those segregating appropriately for an autosomal recessive disorder and predicted to be deleterious. Successive filtering against 568 canine genomes identified a single nucleotide variant in the gene encoding NECAP endocytosis associated 1 ( NECAP1 ): c.544G>A (p.Gly182Arg). Five thousand one hundred and thirty canids of 175 breeds, 10 cross-breeds and 3 wolves were genotyped for c.544G>A. Only the three PRA-affected GS were homozygous (allele frequency in GS, excluding proband family = 0.015). In addition, we identified heterozygotes belonging to Spitz and Dachshund varieties, demonstrating c.544G>A segregates in other breeds of German origin. This study, in parallel with the known retinal expression and role of NECAP1 in clathrin mediated endocytosis (CME) in synapses, presents NECAP1 as a novel candidate gene for retinal degeneration in dogs and other species.

Background: In humans, ADAMTS17 mutations are known to cause Weill-Marchesani-like syndrome, which is characterised by lenticular myopia, ectopia lentis, glaucoma, spherophakia, and short stature. Breed-specific homozygous mutations in ADAMTS17 are associated with primary open angle glaucoma (POAG) in several dog breeds, including the Petit Basset Griffon Vendeen (PBGV) and Shar Pei (SP). We hypothesised that these mutations are associated with short stature in these breeds., Methods: Two hundred thirty-three PBGV and 66 SP were genotyped for their breed-specific ADAMTS17 mutations. The height of each dog was measured at the withers. We used linear (per allele) regression to assess the association between ADAMTS17 mutations and height as a continuous variable, and linear regression and likelihood ratio tests to assess the shape of the association by comparing a general model with a linear (per allele) model., Results: The adjusted mean heights of affected, carrier, and clear PBGV were 33.49 cm ( n  = 21, 95% CI 32.78-34.19 cm), 34.88 cm ( n  = 85, 95% CI 34.53-35.25 cm), and 34.92 cm ( n  = 121, 95% CI 34.62-35.21 cm), respectively. The mean heights of affected, carrier, and clear SP were 43.96 cm ( n  = 9, 95% CI 41.88-46.03 cm), 47.56 cm ( n  = 28, 95% CI 45.50-48.63 cm), and 48.95 cm ( n  = 23, 95% CI 47.80-50.11 cm), respectively. There was a significant difference between the height of affected and clear animals in the PBGV ( P  = 0.001) and the SP ( P  = < 0.0001)., Conclusions: ADAMTS17 POAG mutations are significantly associated with height in these breeds., Competing Interests: Competing interestsTwo of the authors (CM and SR) are employed by the Animal Health Trust that provides commercial DNA testing for mutations in ADAMTS17.

Purpose: To investigate the genetic basis of primary closed angle glaucoma (PCAG) in European Basset Hounds using genome-wide association and RNA sequencing strategies., Methods: DNA samples from 119 European Basset Hounds were genotyped on the 170 K SNP CanineHD BeadChip array (Illumina) comprising 37 with normal iridocorneal angles (controls), 57 with pectinate ligament abnormality (PLA cases), and 25 with PCAG (PCAG cases). Genome-wide association studies (GWASs) of the PLA and PCAG cases were conducted. Whole transcriptome sequences of iridocorneal angle tissues from five Basset Hounds with PCAG were compared with those from four dogs with normal eyes to investigate differences in gene expression between the affected and unaffected eyes in GWAS-associated loci. A variant in NEB , previously reported to be associated with PCAG in American Basset Hounds, was genotyped in cohorts of European Basset Hounds and non-Basset Hounds., Results: The GWASs revealed 1.4 and 0.2 Mb regions, on chromosomes 24 and 37, respectively, that are statistically associated with PCAG. The former locus has previously been associated with glaucoma in humans. Whole transcriptome analysis revealed differential gene expression of eight genes within these two loci. The NEB variant was not associated with PLA or PCAG in this set of European Basset Hounds., Conclusions: We identified two novel loci for canine PCAG. Further investigation is required to elucidate candidate variants that underlie canine PCAG.

OBJECTIVE To evaluate the coding regions of ADAMTS17 for potential mutations in Chinese Shar-Pei with a diagnosis of primary open-angle glaucoma (POAG), primary lens luxation (PLL), or both. ANIMALS 63 Shar-Pei and 96 dogs of other breeds. PROCEDURES ADAMTS17 exon resequencing was performed on buccal mucosal DNA from 10 Shar-Pei with a diagnosis of POAG, PLL, or both (affected dogs). A candidate causal variant sequence was identified, and additional dogs (53 Shar-Pei [11 affected and 42 unaffected] and 95 dogs of other breeds) were genotyped for the variant sequence by amplified fragment length polymorphism analysis. Total RNA was extracted from ocular tissues of 1 affected Shar-Pei and 1 ophthalmologically normal Golden Retriever; ADAMTS17 cDNA was reverse transcribed and sequenced, and ADAMTS17 expression was evaluated by quantitative reverse-transcription PCR assay. RESULTS All affected Shar-Pei were homozygous for a 6-bp deletion in exon 22 of ADAMTS17 predicted to affect the resultant protein. All unaffected Shar-Pei were heterozygous or homozygous for the wild-type allele. The variant sequence was significantly associated with affected status (diagnosis of POAG, PLL, or both). All dogs of other breeds were homozygous for the wild-type allele. The cDNA sequencing confirmed presence of the expected variant mRNA sequence in ocular tissue from the affected dog only. Gene expression analysis revealed a 4.24-fold decrease in the expression of ADAMTS17 in ocular tissue from the affected dog. CONCLUSIONS AND CLINICAL RELEVANCE Results supported that the phenotype (diagnosis of POAG, PLL, or both) is an autosomal recessive trait in Shar-Pei significantly associated with the identified mutation in ADAMTS17.