Acute odontogenic infection combined with crowned dens syndrome: a case report.

BACKGROUND: Calcium pyrophosphate dihydrate crystal deposition disease is a condition in which calcium pyrophosphate dihydrate crystal is deposited in joint cartilage and ligaments. Calcium pyrophosphate dihydrate crystal deposition disease that involves calcification around the odontoid process of the second cervical vertebra is called crowned dens syndrome. Crowned dens syndrome is accompanied by fever in addition to acute and intense neck, posterior head, and temporal pain; thus, distinguishing crowned dens syndrome may be difficult in the presence of odontogenic infection. To the best of our knowledge, this is the first report describing a patient with crowned dens syndrome with coexisting odontogenic infection. CASE PRESENTATION: A 75-year-old Japanese woman was examined in the Emergency Department of this hospital due to a chief complaint of worsened buccal swelling on the left side. An odontogenic infection was considered, and she underwent her first examination. She presented with a body temperature of 37.4 °C, marked swelling and tenderness of her left lower eyelid through to her left cheek, and pain on the left temporal area. Blood tests revealed a leukocyte count of 6700/µL and a C-reactive protein level of 7.15 mg/dL. There was swelling and pain around the gingiva and acute purulent apical periodontitis of left maxillary second premolar. Cellulitis of the left cheek was diagnosed. After performing drainage of the pus, antibiotic treatment was initiated. Although her clinical symptoms improved, blood tests on day 9 of hospitalization revealed a leukocyte count of 6500/µL and a C-reactive protein level of 25.62 mg/dL, which were indicative of worsening symptoms. Computed tomography was performed to evaluate remote infection and images revealed a calcification around the odontoid process of her second cervical vertebra. When she was referred to the Orthopedic Surgery Department, pseudogout of the cervical spine was diagnosed. Subsequently, oral acetaminophen was initiated, and both her leukocyte count and C-reactive protein improved markedly. CONCLUSIONS: In the presence of persistent fever and abnormally high leukocyte and C-reactive protein indicative of an inflammatory reaction, coexistence of pseudogout should be considered. In particular, when symptoms of temporal pain are present, the possibility of pseudogout of the cervical spine must be considered in the differential diagnosis.

Two cases of pressure ulcers related to acute calcium pyrophosphate crystal arthritis: A new concept of "disease-specific unexpected external forces".

Sudden-onset immobilisation generates unexpected external forces over bony prominences and is a potential cause of pressure ulcers. Here, we report two cases of deep pressure ulcers in patients with acute monoarthritis as a result of calcium pyrophosphate (CPP) crystal deposition (pseudogout). The patients were women in their 80 who could perform activities of daily living by themselves. They developed pressure ulcers while living in their own home. Because acute CPP crystal arthritis is known to develop in relatively healthy elderly patients, patients and caregivers do not expect sudden-onset immobilisation. In addition, larger joints are preferentially involved in acute CPP crystal arthritis, leading to the inability of patients to change positions themselves. Therefore, acute CPP crystal arthritis should be recognised as a potential causal disease for pressure ulcers. This case report further highlights a new concept of "disease-specific unexpected external force", which is beneficial for the prevention of pressure ulcers.

Calcium crystal deposition diseases - beyond gout.

The most common types of calcium-containing crystals that are associated with joint and periarticular disorders are calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate (BCP) crystals. Several diverse but difficult-to-treat acute and chronic arthropathies and other clinical syndromes are associated with the deposition of these crystals. Although the pathogenic mechanism of calcium crystal deposition is partially understood, much remains to be investigated, as no drug is available to prevent crystal deposition, permit crystal dissolution or specifically target the pathogenic effects that result in the clinical manifestations. In this Review, the main clinical manifestations of CPP and BCP crystal deposition are discussed, along with the biological effects of these crystals, current therapeutic approaches and future directions in therapy.

Disease-Associated Particulates and Joint Inflammation; Mechanistic Insights and Potential Therapeutic Targets.

It is now well established that intra-articular deposition of endogenous particulates, such as osteoarthritis-associated basic calcium phosphate crystals, gout-associated monosodium urate crystals, and calcium deposition disease-associated calcium pyrophosphate crystals, contributes to joint destruction through the production of cartilage-degrading enzymes and pro-inflammatory cytokines. Furthermore, exogenous wear-debris particles, generated from prosthetic implants, drive periprosthetic osteolysis which impacts on the longevity of total joint replacements. Over the last few years, significant insight has been gained into the mechanisms through which these particulates exert their effects. Not only has this increased our understanding of the pathological processes associated with crystal deposition but it has also led to the identification of a number of therapeutic targets to treat particulate-associated disease. In this review, we discuss recent developments regarding the cellular events triggered by joint-associated particulates, as well as future directions in therapy for particulate-related arthropathies.

Crystal arthritides - gout and calcium pyrophosphate arthritis : Part 1: Epidemiology and pathophysiology.

Gout and calcium pyrophosphate deposition disease (CPPD, pseudogout) are still the most frequent inflammatory arthritides in multimorbid elderly patients. Gout and CPPD are different diseases and based on different pathophysiological principles. Gout is closely associated with the metabolic syndrome and is an independent risk factor for cardiovascular mortality. The prevalence of asymptomatic hyperuricemia is estimated to be 10-20% of adults in industrial nations and prevalence is strongly associated with age. More than 7% of persons aged over 65 years suffer from clinically manifest gout. The underlying pathophysiological principle is an imbalance between the formation and elimination of uric acid. The degradation of the purine bases adenine and guanosine to uric acid is catalysed by xanthine oxidase and genetic polymorphisms and mutations play an important role in absorption and excretion processes. Furthermore, carrier proteins, such as URAT-1 or OAT-4 also have an influence on these processes. An imbalance of the physiological processes results in the solubility product being exceeded, which in consequence leads to crystallization of urate. This induces a cascade of massive inflammatory reactions at the molecular and cellular level with the activation of cytokines. The inflammatory process can be stopped by neutrophil extracellular traps (NETs) that modulate aggregation and degradation of chemokines and cytokines and partitioning of crystallized urate against immune cells. Calcium pyrophosphate dehydrate (CPP) crystals are formed in the cartilage and CPP deposition can be found in 30% of people aged over 80 years. Inorganic pyrophosphate (PPi) is synthesized in chondrocytes and plays an important part in the formation of calcium pyrophosphate crystals. The degradation is catalyzed by inorganic pyrophosphatases. If there is dysregulation of this homeostasis more PPi is produced, which ultimately contributes to the formation of the CPP crystals.

Methotrexate: should it still be considered for chronic calcium pyrophosphate crystal disease?

Chronic calcium pyrophosphate crystal arthritis is a clinical consequence of the formation and deposition of these crystals in joints and can result in persistent arthritis. Curative treatment would require the removal of crystals from joints and tissues, but to date all agents tested have proven ineffective. Management of the inflammatory manifestations of chronic calcium pyrophosphate disease includes glucocorticoids, non-steroidal anti-inflammatory drugs, or colchicine, and responses are usually satisfactory. However, in some patients, the response to these agents is poor or they are contraindicated. Methotrexate had been reported as a promising option in small case series; however, in a recent issue of Arthritis Research & Therapy, a clinical trial failed to confirm the anticipated benefits. Here, we discuss some issues that might have influenced the results of the study, before deciding to abandon methotrexate as a therapeutic option for patients with chronic calcium pyrophosphate arthritis.

A Profilometry-Based Dentifrice Abrasion Method for V8 Brushing Machines Part II: Comparison of RDA-PE and Radiotracer RDA Measures.

OBJECTIVE: The purpose of this study was to compare the abrasivity of commercial dentifrices by two techniques: the conventional gold standard radiotracer-based Radioactive Dentin Abrasivity (RDA) method; and a newly validated technique based on V8 brushing that included a profilometry-based evaluation of dentin wear. This profilometry-based method is referred to as RDA-Profilometry Equivalent, or RDA-PE. METHODS: A total of 36 dentifrices were sourced from four global dentifrice markets (Asia Pacific [including China], Europe, Latin America, and North America) and tested blindly using both the standard radiotracer (RDA) method and the new profilometry method (RDA-PE), taking care to follow specific details related to specimen preparation and treatment. RESULTS: Commercial dentifrices tested exhibited a wide range of abrasivity, with virtually all falling well under the industry accepted upper limit of 250; that is, 2.5 times the level of abrasion measured using an ISO 11609 abrasivity reference calcium pyrophosphate as the reference control. RDA and RDA-PE comparisons were linear across the entire range of abrasivity (r2 = 0.7102) and both measures exhibited similar reproducibility with replicate assessments. RDA-PE assessments were not just linearly correlated, but were also proportional to conventional RDA measures. CONCLUSION: The linearity and proportionality of the results of the current study support that both methods (RDA or RDA-PE) provide similar results and justify a rationale for making the upper abrasivity limit of 250 apply to both RDA and RDA-PE.

Abrasion of eroded dentin caused by toothpaste slurries of different abrasivity and toothbrushes of different filament diameter.

OBJECTIVE: This study aimed to evaluate the impact of toothpaste slurry abrasivity and toothbrush filament diameter on abrasion of eroded dentin in vitro. METHODS: Eroded dentin samples (hydrochloric acid, pH 2.6, 15s) were brushed with 40 strokes in an automatic brushing machine using manual toothbrushes with different filament diameter (0.15, 0.20 or 0.25 mm). The toothbrushes were applied with a control slurry free of abrasive particles (RDA-value 10) or toothpastes slurries with different abrasivity (RDA-values 20, 50 or 100). Each erosive-abrasive cycle was followed by storage of the dentin samples in artificial saliva for 3h. After each 4 cycles, the samples were stored in artificial saliva for 15 h. After 60 cycles, dentin loss was measured by profilometry and statistically analysed by ANOVA and linear regression analysis. RESULTS: Dentin loss increased along with the RDA-value of the toothpaste slurries. The impact of the filament diameter on dentin loss was less evident compared to the RDA-value. However, toothbrushes with smaller filament stiffness caused higher dentin wear in all toothpaste slurry groups (RDA 20, 50 and 100) except for the paste-free control group (RDA 10). CONCLUSION: Abrasion of eroded dentin increased along with the RDA-value of the toothpaste slurry and with decreasing filament diameter of the toothbrush.

Control of brushing variables for the in vitro assessment of toothpaste abrasivity using a novel laboratory model.

OBJECTIVES: Design and construct a tooth-brushing simulator incorporating control of brushing variables including brushing force, speed and temperature, thereby facilitating greater understanding of their importance in toothpaste abrasion testing methodologies. METHODS: A thermostable orbital shaker was selected as a base unit and 16- and 24-specimen brushing rigs were constructed to fit inside, consisting of: a square bath partitioned horizontally to provide brushing channels, specimen holders for 25 mm diameter mounted specimens to fit the brushing channels and individually weighted brushing arms, able to support four toothbrush holders suspended over the brushing channels. Brush head holders consisted of individually weighted blocks of Delrin, or PTFE onto which toothbrush heads were fixed. Investigating effects of key design criteria involved measuring abrasion depths of polished human enamel and dentine. RESULTS: The brushing simulator demonstrated good reproducibility of abrasion on enamel and dentine across consecutive brushing procedures. Varying brushing parameters had a significant impact on wear results: increased brushing force demonstrated a trend towards increased wear, with increased reproducibility for greater abrasion levels, highlighting the importance of achieving sufficient wear to optimise accuracy; increasing brushing temperature demonstrated increased enamel abrasion for silica and calcium carbonate systems, which may be related to slurry viscosities and particle suspension; varying brushing speed showed a small effect on abrasion of enamel at lower brushing speed, which may indicate the importance of maintenance of the abrasive in suspension. CONCLUSIONS: Adjusting key brushing variables significantly affected wear behaviour. The brushing simulator design provides a valuable model system for in vitro assessment of toothpaste abrasivity and the influence of variables in a controlled manner. Control of these variables will allow more reproducible study of in vitro tooth wear processes.

Evaluation of dentin abrasion during professional tooth cleaning in an in vitro model.

OBJECTIVES: Professional tooth cleaning (PTC) may lead to loss of exposed dentin. The aim of the present study was to determine the absolute loss of dentin during PTC using various product combinations with an in vitro model. MATERIAL AND METHODS: Dentin specimens (72) were randomly assigned to nine groups. In four groups each, prophy brushes and prophy cups were used in combination with four different abrasives (calcium pyrophosphate, pumice, Hawe cleanic, Nupro coarse). In the ninth group, a rubber cup with embedded fluoride and abrasives was used (pasteless prophy cup). The treatment time was 37 s. Surface loss was determined by profilometry. RESULTS: The surface loss in the nine groups was as following: (1) brush/calcium pyrophosphate: 6.18 microm (a); (2) brush/pumice: 5.51 microm; (3) brush/Nupro coarse: 10.10 microm (b); (4) brush/Hawe cleanic: 1.88 (a, b); (5) prophy cup/calcium pyrophosphate 2.07 (c); (6) prophy cup/pumice: 6.07 microm; (7) prophy cup/Nupro coarse: 5.93 microm (c); (8) prophy cup/Hawe cleanic: 4.93 microm (c); (9) pasteless prophy cup: 11.86 microm (c). Groups with the same letter in parentheses are statistically significant different at p<0.05. In a pooled analysis, no statistically significant difference between brushes and prophy cups was found. CONCLUSION: In the present study, the surface loss of about eight PTC procedures was simulated. Hence, the dentin loss ranged between 0.24 and 1.48 microm per PTC. Therefore, PTC does not seem to be a main factor in dentin loss.

Inflammatory microcrystals alter the functional phenotype of human osteoblast-like cells in vitro: synergism with IL-1 to overexpress cyclooxygenase-2.

Chronic crystal-associated arthropathies such as gout and pseudogout can lead to local bone destruction. Because osteoblasts, which orchestrate bone remodeling via soluble factors and cell-to-cell interactions, have been described in contact with microcrystals, particularly in uratic foci of gout, we hypothesized that microcrystals of monosodium urate monohydrate (MSUM) and of calcium pyrophosphate dihydrate (CPPD) could alter osteoblastic functions. MSUM and CPPD adhered to human osteoblastic cells (hOB) in vitro and were partly phagocytized as shown by scanning electron microscopy. MSUM and CPPD dose-dependently stimulated the production of PGE(2) in hOB as assessed by enzyme immunoassay, a response that was synergistically enhanced in the presence of IL-1. The mechanism of this synergism was, at least in part, at the level of the expression of cyclooxygenase-2 as evaluated by immunoblot analysis. MSUM and CPPD also stimulated the expression of IL-6 and IL-8 and reduced the 1,25-dihydroxyvitamin D(3)-induced activity of alkaline phosphatase and osteocalcin in hOB (with no synergism with IL-1). MSUM- or CPPD-stimulated expression of IL-6 in hOB pretreated with the selective cyclooxygenase-2 inhibitor NS-398 was increased, unlike that induced by IL-1 alone which was partially reduced. MSUM-, CPPD- or IL-1-induced expression of IL-8 was unchanged by pretreating hOB with NS-398. These results suggest that inflammatory microcrystals alter the normal phenotype of hOB, redirecting them toward reduced bone formation and amplified osteoblast-mediated bone resorption, abnormalities that could play a role in the bone destruction associated with chronic crystal-induced arthritis.

Artropatía por depósito de cristales de dihidrato de pirofosfato de calcio / Calcium pyrophosfate dihydrate crystal deposition disease: review

Los autores estudiaron las características radiológicas en 67 pacientes con artropatía por depósito de cristales de dihidrato de pirofosfato de calcio encontrados en un total de 2.565 pacientes con articulaciones dolorosas no traumáticas; 2 por ciento de los casos presentaron artropatía por pirofosfato. La radiología convencional fue generalmente diagnóstica en todos los casos cuando se analizaron signos específicos para diferenciar la artropatía por pitofosfato de otras artropatías como la osteoartritis, considerando: a) condocalcinosis (94 por ciento), b) articulación no afectada usualmente en la osteoartritis primaria (22 por ciento) y c) compartimientos no comúnmente comprometidos en la osteoartritis (29 por ciento). Todos los pacientes presentaron además signos de artropatía degenerativa

Comparison of the acute inflammation induced by calcium pyrophosphate dihydrate, apatite and mixed crystals in the rat air pouch model of a synovial space.

Pure monoclinic or triclinic calcium pyrophosphate dihydrate (CPPD) crystals, apatite crystals or mixtures of these crystals were injected into the synovial-like space created by the rat air pouch to compare the acute inflammation induced by these crystals. Fluids were withdrawn 6 h after injection and examined for leukocyte counts, protease, prostaglandin E2 (PGE2) and tumor necrosis factor (TNF) levels. CPPD crystals (especially monoclinic CPPD) induced higher numbers of leukocytes, and more protease, PGE2 and TNF than apatite. CPPD seemed to play a predominant role in the acute inflammation induced by mixed crystals.

Arthropathies associated with calcium-containing crystals.

Monosodium urate crystals are clearly related to acute attacks of gout and to the hard tissue destruction of chronic tophaceous gout. Fortunately, the acute attacks are readily treated with anti-inflammatory drugs, and destructive changes due to tophi may be prevented or reversed, at least in part, by the intelligent control of serum urate levels. Control of gout is one of the premier success stories of modern medicine. In contrast, the number of patients who have arthritis associated with crystals that contain calcium appears to be rising--perhaps a function of better recognition, perhaps related to the aging of the population. CPPD and BCP crystals can be associated with acute or subacute inflammation, but as in acute gout, it is easily controlled with anti-inflammatory drugs or by local injections of corticosteroids. A direct relationship of BCP and CPPD crystals to the associated destructive arthropathies has been hypothesized and is supported by clinical observations, animal studies, and in vivo experiments. Unlike gout, which is usually associated with a systemic metabolic abnormality (i.e., hyperuricemia), calcium crystals deposition seem to be a localized phenomenon, although numerous local sites in several joints are often involved in a given patient. Tissue degeneration in gout clearly follows (tophaceous) crystal deposition. Calcium crystal deposition may follow, rather than precede, destructive joint changes. Alternatively, both destructive changes and crystal deposition may derive independently from a common, still obscure, biochemical abnormality of joint tissues. P. A. Dieppe and colleagues believe that calcium crystal deposition follows either primary or secondary tissue degeneration but that the crystals exert a positive feedback effect (amplification loop) that accelerates degeneration. Each of those formulations of a pathogenetic role for crystals may be true in a given case, analogous to the etiology of primary and secondary forms of hyperuricemia and to sodium urate crystal deposition coexistent with osteoarthritis (tophus formation in Heberden's nodes). Conclusive proof of a significant role for BCP or CPPD crystals in the pathogenesis of human joint tissue damage depends on interrupting the postulated disease mechanism and showing that this prevents joint deterioration and leads to significant repair of existing damage. Our current position is somewhat analogous to that of our colleagues who had to contend with management of gouty arthritis before the advent of effective drugs for control of hyperuricemia.

An international collaborative study of laboratory methods for assessing abrasivity to dentin.

An International Collaborative Study was conducted in which one surface profile and two radiotracer methods for assessing abrasivity of dentifrices on human dentin were compared. The study consisted of two phases: an open phase in which participating laboratories used the method they routinely practiced; and a controlled phase in which an expert team for each method performed the abrasion tests using all three methods. Four test pastes of known abrasivity were evaluated by each method. Similar abrasivity values for the test pastes were obtained with the radiotracer methods, whereas the surface profile method produced significantly different values. The precision levels of the radiotracer methods were similar, and both were superior to those obtained by the surface profile method. The time needed to perform the tests by the ADA radiotracer method was significantly less than that needed by the other methods. These findings suggest that the ADA radiotracer method will be useful in assessing abrasivity of dentifrices.