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Abstract

Purpose

Identify characteristics predictive of CPPD in the lumbar spine and evaluate the impact of CPPD on perioperative adverse events.

Methods

A cohort of patients who underwent open lumbar decompressions for spinal stenosis at a single academic tertiary referral center from 1/1/2001 to 1/31/2021 with pathology-proven pseudogout were compared with an age, sex and BMI propensity-matched non-CPPD cohort. The primary outcome was incidental durotomy. Secondary outcomes were 90-day reoperations and all-cause readmissions, chronic pain utilization and motor deficits. Independent associations between patient factors, operative characteristics and CPPD with adverse events were identified using step-wise multivariate logistic regressions.

Results

A total of 139 patients diagnosed with CPPD based on operative pathology (mean age 68.4 ± 10.7 years, 49.6% female, mean BMI 28.9 ± 6.1) were compared with a matched cohort of 133 patients. Active smoking (OR 3.1, 95% CI 1.3 to 7.6) and a prior epidural steroid injection (OR 2.5, 95% CI 1.4 to 4.3) were independently associated with lumbar CPPD. CPPD was associated with an increased likelihood of durotomy (OR 2.2, 95% CI 1.1 to 4.5).

Conclusions

CPPD was more prevalent in active smokers and those who received an epidural steroid injection. Durotomies were more common in patients with CPPD.

Keywords

pseudogout calcium pyrophosphate deposition disease lumbar laminectomy dural tear

Introduction

Calcium pyrophosphate deposition disease (CPPD), or pseudogout, is a crystal deposition arthropathy of the synovial and periarticular tissues. The clinical manifestations of CPPD vary widely, ranging from no symptoms at all to chronic inflammatory arthritis.³⁰ CPPD can be hereditary or sporadic and has been associated with parathyroid dysfunction and magnesium and phosphate dysmetabolic syndromes.^4,9,12,29 CPPD of the joints of the appendicular skeleton is commonly mistaken for a feature of degenerative osteoarthritis and is consequently underdiagnosed on conventional X-rays. Thirty percent of harvested knee surgical specimens with known osteoarthritis had CPPD crystals on pathologic analysis.^5,7,18

CPPD is less commonly reported in the spine than in the appendicular skeleton. Spinal synovial calcinosis may present as CPPD crystals surrounded by a foreign body giant cell and histiocytic reaction, which previously led to its misdiagnosis as a neoplasm.²³ The increased use and availability of magnetic resonance imaging (MRI) has helped distinguish CPPD on pre-operative imaging as hypo- or isointense on sagittal T1- or T2 weighted images. Furusawa et al⁸ in their analysis of ligamentum flavum samples that contained calcium deposits noted areas of marked elastic fiber degeneration and the formation of nodular granulomas, which the authors hypothesized were the nidus for calcium crystal deposition. Yayama et al²⁶ reported that these calcium deposits were surrounded by areas of neoangiogenesis and hypertrophic chondrocytes, which may be involved in the formation of CPPD crystals.²⁵ This pathologic environment is suggestive of chronic relapsing inflammation, predisposing to scar formation that could involve the dura.

This work evaluated a 20-year hospital experience treating patients with pathology-confirmed CPPD of the lumbar spine who underwent open decompression for spinal stenosis with matched non-CPPD patients over that same period. We hypothesized that the inflammatory environment inherent in CPPD of the lumbar spine would predispose to higher durotomy, 90-day readmission, and 90-day unplanned return to the OR rates compared with matched institutional controls.

Methods

This was an institutional review board-approved (Partners Human Research Committee 2016P002658) retrospective analysis of patients who underwent an open lumbar decompression with or without fusion at a single large academic tertiary referral medical center from 1/1/2001 to 1/31/2021. Inclusion criteria were patients 18 years and older who underwent a posterior decompression for lumbar stenosis. Patients with an active malignancy, active or chronic spinal infection, pseudoarthrosis from a prior lumbar surgery, or who underwent surgery without an open decompression were excluded from this work.

CPPD was diagnosed via intraoperative specimens sent by the operative surgeon from those patients in whom CPPD was suspected. Features that prompted the submission of pathologic specimens were tophaceous deposits within the synovial tissues, ligamentum flavum, or interspinous ligaments or tophaceous material within a facet cyst (Figures 1 and 2). CPPD was diagnosed by the pathologist if positively birefringent crystals were present in the specimen on microscopic analysis.

Figure 1.

Intraoperative image of a tophaceous deposit obtained during a lumbar decompression that was confirmed to be CPPD.

Figure 2.

(A) The characteristic rhomboid shape of the CPPD crystals could be observed within the ligamentum flavum after hematoxylin and eosin staining; (B) a black elastin fiber stain was performed on 1 of the samples to further outline CPPD crystals among the elastin fibers; (C) polarized light microscopy demonstrated the presence of positively birefringent crystals, confirming the diagnosis of CPPD.

CPPD patient records were identified via free text search of pathology records using our institutional Research Patient Data Registry (RPDR), while non-CPPD patients were isolated for matching from those patients who carried an International Classification of Diseases 10th revision (ICD10) diagnosis code for lumbar stenosis and Current Procedural Terminology (CPT) codes for lumbar decompression. The institutional comparison group was generated via propensity score matching using one-to-one nearest-neighbor matching in a random order without replacement and a caliper fixed at 0.005 based on a propensity score calculated through a logistic regression model that included age, sex, and body mass index. Clinical and outcome data for both groups were obtained via medical record review.

The primary outcome was incidental durotomy. Secondary outcomes were surgical site infections, 90-day reoperations, 90-day all-cause readmissions, chronic pain/opioid utilization, and 3-month post-operative motor deficits.

Identification of the primary and secondary outcomes for both the CPPD and non-CPPD cohorts was performed via direct review of operative records and discharge summaries. Additional information obtained via chart review included ethnicity, comorbidities, which were defined using the age-adjusted Charlson comorbidity index (ACCI), smoking status, hypothyroidism, previously diagnosed gout and nephrolithiasis, spine surgery history, pre-operative epidural steroid injections, pre- and 3-month post-op neurologic deficits, and long-term pain management.

Statistical analysis was performed using SPSS 28.0.1 (IBM, Armonk, NY). Our sample was one of the convenience, including all patients with pathologic evidence of lumbar pseudogout and eligible matched non-CPPD patients. Univariate statistical comparisons were performed using unpaired Student’st test or Fisher’s exact test as indicated, with P < 0.05 considered statistically significant. Patient factors independently associated with CPPD were identified using a step-wise multivariate logistic regression. Additional step-wise multivariate logistic regressions including both patient and surgical factors were performed to identify independent associations with 90-day reoperations, 90-day readmissions, durotomies, chronic pain/opioid utilization, and 3-month post-operative motor deficits. Data are written as mean ± standard deviation and percentages for univariate comparisons, and odds ratio (95% confidence interval) for the regressions.

Results

A total of 139 patients were diagnosed with CPPD based on operative pathology and were propensity-matched with 139 patients without a CPPD diagnosis. After screening, six patients in the matched cohort were excluded due to inappropriate surgical coding (n = 4) and unavailable clinical and surgical records (n = 2), leaving a final non-CPPD sample of 133 patients. Mean follow-up was 3.7 ± 3.4 years.

Patient demographics, including age, sex, BMI, and comorbidities, for the CPPD cohort are compared in Table 1. Age, sex, and BMI were equivalent, confirming the propensity match. The CPPD group was 97.8% white, with 1 black, 1 Hispanic, and 1 Asian patient each (1/139, 0.7% each), a diversity that was equivalent to the matched group (94.7% white, P = 0.2). The ACCI equivalent between groups (4.4 ± 2.0 in the CPPD group vs 4.3 ± 2.0 in the non-CPPD group, P = 0.9) and the proportion of patients who were either ASA III or IV in both groups were also equivalent (58/139, 41.7% with CPPD vs 47/133, 35.3% without CPPD, P = 0.3). Rates of smoking and nephrolithiasis were equivalent. A significantly larger number of patients with CPPD had a prior epidural steroid injection (108/139, 77.7% vs 84/133, 63.2% in controls, P = 0.0003).

Table 1.

CPPD vs Non-CPPD Cohort Comparison.

	CPPD (n = 139)	Non-CPPD (n = 133)	P-Value
Demographics
Age (years)	68.4 ± 10.7	67.2 ± 11.5	0.4
Sex (% female)	49.6% (69/139)	57.1% (76/133)	0.2
BMI	28.9 ± 6.1	29.2 ± 5.1	0.9
Ethnicity (% white)	97.8% (136/139)	94.7% (126/133)	0.2
ACCI	4.4 ± 2.0	4.3 ± 2.0	0.9
ASA III or IV	41.7% (58/139)	35.3% (47/133)	0.3
Active smoker	14.4% (20/139)	9.0% (12/133)	0.2
Hypothyroid	15.1% (21/139)	25.6% (34/133)	*0.04
Nephrolithiasis	5.0% (7/139)	10.5% (14/133)	0.1
Gout diagnosed outside of the spine	8.6% (12/139)	6.8% (9/133)
Pre-op motor deficit	32.3% (45/139)	27.1% (36/133)	0.2
History of a prior epidural steroid injection	77.7% (108/139)	63.2% (84/133)	* 0.0003
Surgical characteristics
Revision procedure	25.9% (36/139)	26.3% (35/133)	>0.99
Interbody placement	12.2% (17/139)	15.0% (20/133)	0.6
Surgical levels	2.3 ± 1.7	2.1 ± 1.3	0.09
Post-operative outcomes
3-month post-op motor deficit	16.5% (23/139)	8.3% (10/133)	*0.03
Chronic opioid/pain clinic	28.1% (39/139)	20.3% (27/133)	0.2
Durotomy	19.4% (27/139)	9.8% (13/133)	*0.03
90-day return to OR	9.4% (13/139)	4.5% (6/133)	0.2
90-day all-cause readmission	15.8% (22/139)	10.5% (14/133)	0.3

The number of revision procedures, interbody placements, and decompressed levels were equivalent between groups. Patients with CPPD had a significantly higher incidence of dural tears (27/139, 19.4% of CPPD vs 13/133, 9.8% of non-CPPD, P = 0.03), but equivalent 90-day reoperations (13/139, 9.4% vs 6/133, 4.5% without CPPD, P = 0.2) and all-cause readmission rates (22/139, 15.8% with CPPD vs 14/133, 10.5% without CPPD, P = 0.3). There was no difference in the incidence of surgical site infections between groups (5/139, 3.6% with CPPD vs 4/133, 3.0% without CPPD, P > 0.99). While pre-operative motor weakness was equivalent between groups, a higher proportion of patients with CPPD had motor deficits 3-month post-operatively (23/139, 16.5% vs 10/133, 7.5% without CPPD, P = 0.03). Table 2 shows the indications for a 90-day reoperation in the CPPD group.

Table 2.

Indications for a Return to the OR in the CPPD Group.

Indication	Number of Patients (n = 14 Total)
Recurrent disc herniation	1
Dural tear drain or repair	3
Infection/wound complication	6
Malpositioned hardware	1
Persistent radiculopathy	2
Epidural hematoma	1

When analyzed using multivariate logistic regression, pre-operative predictors of CPPD were active smoking (OR 3.1, 95% CI 1.3 to 7.6) and a prior epidural steroid injection (OR 2.5, 95% CI 1.4 to 4.3). Hypothyroidism was negatively predictive of CPPD (OR 0.5, 95% CI 0.3 to 0.9). Independent predictors of durotomy were CPPD (OR 2.2, 9.5% CI 1.1 to 4.5), increasing ACCI (OR 1.2, 95% CI 1.002 to 1.5), and a larger number of surgical levels (OR 1.4, 95% CI 1.1 to 1.8). Fewer dural tears occurred in patients who underwent interbody procedures (transforaminal or posterior lumbar interbody fusions) (OR 0.7, 95% CI 0.008 to 0.5). Predictors of 3-month post-operative motor deficits were pre-operative deficits (OR 13.5, 95% CI 5.1 to 35.7), a larger number of surgical levels (OR 1.4, 95% CI 1.01 to 1.8), and male sex (OR 2.6, 95% CI 1.1 to 6.2). Chronic pain/opioid utilization was associated with smoking (OR 3.0, 95% CI 1.3 to 7.1), revision surgery (OR 2.3, 95% CI 1.3 to 4.3), a prior epidural injection (OR 2.2, 95% CI 1.1 to 4.5), and increased BMI (OR 1.1, 95% CI 1.03 to 1.1). Non-white ethnicity was associated with a 90-day readmission (OR 4.6, 95% CI 1.4 to 14.8), and a prior epidural steroid injection was associated with a lower likelihood of a 90-day return to the OR (OR 0.4, 95% CI 0.2 to 1.0).

Discussion

CPPD is a crystalline deposition disease that affects both the axial and appendicular anatomy. In a matched cohort analysis of patients who underwent open lumbar decompressions over a 20-year period, smoking and a prior epidural steroid injection were independently associated with biopsy-proven CPPD of the lumbar spine, which in turn was independently associated with an intraoperative dural tear. Findings suggest that CPPD as a systemic disease can have a clinically consequential impact on spine surgery outcomes.

With a clinical presentation that commonly overlaps with that of osteoarthritis and the need for non-routine pathologic confirmation,²¹ CPPD of the spine is likely to be underdiagnosed. Consequently, the current body of literature describing CPPD of the spine largely consists of case reports and small case series. Moshrif et al¹⁷ in their series of 152 patients with CPPD diagnosed anywhere in the skeleton reported that 37/152 (24.3%) of CPPD diagnoses were in the spine, with a roughly even distribution between the lumbar and cervical spine. Manifestations of CPPD of the spine in their series included pain and inflammation, destructive arthropathy, and MRI features consistent with discitis. Additional reported spinal pathology attributed to CPPD included pseudotumor formation causing myelopathy or cervicomedullary compression^22,27 and recurrent sterile fluid collections in the lumbar spine.¹¹ The most common manifestation of CPPD in the present work was the presence of white, tophaceous, calcified deposits within the ligamentum flavum and facet joints. This material is similar visually to what would be expected in patients who have had a prior epidural steroid injection, which likely explains why a steroid injection was associated with CPPD. In addition to the surgical challenge posed by these deposits, tophaceous deposits may represent rapid clinical symptom progression. Cabre et al² in their series of 6 patients who underwent posterior decompression for cervical myelopathy due to a calcified ligamentum flavum of the cervical spine noted that symptom onset was rapid (within 6 months) and that all patients had severe motor dysfunction at the time of surgery. Rapid symptom progression in the setting of CPPD of the cervical spine has been repeatedly noted.^14,16 However, symptom progression was not observed by Ariyawatkul et al¹ in their comparative study of patients with vs without CPPD of the lumbar spine, although their sample sizes were very small (18 CPPD patients vs 16 non-CPPD). While we did not observe a markedly larger number of short-term reoperations due to continued stenosis, this work was not able to compare long-term reoperation rates and indications. Evaluating the potential for minimally invasive or partial laminectomies to definitively treat lumbar stenosis in the setting of CPPD is also required. Systemic control of CPPD may be considered in patients with known appendicular pathology. While causality cannot be shown by the present work, it is possible that CPPD deposits may be avoidable in patients with a previous diagnosis, thereby avoiding complex surgery or the need for a procedure at all. However, such a conjecture requires prospective validation.

A large proportion of the indications for a 90-day return to the OR in the CPPD group were for wound-related complications, including epidural hematomas, deep infections, and dural tears. As our cohorts had equivalent ACCIs, this difference is unlikely to be related to patient comorbidity, although frailty was not evaluated in the present work. However, it is possible that these infections/wound complications are related to a CPPD flare. Kensuke et al¹⁵ reported two cases of patients who underwent irrigation and debridement for a presumed infection after a total knee arthroplasty. Despite clinical and laboratory signs of infections, cultures did not grow but CPPD crystals were discovered.¹⁵ Acute pseudogout flares in the early and late post-operative period have been repeatedly reported after total joint arthroplasty^6,13,24 and anterior cruciate ligament reconstruction.²⁸ A single report of an acute post-operative pseudogout flare following lumbar spine surgery by Ogawa et al¹⁹ described a patient with increased lower back pain and a fluid collection 4 weeks after a transforaminal lumbar interbody fusion. A biopsy was negative for infection, and the patient recovered after conservative management. It is therefore possible that acute pseudogout flares contributed to the reoperation rate of patients with CPPD of the lumbar spine in the present work. However, as George et al¹⁰ reported that CPPD can be coincident with positive cultures in patients with prosthetic joint infections, it is difficult to validate this finding without uniform crystalline testing in a prospective study.

The findings of the present work appear to confirm our hypothesis that CPPD is surgically consequential. Dural adhesions due to invasive tophaceous deposits should be expected and meticulously dissected. We recommend consideration of a wider decompression in those patients in whom CPPD is suspected. It is unclear if a rheumatology consult is beneficial to those patients with pathologic confirmation of CPPD. Multiple works describe the use of colchicine and non-steroidal anti-inflammatory drugs (NSAIDs) in the management of patients with more acute signs of CPPD around the spine, such as sacroiliitis and discitis.¹⁷ Current societal guidelines for the management of CPPD, notably that of the European Alliance of Associations for Rheumatology (EULAR), highlight the unproven nature of any specific treatment for the chronic manifestations of CPPD and the potential for side effects after the long-term use of NSIADs (gastrointestinal bleeding) and colchicine (diarrhea and dyspepsia).³¹ Methotrexate³ and hydroxychloroquine²⁰ were evaluated in clinical trials in the treatment of chronic refractory symptomatic CPPD, but no firm recommendations were made and it is unclear if patients with CPPD of the lumbar spine should be considered to have “chronic, refractory disease.”

There are several limitations to this work beyond those intrinsic to retrospective analyses. First is the nature of the identification of the CPPD patients, which was based on surgeon observation of tophaceous deposits and prior experience with CPPD diagnoses. This work can therefore only report on those with these disease manifestations. If CPPD is in fact more common and tophaceous deposits are more severe disease manifestations, the resulting selection bias would result in an overcalculation of the incidence of dural tears and motor weakness in patients with CPPD. This is particularly important given the way in which CPPD and non-CPPD patients were selected. While CPPD patients were identified via pathologic analysis, non-CPPD patients were randomly selected among those without a CPPD diagnosis. It is not just probable but likely that some in the non-CPPD group actually had CPPD, just without clinical manifestations. Our findings must therefore be validated with a prospective analysis that utilizes sequential and standardized sampling criteria. Second, our matched cohort was derived from operative and diagnosis codes, which may be inconsistently entered and were prone to miscoding due to changes in the diagnosis code system over the study period. This is evidenced by the six patients excluded from the non-CPPD cohort of the present work. Finally, we did not have standardized CT and MRI imaging for all CPPD patients, making it unclear how many of these patients would demonstrate pre-operative evidence of this disease on advanced imaging. Despite these limitations, we believe that our findings strongly indicate the more challenging nature of patients with CPPD of the lumbar spine, meriting further investigation.

Conclusion

In a matched cohort analysis of pathologically confirmed CPPD of the lumbar spine over a 20-year period, CPPD was independently associated with a durotomy. While these observations require confirmation with a prospective sequential cohort analysis, this work presents the largest single institutional cohort of CPPD of the lumbar spine to our knowledge, uniquely permitting early insights into this underdiagnosed pathology.

Footnotes

Ethical Statement

Author Contributions

David O Osei-Hwedieh: Conceptualization, Formal analysis, Methodology, Writing - original draft, Writing - review & editing.

Mitchell Fourman: Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Writing - original draft, Writing - review & editing.

Derrick Williams: Data curation, Investigation, Methodology, Writing - review & editing.

David Shin: Data curation, Formal analysis, Investigation, Writing - review & editing.

Tom de Groot: Investigation, Methodology, Writing - review & editing.

Taikhoom Dahodwala: Investigation, Methodology, Writing - review & editing.

Duncan C Ramsey: Investigation, Methodology, Writing - review & editing.

Joseph H Schwab: Conceptualization, Investigation, Methodology, Project administration, Supervision, Writing - original draft, Writing - review & editing.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The datasets used for the analysis presented in this work can be obtained from the authors upon reasonable request.*

References

Ariyawatkul

Pichaisak

Chavasiri

Vamvanij

Wilartratsami

Luksanapruksa

. The role of calcium pyrophosphate dihydrate deposition in the postoperative outcome of lumbar spinal stenosis patients. Asian Spine J. 2019;13:1001-1009.

Cabre

Pascal-Moussellard

Kaidomar

, et al. Six cases of cervical ligamentum flavum calcification in Blacks in the French West Indies. Jt Bone Spine. 2001;68:158-165.

Chollet-Janin

Finckh

Dudler

Guerne

P-A

. Methotrexate as an alternative therapy for chronic calcium pyrophosphate deposition disease: an exploratory analysis. Arthritis Rheum. 2007;56:688-692.

Chuck

Pattrick

Hamilton

Wilson

Doherty

. Crystal deposition in hypophosphatasia: a reappraisal. Ann Rheum Dis. 1989;48:571-576.

Derfus

Kurian

Butler

, et al. The high prevalence of pathologic calcium crystals in pre-operative knees. J Rheumatol. 2002;29:570-574.

Forlizzi

Ryan

Galow

Shang

Polakoff

. Acute pseudogout presenting as an exception to Musculoskeletal Infection Society criteria in total knee arthroplasty: a case report. AME Case Rep. 2020;4:21.

Fuerst

Bertrand

Lammers

, et al. Calcification of articular cartilage in human osteoarthritis. Arthritis Rheum. 2009;60:2694-2703.

Furusawa

Baba

Maezawa

, et al. Calcium crystal deposition in the ligamentum flavum of the lumbar spine. Clin Exp Rheumatol. 1997;15:641-647.

Geelhoed

Kelly

. Pseudogout as a clue and complication in primary hyperparathyroidism. Surgery. 1989;106:1036-1041.

10.

George

Ernste

Tande

Osmon

Mabry

Berbari

. Clinical presentation, management, and prognosis of pseudogout in joint arthroplasty: a retrospective cohort study. J bone Jt Infect. 2019;4:20-26.

11.

Grobost

Vayssade

Roche

Kemeny

J-L

Soubrier

. Axial calcium pyrophosphate dihydrate deposition disease revealed by recurrent sterile spondylodiscitis and epidural abscess. Jt Bone Spine. 2014;81:180-182.

12.

Guañabens

Mumm

Möller

, et al. Calcific periarthritis as the only clinical manifestation of hypophosphatasia in middle-aged sisters. J bone Miner Res Off J Am Soc Bone Miner Res. 2014;29:929-934.

13.

Hirose

Wright

. Calcium pyrophosphate dihydrate deposition disease (pseudogout) after total knee arthroplasty. J Arthroplast. 2007;22:273-276.

14.

Hugues

Baille

. Compression de la jonction bulbomédullaire, complication rare de la chondrocalcinose. Prat Neurol - FMC. 2021;12:237-241.

15.

Koyama

Ohba

Sato

Haro

. Pseudogout mimicking infection following total knee arthroplasty: a report of two cases. JBJS Case Connect. 2012;2:e3.

16.

Mori

Imai

Nishizawa

Matsusue

. Cervical myelopathy due to calcification of the posterior atlantoaxial membrane associated with generalized articular deposition of calcium pyrophosphate dihydrate: a case report and review of the literature. J Orthop Sci. 2015;20:1136-1141.

17.

Moshrif

Laredo

Bassiouni

, et al. Spinal involvement with calcium pyrophosphate deposition disease in an academic rheumatology center: a series of 37 patients. Semin Arthritis Rheum. 2019;48:1113-1126.

18.

Nalbant

Martinez

JAM

Kitumnuaypong

Clayburne

Sieck

Schumacher

HRJ

. Synovial fluid features and their relations to osteoarthritis severity: new findings from sequential studies. Osteoarthr Cartil. 2003;11:50-54.

19.

Ogawa

Nagatsuma

Kubota

, et al. Acute lumbar spinal pseudogout attack after instrumented surgery. Spine. 2012;37:E1529-E1533.

20.

Rothschild

Yakubov

. Prospective 6-month, double-blind trial of hydroxychloroquine treatment of CPDD. Compr Ther. 1997;23:327-331.

21.

Serling-Boyd

Wallace

Jarolimova

Arvikar

Miloslavsky

. An 80-year-old man with fevers, altered mental status, and joint effusions. Arthritis Care Res. 2020;72:293-300.

22.

Sethi

Garg

Sharma

Ahmad

Sharma

. Cervicomedullary compression secondary to massive calcium pyrophosphate crystal deposition in the atlantoaxial joint with intradural extension and vertebral artery encasement. Surg Neurol. 2007;67:200-203.

23.

Slavin

Wen

Kumar

Evans

. Familial tumoral calcinosis. A clinical, histopathologic, and ultrastructural study with an analysis of its calcifying process and pathogenesis. Am J Surg Pathol. 1993;17:788-802.

24.

Sonsale

Philipson

. Pseudogout after total knee arthroplasty. J Arthroplast. 2007;22:271-272.

25.

Yamakawa

Iwasaki

Masuda

, et al. Cartilage intermediate layer protein expression in calcium pyrophosphate dihydrate crystal deposition disease. J Rheumatol. 2002;29:1746-1753.

26.

Yayama

Kobayashi

Sato

, et al. Calcium pyrophosphate crystal deposition in the ligamentum flavum of degenerated lumbar spine: histopathological and immunohistological findings. Clin Rheumatol. 2008;27:597-604.

27.

Yurube

Iguchi

Kinoshita

Sadamitsu

Kakutani

. Upper cervical compression myelopathy caused by the retro-odontoid pseudotumor with degenerative osteoarthritis and calcium pyrophosphate dihydrate disease: a case report and literature review. Neurospine. 2021;18:903-913.

28.

Zaman

Sabir

Mills

Charalambous

. Pseudogout: a rare cause of acute arthritis following arthroscopic anterior cruciate ligament reconstruction. Knee Surg Relat Res. 2015;27:194-196.

29.

Zeng

Wei

Terkeltaub

, et al. Dose-response relationship between lower serum magnesium level and higher prevalence of knee chondrocalcinosis. Arthritis Res Ther. 2017;19:236.

30.

Zhang

Doherty

Bardin

, et al. European League against Rheumatism recommendations for calcium pyrophosphate deposition. Part I: terminology and diagnosis. Ann Rheum Dis. 2011;70:563-570.

31.

Zhang

Doherty

Pascual

, et al. EULAR recommendations for calcium pyrophosphate deposition. Part II: management. Ann Rheum Dis. 2011;70:571.

Calcium Pyrophosphate Deposition Disease is Independently Associated With a Durotomy During an Open Lumbar Decompression: Results of a Propensity-Matched Cohort Analysis

Abstract

Purpose

Methods

Results

Conclusions

Keywords

Introduction

Methods

Results

Discussion

Conclusion

Footnotes

Ethical Statement

Author Contributions

Funding

Declaration of conflicting interests

Data Availability Statement

References