Forestier Disease

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Original Editors Lisa Pernet

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Search Strategy[edit | edit source]

Databases: Pubmed, web of knowledge, google scholar, science direct 
Search terms: forestier disease, diffuse idiopathic skeletal hyperostosis, treatment DISH, physical therapy DISH, diagnosis diffuse idiopathic skeletal hyperostosis, DISH AND physical therapy, medical managment AND DISH, Forestier disease AND treatment, differential diagnosis DISH, differential diagnosis forestier disease, DISH AND osteoarthritis, DISH AND ankylosing spondylitis.


Search timeline: 15/02/2014- 30/04/2014
 

Definition/Description[edit | edit source]

Forestier disease or diffuse idiopathic skeletal hyperostosis is a condition characterized by thickening, calcification and ossification of soft tissues, mainly ligaments, joint capsules and insertions of muscles and tendons (entheses). Another aspect of the disease is the formation of large, flowing osteophytes due to abnormal bone growth (Mader R 2005(A1), Sarzi-Puttini P 2004(A1), Mader R 2009(A1),Mader R. 2013 (1A)) [1] [2] [3][4]. 


These ossifications are mostly seen in the axial skeleton, of which the thoracic region is the main location (Mader R 2005(A1), Mader R 2002(C), Mader R. 2009 (1A)) [1] [5][6]. Also peripheral entheses may be affected: peripatellar ligaments, Achilles tendon insertion, plantar fascia, shoulders, olecranon and metacarpophalangeal joints (Mader R 2005(A1), Sarzi-Puttini P 2004(A1), Mader R 2009(A1)) [1] [2] [3].


Forestier disease or DISH has also been described by various other names, such as spondylosis hyperostotica, spondylitis ossificans ligamentosa, senile ankylosing hyperostosis, physiological vertebral ligamentous calcification and others (Giles LGF 2001, Artner. 2012(5)) [7][8]. 
 

Clinically relevant anatomy[edit | edit source]

The most common characteristic of DISH is the ossification of the anterior longitudinal ligament of the spine (and various extraspinal ligaments, most commonly in the shoulders, elbows and metacarpophalangeal joints (Sarzi-Puttini P 2004 (1A))[2]. The anterior longitudinal ligament is most affected at the level of the thoracic spine (Sarzi-Puttini P 2004 (1A))[2].

Epidemiology/Etiology[edit | edit source]

Forestier disease (DISH) is most common in the elderly population (>50 years old) and the prevalence increases with age (Mader R 2005(A1), Sarzi-Puttini P 2004(A1), Holton KF 2011 (2B))[1][2] [9]. According to US prevalence estimates, man are more frequently affected (25%) than women (15%) in a population age 50 and older. (Holton KF 2011 (2B), Perlaza 2012 (4))[9][10]

Although the etiology of the disease is not fully understood, studies have already shown that the clinical features are related to the formation of new bone. It is assumed that several metabolic factors affect the onset of the disease (Holton KF 2011(B), Mader R 2002(C), Sarzi-Puttini P 2004(A1), Westerveld LA 2009(C)) [9] [5] [2] [11].

Etiologic / Risk factors associated with various metabolic conditions [1] [2] [3] [11]:
(Mader R 2005(A1), Sarzi-Puttini P 2004(A1), Mader R 2009(A1), Westerveld LA 2009(C))

  • waist circumference
  • BMI / Obesity
  • hyperinsulinemia
  • diabetes mellitus
  • hyperuricemia
  • dyslipidemia
  • hypertension
  • coronary artery disease
  • gout
     

Characteristics/Clinical Presentation[edit | edit source]

DISH is often asymptomatic (Sarzi-Puttini P 2004(A1), Al-Herz A 2008(B)) [2] [12], this is why the diagnosis is usually made on the basis of the radiographic images. Many years the clinical manifestations have been considered as minor and non significant (Olivieri I 2007 (4))[13]. When the disease becomes symptomatic, the main clinical features are pain (not always[14]), stiffness and decreased mobility (ROM) (Sarzi-Puttini P 2004(A1), Olivieri I 2007(D)) [2] [13]. Side-bending is the motion that decreases the most. Apparently the right side of the thoracic spine is more often affected than the left side, the exact cause of it is not found[14].

Possible additional problems/complications can occur when there are calcifications and osteophytes in the cervical and lumbar spine (Mader R 2002(C), Sarzi-Puttini P 2004(A1), Westerveld LA 2009(C), Artner 2012(5)) [5] [2] [11][8]:

  • dysphagia (caused by compression of osteophytes): Dysphagia is often related to DISH. It can occur because of mechanical obstruction or impingment of the osteophytes at the larynx or pharynx (Reuven 2008 (5))[15].
  • oesophagal obstruction
  • hoarseness
  • atlantoaxial subluxation
  • ossification of the posterior longitudinal ligament
  • spinal cord injury
  • dyspnea
  • foreign body sensation
  • neurologic manifestations duo to compression of the spinal cord
  • hypercholesterinemia (resulting in cardiovacular comorbidities)
  • peripheral joint affection

Differential Diagnosis[edit | edit source]

Dish often coexists with osteoarthritis (Mader R 2005(A1), Sarzi-Puttini P 2004(A1), Mader R 2009(A1)) [1] [2] [3]. Although they both occur in the same age group, there are clear differences between the two conditions on which we can make a distinction:  - gender: women (OA) – men (DISH)
                  - affected structure: cartilage (OA) – entheses (DISH)
                  - different peripheral sites (Mader R 2002(C)) [5]  


Both diseases affect the axial skeleton and peripheral entheses (Yagan 1990 (4))[16]. In both disorders similar postural abnormalities can be found as a result of the decrease in spinal mobility. Differential diagnosis is based on radiological features and clinical signs. An important difference is the age at which the diseases start. Ankylosing spondylitis already starts at an earlier age than DISH.

When we compare the symptoms we see some differences:
The symptoms of AS consist of inflammatory back pain and buttock pain, reduced spinal movement, and progressive typical postural abnormalities known as “Bechterew stoop.”
DISH is more considered as a disease with an asymptomatic course or with mild dorsolumbar pain and/or some restriction of spinal motion (Olivieri 2013 (5)[17].

DISH patients have a higher chance to report a past history of upper extremity pain, medial epicondylitis of the elbow, enthesitis of the patella or heel, or dysphagia than spondylosis patients (Mata 1997 (3B))[18].

Diagnostic Procedures[edit | edit source]

Because of the absence of validated diagnostic criteria, different sets of classifications criteria are commonly used (Reuven 2008 (5))[15]. The diagnosis of DISH is based on radiological findings, defined by Resnick and Niwayana. This allows a differentiation of the entity towards ankylosing spondylitis (Artner 2012 (5))[8]. According to this definition, the presence of flowing calcifications and ossifications mainly along the anterolateral aspect (anterior longitudinal ligament) of at least 4 contiguous vertebrae (across 3 intervertebral disc spaces) with preserved disc height is indicative of the condition (Mader R 2005 (A1), Holton KF 2011 (B), Sarzi-Puttini P 2004(A1), Olivieri I 2007(D)) [1] [9] [2] [13]. According to Resnick and Niwayana, absence of apophyseal joints or sacroiliac inflammatory changes is the last criteria (Reuven 2008 (5))[15].Sometimes the ossification of the anterior longitudinal ligament can be associated with the ossification of the posterior longitudinal ligament or the calcification of the ligamentum flavum. It occurs often in different spinal regions (Artner. 2012 (5))[8].

When a patient meets these criteria, one can use the classification system established by Mata (1998). With this scoring system the amount of ossification of each vertebral level and the degree of bridging of the disc space can be assessed (Holton KF 2011 (B)) [9]. 


Mata scoring system:

  • 0: no ossification
  • 1: ossification without bridging
  • 2: ossification with incomplete bridging
  • 3: ossification with complete bridging


Whereas conventional radiography can only be used for the diagnosis of DISH, CT and MRI can be used to detect complications associated with the disease (Sarzi-Puttini P 2004(A1)) [2].

Outcome Measures[edit | edit source]

  • Measurements of spinal mobility (Olivieri I 2007(D)) [13]: - schöber test
                                                                                        - finger-to-floor distance
                                                                                        - lumbar lateral flexion
                                                                                        - chest expansion
                                                                                        - occiput-to-wall distance
                                                                                        - flexion and extension of the cervical spine

Examination[edit | edit source]

Radiography of the thoracic and lumbar spine is the single most useful imaging modality in the diagnosis of DISH. Computed tomography (CT) scanning can be used to evaluate complications, such as fracture, or symptoms that can be caused by pressure effects on the trachea, esophagus, and veins. Bone scanning and magnetic resonance imaging (MRI) are also used but they do not play a significant role in the diagnosis of DISH (Baraliakos 2011 (2B), Cammisa 1998 (5))[19][20].

Medical management[edit | edit source]

The management of DISH consist primarily of a conservative approach such as symptomatic therapy (Artner 2012 (5)[8] , if this is not effective, surgery is often the only remaining option (Sarzi-Puttini P 2004(A1)) [2]. Surgery is rarely used, except in cases where nerve roots or the spine are compressed because of the extra bone growth. Symptoms of difficulty with swallowing can be decreased by taking out the spurs trough surgery[14].Only few therapeutic interventions have been described for DISH, because this disease is often seen as a part of osteoarthritis. Currently, people often assume that most treatments for OA can also be useful for the treatment of DISH (Mader R 2005 (A1)) [1].


Main treatment goals (Mader R 2005 (A1)) [1]: - reduce pain and stiffness
                                                                       - prevent, retard or arrest progression 
                                                                       - treatment of associated metabolic disorders
                                                                       - prevent complications  

Several therapeutic modalities can be used to reduce pain, including both medical and physical therapy treatments. The medical aspect, mainly includes the use of NSAIDs (nonsteroidal anti-inflammatory drugs) and mild analgesics and occasionally, in severely symptomatic cases, local corticosteroid injections (Mader R 2005 (A1), Sarzi-Puttini P 2004(A1), Al-Herz A 2008(2B)) [1] [2] [12]. Local heat can be used to reduce pain temporary (Mader R 2005 (A1), Al-Herz A 2008(B)) [1] [12]. 


To treat the painful disorders of the spine (or extremity) joints, several therapeutic modalities can be used. The medical treatment includes the use of NSAIDs (nonsteroidal anti-inflammatory drugs) and mils analgesics and occasionally, in severely symptomatic cases, local corticosteroid injections (Mader R 2005 (1A), Sarzi-Puttini P 2004(1A), Al-Herz A 2008(2B), Artner 2012 (5)) [1][2][12][8] Several studies also recommend local heat to reduce the pain temporary of the affected joint sections. The complaints can also be postively influenced by wearing appropriate bandages or by local injection treatment with anesthetic and cortisone additive. (Artner. 2012 (5))[8].

Since it is believed that DISH is related to several metabolic diseases (eg, diabetes mellitus, obesity, hyperuricemia, hypertension, coronary heart disease…) and risk factors, one will also have to intervene on these disorders. Many of these factors are in turn related to obesity, so as a physiotherapist one must encourage patients to adopt a healthier, active lifestyle and thus promote weight loss. Moreover, light aerobic activity leads to reduced pain and stiffness (Mader R 2005 (A1), Artner 2012 (5)) [1][8].
 

Physical Therapy Management[edit | edit source]

If DISH is symptomatic, there are often complaints of stiffness that can lead to limitations of movement of the spine. In this case, it is useful to add stretching and mobility exercises to the rehabilitation program to maintain or regain range of motion (Al-Herz A 2008(B))[12]. Regular exercises such as walking can also be recommended for the stifness and pain[14]. Currently there is a lack of specific therapeutic interventions but correction of the associated metabolic derangements seems to have a positive effect and is therefore recommended (Reuven 2008 (5), Artner 2012 (5))[15][8].

Many of the metabolic and cardiovascular complications of factors can be related to obesity. The physiotherapist must encourage the patients to adopt a healthier, active lifestyle and thus promote weight loss. Aerobic activity also leads to reduced pain and stifness. (Mader R 2005 (1A), Artner 2012 (5))[1][8]. 
If surgery has been done physical therapy will help you to return to your normal activities. The therapy after surgery is similar to the conservative treatment and includes stretching, increasing range of motion, walking,... Repeat examination and imaging studies will be done to evaluate the progression[14].

Key Research[edit | edit source]

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References[edit | edit source]

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  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 Mader R, Current therapeutic options in the management of diffuse idiopathic skeletal hyperostosis. Expert Opinion Pharmacother 2005, 6(8): p.1313-1318 (level A1)
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 Sarzi-Puttini P, New developments in our understanding of DISH. Curr Opin Rheumatol 2004, vol.16: p.287-292 (level A1)
  3. ↑ 3.0 3.1 3.2 3.3 Mader R, Sarzi-Puttini P, Extraspinal manifestations of diffuse idiopathic skeletal hyperostosis. Rheumatology 2009, 48: p.1478-1481 (level A1)
  4. ↑ Mader R., Verlaan J., Buskila D., Diffuse idiopathic skeletal hyperostosis: clinical features and pathogenic mechanisms., Nat Rev Rheumatol., 2013, 9(12):741-50 (level 1A)
  5. ↑ 5.0 5.1 5.2 5.3 Mader R, Clinical manifestations of diffuse idiopathic skeletal hyperostosis of the cervical spine. Semin Arthritis Rheum 2002, vol 32, no 2, p.130-135 (level C)
  6. ↑ Mader R., Novofestovski I, Adawi M., Lavi I, , Metabolic Syndrome and Cardiovascular Risk in Patients with Diffuse Idiopathic Skeletal Hyperostosis., Semin Arthritis Rheum, 38 (2009), pp. 361–365 (Level of evidence: 2B)
  7. ↑ Giles LGF, Singer KP, Vol.3: Clinical anatomy and management of cervical spine pain. Butterworth Heinemann, 2001, second edition, p.103-104
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9 Artner J., Leucht F., Cakir B., Reichel H., Lattig F., Diffuse idiopathic skeletal hyperostosis: current apsects of diagnostics and therapy., 2012, Orthopade. 2012 Nov;41(11):916-22 (Level of evidence: 5)
  9. ↑ 9.0 9.1 9.2 9.3 9.4 Holton KF, Diffuse idiopathic skeletal hyperostosis and its relation to back pain among older men: the MrOS Study. Semin Arthritis Rheum 2011, Mar. 3 [Epub ahead of print] (level B)
  10. ↑ PERLAZA, N. A. Diffuse idiopathic skeletal hyperostosis of cervical column: a clinical anatomy and functional approach. Int. J. Morphol., 30(2):499-503, 2012. (Level 4)
  11. ↑ 11.0 11.1 11.2 Westerveld LA, Spinal fractures in patients with ankylosing spinal disorders: a systematic review of the literature on treatment, neurological status and complications. Eur Spine J 2009, vol.18: p.145-156 (level C)
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 Al-Herz A, Exercise therapy for patients with diffuse idiopathic skeletal hyperostosis. Rheumatol 2008, 27: p.207-210 (level B)
  13. ↑ 13.0 13.1 13.2 13.3 13.4 Olivieri I, Diffuse Idiopathic skeletal hyperostosis may give the typical postural abnormalities of advanced ankylosing spondylitis. Rheumatology 2007, vol.46: p. 1709-1711 (level D)
  14. ↑ 14.0 14.1 14.2 14.3 14.4 The methodist hospital system, methodist orthopedics, a patient’s guide to diffuse idiopathic skeletal hyperostosis (DISH), 2006 (Level of evidence: 5)
  15. ↑ 15.0 15.1 15.2 15.3 Reuven M., diffuse idiopathic skeletal hyperostosis: time for a change, The journal of Rheumatology 2008, 35:3, 377-379 (Level of evidence: 5)
  16. ↑ Yagan R, Khan M., Confusion of roentgenographic differential diagnosis in ankylosing hyperostosis (Forestier’s disease) and ankylosing spondylitis, Khanma, Ankylosingspondylitis and related spondyloarthropathie, Spine: state of the art review, Vol 4, Philadelphia: Haley & Belfus, 1990:561-75 (Level of evidence: 4)
  17. ↑ Olivieri I, Salvatore, Palazzi C., Padula A., 2013, Spondyloarthritis and diffuse idiopathic skeletal hyperostosis: two different diseases that continue to intersect. J Rheumatol. (Level of evidence: 5)
  18. ↑ Mata S., Fortin P., Fitzcharles M., Starr M., Joseph L., Watts C., Gore B., Rosenberg E., Chhem R., Esdaile J., 1997 A controlled study of diffuse idiopathic skeletal hyperostosis. Clinical features and functional status. (Level of evidence:3B)
  19. ↑ Baraliakos X, Listing J., Buschmann J., Comparing new bone formation in ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis patients- a retrospective cohort study over 6 years, 2011, Arthritis Rheum (Level of evidence: 2B)
  20. ↑ Cammisa M, De Serio A., Guglielmi G., Diffuse idiopathic skeletal hyperostosis, Eur J Radiol. 1998 MAY; 1:S7-11 (Level of evidence : 5)
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