Primary Care Diabetes 17 (2023) 548–553

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Primary Care Diabetes

journal homepage: www.journals.elsevier.com/primary-care-diabetes

Diabetes mellitus-related musculoskeletal disorders: Unveiling the cluster

of diseases
Viktória Csonka a, Cecília Varjú b, Marcell Lendvay b, 1, *
a
Department of Rheumatology, Somogy County Kaposi Mór Teaching Hospital, Kaposvár, Hungary
b
Department of Rheumatology and Immunology, Medical School, University of Pécs, Pécs, Hungary

A R T I C L E I N F O A B S T R A C T

Keywords: The current study ushers in a comprehensive review in clinical research to demonstrate the prevalence of
Diabetes mellitus musculoskeletal (MSK) complications in diabetes mellitus and the most relevant clinical aspects. In particular,
Musculoskeletal revealing the early symptoms of the disorders, the pathology lurking behind the complications and their optimal
Prevalence of musculoskeletal complications
management. In diabetes mellitus, MSK complications are common and are largely due to similar pathogenetic
Advanced glycation end products
Diabetic foot
factors responsible for the internal organ complications associated with diabetes leading to chronic low-intensity
inflammatory processes. MSK disorders develop by vasculopathy, neuropathy, arthropathy or combinations of
the above, which are not specific to diabetes. However, their prevalence is significantly increased in diabetes and
contributes to the disability impairing patients’ quality of life. Locomotor disease affects approximately
34.4–83.5 % of patients suffering from type-2 diabetes mellitus. Several musculoskeletal abnormalities (cheir­
oarthropathy, Dupuytren’s contracture, trigger finger, ect.) can be diagnosed upon physical examination,
although certain symptoms (frozen shoulder, neurogenic arthropathy, septic arthritis, etc.) require differential
diagnostic considerations. Early identification regarding characteristic symptoms in the treatment reducing
inflammation and pain, followed with increasingly strenuous exercise therapy, aligned with optimal manage­
ment of carbohydrate metabolism, proves essential in alleviating MSK complications.

1. Introduction 1.1. The prevalence of MSK complications

Diabetes mellitus (DM) is a complex metabolic disorder, in which the
carbohydrate metabolism is the most deteriorated pathway. Absolute
(Type-1, T1DM) or relative (Type-2, T2DM) lack of insulin is crucial in
the development of the disease [1].
Globally, the prevalence of diabetes mellitus among 20–79-year-
olds, according to the International Diabetes Federation , current as of
2021, was estimated to be 10.5 % (535 million individuals) [2].
The prevalence and the life expectancy of patients afflicted with DM
are on the increase in recent years, resulting in the increased occurrence
of DM-related and quality-of-life diminishing musculoskeletal (MSK)
complications.
In this review, we aim to depict the prevalence of MSK complica­
tions, the most important clinical aspects, emphasizing early signs and
optimal management of the disorders and the pathology lurking behind
the representative MSK manifestations in DM.
Admittedly there are not a plethora of studies thoroughly investi­
gating the MSK condition of patients afflicted with DM. According to a
Danish study, the prevalence of MSK pain was significantly increased
(1.7–2.1-times) in patients suffering from T2DM when compared to in­
dividuals without diabetes. The pain was associated with a high body
mass index (BMI), reduced test results of the health-related quality of life
(HRQoL) and physical capability [3]. Majjad et al. [4] measured the
prevalence of MSK complications in 376 subjects with DM. MSK disor­
ders occurred more frequently in T2DM individuals when contrasted
T1DM (37.4 %, versus 17.2 %). The median age of the participants was
54 years of age. Notably, 34.4 % (129 individuals) suffered from at least
one MSK disorder. Osteoarthritis (OA) was the most common disorder,
seen in 19.4 % (73 individuals). Shoulder capsulitis appeared in 12.5 %.
Carpal tunnel syndrome (CTS) was present in 33 subjects (8.8 %). Fe­
male gender, obesity, above 50 years of age and nephropathy were
associated with increased odds of OA. In this study, haemoglobin A1c

* Corresponding author at: Department of Rheumatology and Immunology, Medical School, University of Pécs, Akác utca 1., Pécs H-7632, Hungary.
E-mail address: lendvay.marcell@pte.hu (M. Lendvay).
1
ORCID iD: https://orcid.org/0000-0001-6684-0924

https://doi.org/10.1016/j.pcd.2023.08.003

Available online 27 August 2023

1751-9918/© 2023 The Authors. Published by Elsevier Ltd on behalf of Primary Care Diabetes Europe. This is an open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/).
V. Csonka et al.
Scleredema of Bushke
Adhesive capsulitis
of the shoulder
Osteoporosis
Diffuse idiopathic
skeletal hyperostosis
Diabetic hand
(Cheiroarthropathy,
Trigger finger,
Dupuytren's contracture,
Carpal tunnel syndrome)
Osteoarthritis
Diabetic foot
Fig. 1. Common musculoskeletal complications of diabetes mellitus.
(HgA1c) levels did not seemingly appear to be associated with the
development of MSK disorders [4].
Abourrazzak et al. [5] classified the MSK manifestations of 116 pa­
tients suffering from T2DM into articular and extraarticular subgroups.
OA of the knee ranks as the most frequent complication (49 %). The most
common extraarticular rheumatological manifestations include the
following: CTS (29 %), adhesive capsulitis of the shoulders (23 %) and
hand contractures (cheiroarthropathy) (16 %). A significant association
was demonstrated between vascular complications (mainly in patients
suffering from retinopathy) and the development of extraarticular
manifestations, such as CTS (p < 0.0001) and Dupuytren’s contracture
(p = 0.01), whereas diabetic neuropathy was associated with the
expanding occurrence of adhesive capsulitis of the shoulder (p = 0.004).
Ramchurn et al. [6] in a cross-sectional study compiled a group of 96
individuals with established diabetes and examined these subjects for
the presence of locomotor disease affecting the upper limbs and
revealed, MSK disease was present in 75 % of the patients. Shoulder
adhesive capsulitis (25 %), tenosynovitis (29 %), and limited joint
mobility (28 %) were the most common manifestations and appeared
more frequently when compared with the control group. In this study
adhesive capsulitis coincided with other upper limb abnormalities and
substantially predicted the presence of retinopathy and/or neuropathy:
microvascular complications in individuals suffering from upper ex­
tremity manifestations were present in 75 %, whereas in patients
without upper limb findings, microvascular complications were only
present in 33 %. The mean HbA1c was significantly higher in patients
with combined shoulder and hand complications (9.1 %) than in those
unaffected by upper limb manifestations (8.0 %) [p = 0.018].
According to an Iranian review, MSK prevalence may be as high as
83.5 % in patients afflicted with T2DM [7].
2. The effects of diabetes mellitus on bone metabolism, joints
and periarticular tissues
Since a wide spectrum of MSK disorders may develop in patients with
DM, linked with metabolic disorders, the underlying pathogenesis is also
multifaceted.
Evidence is expanding in association with the relationship between
carbohydrate metabolic disorder and bone metabolic disorder. In T1DM,
due to the lack of insulin and its consequences, the decreased levels of
insulin-like growth factor (IGF-1) and the insulin-like growth factor-
binding protein 3 (IGFBP-3), differentiation, quantity and function of
osteoblasts diminish, which leads to decreased bone turnover, thus
549
Primary Care Diabetes 17 (2023) 548–553
Cerebrovascular disorders
Retinopathy
Cardiovascular disease
Nephropathy
Peripheral vascular disease
Neuropathy
resulting in apparent osteoporosis. In T2DM, advanced glycation end
products (AGEs) are crucial in the development of bone metabolism
damage and in many other MSK manifestations of DM. [8].
Glycosylation of collagen structures damages the organic matter
diminishing the flexibility of bones. AGEs binding to their receptors
(RAGEs) increases osteoblast apoptosis over the long term and
decreasing differentiation of myeloid stem cells towards developing into
osteoblasts. Inevitably, AGEs induce the receptor expression of osteo­
clasts through receptor activator nuclear factor kappa beta ligands
(RANKL) resulting in increased bone resorption [8,9].
AGEs are heterogeneous molecules originating from non-enzymatic
products of the reaction of glucose or other sugar derivates with pro­
teins or lipids. AGEs accumulate in all tissues ultimately inflicting
damage. AGEs build-up has been confirmed in MSK tissues, including
bones, cartilages, muscles, tendons, ligaments and nerves, in which they
adversely affect biomechanical structures by causing charge changes
and forming collagen cross-linkages. These mechanisms are responsible
for a variety of ageing and diabetes-related pathological conditions, such
as osteoporosis, OA, sarcopenia, tendinopathy, neuropathy and joint
stiffness [10,11].
Chronic, low-grade inflammatory processes play a pivotal role in the
development of DM complications. AGEs activate RAGE and increase
inflammation through intracellular signal transduction: AGEs stimulate
the transcription of NF-κB, the production of vasoactive factors and
cytokines, such as interleukin-1, − 6 (IL-1, IL-6) and tumour necrosis-
factor-α (TNF α).
Another means of provoking inflammatory processes is referred to as
“meta-inflammation”: notably, the reconstruction of body composition
caused by the overloaded metabolism in a metabolic syndrome, which
is, by definition, the co-existence of obesity, T2DM, dyslipidaemia and
hypertension. The aforementioned inflammatory mechanisms are
crucial both in the development and progression of OA and in upper
limb soft tissue rheumatism.
Adipose tissue, functioning as an endocrine organ, produces bio­
logically active molecules, adipokines (i.e., leptin, resistin and adipo­
nectin) and interacts with endothelial cells, macrophages and
consequently, inflammatory cytokines are produced (IL-1, IL-6, TNF α)
and a low intensity, yet chronic systemic inflammation, is also man­
ifested. Regarding all adipokines, leptin plays the most significant role in
the development of OA, due to its pro-inflammatory and catabolic effect
on cartilage. According to recent studies, resistin is crucial in upper-limb
soft-tissue rheumatism, as seen in rotator-cuff calcific tendinopathy [10,
12] (Fig. 1).
V. Csonka et al.
3. Diabetes mellitus-related MSK disorders
3.1. Diabetes mellitus-related MSK disorders of the upper extremities
DM-related complications regarding the upper limbs primarily affect
periarticular soft tissues. One of the most common disorders is diabetic
cheiroarthropathy, which is the only diabetes-specific manifestation
with a prevalence of 3.5–58 % among patients suffering from DM [13].
Moreover, it is more common in T1DM [4–6,13,14]. Skin thickening and
flexion contracture of the fingers are the main characteristics of the
condition, which is easily recognised by a simple physical gesture, the
"prayer sign", which is the inability to put the palms and fingers
together. Finger rigidity and skin thickening can be explicit, therefore, a
differential diagnosis between scleroderma and diabetic cheiroarthrop­
athy must be accomplished. Diabetic cheiroarthropathy is a hand
function-limiting disorder often aggravated by polyneuropathy, thus
limiting daily activities.
Lesions can also be detected via physical examination including the
trigger finger and Dupuytren’s contracture. A minute difference
compared to individuals without DM, is both lesions are more common
in diabetic females than males and may appear on both hands and on
multiple phalanxes. Scar nodules appear on the palms, resulting in
flexion contracture, due to the shortening of the palmar fascia further
deteriorating hand function [4–6,15,16].
In CTS, the symptoms originate from the compression of the median
nerve. The pain worsens during the night, including the numbness of the
palms and the area of fingers I-III is characteristic of CTS, a lengthy
disease course associated with clumsiness of the hand and thenar atro­
phy. It is challenging to differentiate between numbness caused by CTS
and diabetic polyneuropathy of the hands. In the latter, paraesthesia in a
glove-like localisation is the leading symptom. Multiple clinical tests,
including the Phalen-test, the Tinel sign, provoking CTS symptoms, and
electroneurography (ENG) can be beneficial in the differential diag­
nostic process. Since both disorders are common among individuals
suffering from DM, their concurrence may likely be evident. In such
cases, surgical procedures may ease the symptoms of CTS, as opposed to
polyneuropathy, in which pharmacotherapy is favourable [4–6,17].
Adhesive capsulitis of the shoulder bears a higher prevalence among
patients afflicted with DM, it is more common in females and it is often
bilateral. Periarticular soft tissues of the shoulders inflame, oftentimes
provoked by minor trauma and overexertion. Adhesive capsulitis results
in glenohumeral pain, reduced range of motion (ROM), and pain during
the night disturbing the quality of sleep. Shoulder immobilization, due
to pain, leads to frozen shoulder syndrome. Non-steroidal anti-inflam­
matory drugs, intra-articular corticosteroid injections, and exercises as
soon as possible may prevent the development of frozen shoulder syn­
drome. In the acute stage, abruptly developing shoulder pain in DM
presents a differential diagnostic challenge. In such cases, rotator cuff
injury and potential internal organ damage (for instance, in left-sided
shoulder pain, a cardiac pathology) need to be excluded [4,5,18,19].
3.2. Scleredema adultorum of Bushke
Buschke-type scleredema is a scleroderma-like disease presented in
diabetic patients characterized by firm, non-pitting oedema commonly
developing in the neck, spreading to the shoulders and back. The pro­
gressive form of the disorder may limit the ROM in the shoulders. It is a
misdiagnosed condition, despite the fact it can be detected by simple
palpation [20–22]. In the scleredema population, there was a greater
prevalence of dyslipidaemia, stroke and other venous thromboembolic
events when compared with the diabetic patients without
scleredema-associated skin symptoms [20–23].
3.3. Diabetic amyotrophy and muscle infarction
Diabetic amyotrophy or diabetic lumbosacral radiculoplexus
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Primary Care Diabetes 17 (2023) 548–553
neuropathy (DLRPN) is primarily associated with T2DM, however, the
symptoms are vastly different from the typical diabetic polyneuropathy.
DLRPN is defined by acute, one-sided, proximal, lower-limb pain,
mainly affecting thighs and hips, followed by gradually increasing
weakness and atrophy over the span of several weeks. The underlying
condition is likely due to an immune-mediated inflammatory disorder
leading to ischaemic neuropathy. Differential diagnosis includes spinal
nerve compression, tumour, haemorrhage in the pelvis and diabetic
muscle infarction (DMI) [24,25].
Furthermore, DMI presents as acute pain and swelling of the affected
limb (likely in the lower extremities, yet arises to the upper extremities)
in a circumscribed area, which is a rare angiopathic complication. Dif­
ferential diagnosis of DMI includes trauma and deep vein thrombosis. To
set up the diagnosis, in addition to the typical symptoms and local­
isation, the most necessary imaging tools are soft-tissue ultrasound and
particularly, magnetic resonance imaging . There are no specific labo­
ratory tests supporting the diagnosis and even the creatine kinase levels
remain unchanged in more than half of the cases [26,27].
3.4. The disorders of osteogenesis and bone metabolism: osteoporosis and
DISH
The pathophysiology behind the increased risk of fractures in both
T1DM and T2DM largely differs from one another. In T1DM, the bone
mineral content is decreased, whereas in T2DM, the deterioration of
bone quality dominates. The number of fractures is partially elevated
due to frequent falls, which is aligned with polyneuropathy, encepha­
lopathy and retinopathy. Notably, in T2DM, in which bone mineral
density may show normal or even elevated values, it is important to
determine the disease-specific risks for fracture. Although several clin­
ical trials were conducted to determine the diabetes-specific fracture
risk, as of yet, there is no internationally established method [8,28].
Moreover, medications administered during the treatment of DM
influence bone metabolism. Antidiabetic agents heterogeneously impact
bone metabolism. The thiazolidinediones were confirmed in having a
negative effect on bones. The widely used metformin increases BMD and
improves bone quality. The majority of antidiabetic drugs are neutral for
bone metabolism, yet hypoglycaemic agents may increase the risk of
fractures through increased falls. Currently, individual antidiabetic
medication must be adhered to, considering potential comorbidities and
complications.
Diffuse idiopathic skeletal hyperostosis (DISH, Forestier-disease) is
defined by the ossification of the entheses. Extraosseal calcification
develops, which primarily affects the anterior longitudinal ligament of
the spine. DISH often concurs with metabolic disorders and obesity,
subsequently, DISH is common in T2DM. Spondylosis, ankylosing
spondylitis and other seronegative chronic inflammatory spine diseases
must be ruled out, both clinically and radiologically.
DISH diminishes the QoL, leading to significantly limited ROM,
although inducing less severe pain than the other aforementioned spine
diseases. Currently, no specific therapy yet exist, only symptomatic
treatment is possible [29–32].
3.5. Diabetic foot syndrome (DFS) and osteomyelitis
Arguably, the most severe MSK disorder in relation to DM is osteo­
myelitis. A special type of osteomyelitis is often referred to as “tropical
diabetic hand syndrome” ), which occurs chiefly in developing countries
[33]. Poor glycaemic control, neuropathy, angiopathy, malnutrition,
immune deficiency and the fact certain microorganisms become more
virulent as blood glucose concentration levels surge are all risk factors
for bone infections [34–37].
The most well-known MSK consequence of DM is diabetic foot syn­
drome. The two most important risk factors in the development of foot
ulcers in DM are peripheral vascular disease and peripheral neuropathy
(mainly sensory and autonomic). Sensory neuropathy diminishes the
V. Csonka et al. Primary Care Diabetes 17 (2023) 548–553

Injuries
(Inappropriate footwear, pedicure)

Neuropathy
(Sensory, motor, autonomic)
Infections
(Fungal infections of the nails
and skin, bacterial infections) Angiopathy
(Micro, macro)

Increased susceptibility to infection

(Diabetes secondary immunodeficiency)

Charcot arthropathy
Delayed perception in the process due to sensory neuropathy
Damage to skin continuity
Altered statics new pressure points on the sole

Fig. 2. External and internal factors involved in the development of diabetic foot.

Table 1
The prevalence and early symptoms of musculoskeletal disorders in patients with diabetes mellitus in comparison to the general population.
Prevalence in patients General Differential diagnoses Early symptoms
with DM population

Cheiroarthropathy [4–6,13,14] 3.5–58 % - - Osteoarthritis Reduced ability of the hand’s digital dorsiflexion
- Seronegative polyarthritis, RA,
SLE, SSc
- Flexor tenosynovitis
Dupuytren contracture 0.5–32 % 8–15 % - Clavus Soft nodule development at the palmar folds
[4–6,15] - Neurofibroma
- Tendon nodules
Trigger finger [4–6,16,47] 5–11 % 2–3 % - Suppurative tenosynovitis Painful movement in the MCP joints, mainly in the
- Dupuytren contracture thumb
Carpal tunnel syndrome (CTS) [4–6,17] 8.8—29 % 2% - Cervical radiculopathy Tingling sensation in hands
- Diabetic polyneuropathy
- Brachial plexopathy
Adhesive capsulitis [6, 18, 19] 20 − 40 % 3–5 % - Acromioclavicular arthropathy Movement-evoked or night-time shoulder pain
- Myocardial infarction
- Polymyalgia Rheumatica
Diabetic muscle-infarction Case studies, Case studies - Infection Painful swelling portions of the affected muscle,
[26,27] case reports - Polymyositis most often in the thighs
- Deep vein thrombosis
(Diabetic) Scleredema [20–22] 2.5–14 % No data - Systemic sclerosis Skin thickening of the nape
Diabetic amyotrophy [24,25] 1% Rare, case - Muscular dystrophies Sudden onset of unilateral neurogenic type of pain
studies - Intervertebral disc diseases in the thigh and the hip
-Amyloidosis
Osteoarthritis (OA) 27–52 % 14–34 % - Gout Joint pain upon exertion
[43,44] - RA Hip OA typically begins with groin pain upon
-Septic arthritis exertion
Neurogenic arthropathy [41] 0.1–7 % No data -Tabes dorsalis Typically asymptomatic, although may cause mild
- Syringomyelia foot pain or limping.
- Iatrogenic steroid
Septic arthritis [34,35] Higher risk 4–12/100000 - Osteoarthritis Swollen and tender joint
- Rheumatoid arthritis
- Gout
Osteoporosis [8, 9, 28] T1DM is more common 8–10 % - Tumour (compression vertebral Usually asymptomatic, however, may cause back
fracture) pain
- Osteonecrosis
- Osteoarthritis
Diffuse idiopathic skeletal hyperostosis 10–50 % 1.6–42 % - Ankylosing spondylitis Reduced ability of lumbar anteflexion or presence
(DISH) [29–32] - Spondyloarthropathies of mild low back pain
Diabetic foot ulceration [36–39] 1.5–16.6 % - - Charcot arthropathy Swollen, tender joint, primarily develops in feet
- Peripheral arteriovascular
disease (PAD)

RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; SSc: systemic sclerosis;

551
V. Csonka et al.
individual’s sensory awareness, consequently resulting in the patient
being prone to traumatic falls and unable to recognise the shoe is ill-
fitting. [31,38,39]. (Fig. 2).
Charcot neuroarthropathy of the foot is a non-infectious, progressive
inflammatory condition threatening periarticular soft tissues and bones,
leading to subluxation, dislocation and fracture. Extensive destruction of
the midfoot results in the collapse of the arch, leading to oedematous,
deformed and unstable feet, thus more susceptible to pressure ulcers.
The first line of treatment of Charcot neuroarthropathy is the early
immobilisation in a total contact cast, which reduces inflammation and
bone necrosis by alleviating the pressure on the midfoot. Immobilisation
needs to be continued until oedema resolves and evidence of osseous
consolidation is apparent.
Physicians must distinguish between osteomyelitis and Charcot,
since the treatment of the two conditions is vastly different. In addition
to imaging and laboratory tests, tissue sampling may also be necessary
for differentiation. [40,41].
3.6. Osteoarthritis and DM
Osteoarthritis (OA) and T2DM coincide among the elderly. In studies
assessing the MSK status of diabetic patients, knee OA was found to be
the most common MSK abnormality [4,5]. The presence of DM alone
represents a double risk in developing severe OA requiring total
arthroplasty [42]. In addition to the well-known etiological factors (age,
obesity), DM influences the development of OA through specific meta­
bolic pathways. Hyperglycaemia facilitates the accumulation of AGEs,
damaging the cartilage. Other characteristics, including chronic,
low-intensity inflammation caused by synovitis bears a negative impact
on cartilage metabolism. Hyperglycaemia induces the production of
reactive oxygen species (ROS) laying the foundation for inflammation
and eventually cell degradation and apoptosis [43–45].
In the regimen of T2DM and OA interventions, physical activity and
body weight- control plays a key role. As body weight decreases, the
pressure on weight-bearing joints diminishes. From a varied perspective,
metabolic parameters, such as insulin resistance and dyslipidaemia
enhance, accordingly, the metabolic syndrome-associated low-intensity
inflammatory processes mitigate. Physical activity, beyond its beneficial
metabolic effects, improves mobility and reduces joint stiffness and pain
[43, 44, 46].
Table 1 presents the prevalence and the early symptoms of muscu­
loskeletal disorders compared to the standard population.
4. Management of MSK abnormalities in diabetes
Recognising and managing MSK manifestations are increasingly
important aspects of diabetes care since the underlying disease is more
treatable. The optimal management of carbohydrate metabolism is
essential in the remedy of disorders. In many cases, diabetes is only
brought to attention by the complications, which have already devel­
oped. Among MSK abnormalities, diabetic cheiroarthropathy and
Bushke’s scleredema are considered as diabetes-representative abnor­
malities; therefore, their presence is indicative of DM. Other MSK ab­
normalities in diabetic patients are not diabetes-specific, however, their
prevalence in diabetes is significantly increased and their appearance or
progression may differ from the general population [40,48,49].
Currently, specific therapies in the remedy of MSK complications in
DM do not yet exist. There are only a few opportunities in the treatment
of DM and MSK disorders: proper diet, optimal body weight and
movement-based therapy. The MSK pain in patients suffering from DM is
partially nociceptive: tissue damage develops due to inflammation,
ischaemia, joint capsule tightness, etc., and it is partially neuropathic,
which is the result of direct nerve damage. Prudent anti-inflammatory
pain relief along with physiotherapy may ameliorate the condition. If
required, assistive devices such as resting orthoses, can enhance balance,
relieve pain, improve mobility and serve in reducing the load of the
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Primary Care Diabetes 17 (2023) 548–553
affected limb [50].
In the pharmacotherapy of patients with DM, special aspects need to
be considered. Topical application of non-steroidal anti-inflammatory
drugs (NSAIDs) is preferred over the oral route, since long-term systemic
use increases the risk of renal failure, hypertension and cardiovascular
diseases. Furthermore, diabetic patients are already at higher risk of
developing these abnormalities due to their underlying disease [50].
Following the administration of an intraarticular steroid, blood
glucose levels may spike, hence rigorous glycaemic control may prove
beneficial. An alternative solution may be the intervention of an intra­
articular hyaluronate acid, since it does not elevate blood sugar levels
[46].
Slow Acting Symptomatic Drugs in Osteoarthritis (SYSADOA) may
have a positive chondroprotective effect with a favourable risk/reward
ratio. Oral administration of glucosamine to OA patients was not asso­
ciated with significantly elevated levels of HgbA1c, notwithstanding,
glucosamine is involved in glucose metabolism [46].
Administration of opioid analgesics is associated with an increased
risk of falls, which, in the presence of metabolic osteopathy accompa­
nying diabetes, further increases the risk of fractures. If pain cannot be
relieved by utilising conservative therapy and the loss of function is
significant, surgery may be necessary. The combined pharmacological
and non-pharmacological therapeutic methods are used to preserve
mobility, reduced the number of traumatic falls, improved cardiovas­
cular fitness, mood and HRQoL [38, 41, 47, 51].
5. Conclusions
The prevalence of MSK occurrence in T2DM affects approximately
three to eight out of ten patients. DM is a complex, generalised metabolic
disease, gradually deteriorating all tissues and organs in the body. The
pathogenesis consists of increased non-enzymatic glycation of collagen
fibres, growth in the number of collagen cross-links accumulation and
deposition of AGEs in tissues resulting in chronic low-intensity inflam­
matory processes. The most common complications were determined as
DM-related osteoarthritis, adhesive capsulitis of the shoulder, CTS and
Dupuytren contracture. Early recognition of the symptoms aids towards
a conservative and in the majority of cases, effective treatment of MSK
manifestations.
Funding
Project TKP-2021-EGA-10 has been implemented with the support
provided by the National Research, Development and Innovation Fund
of Hungary, financed under the TKP-2021-EGA funding scheme.
Declaration of Competing Interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influence
the work reported in this paper.
Acknowledgements
We wish to express our sincere gratitude to Jon E. Marquette in
proofreading this manuscript.
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